Desferoxamine
desferoxamine
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- Search all fields for: desferoxamine
- Published in 1966 through 1999
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Documents: 1 to 61 of 61
NLM database Documents
Record 1 from database: MEDLINE
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- Title
- Desferoxamine mesylate (Desferal): a contrast-enhancing agent for gallium-37
imaging.
- Author
- Hoffer PB; Samuel A; Bushberg JT; Thakur M
- Address
-
- Source
- Radiology, 1979 Jun, 131:3, 775-9
- Abstract
- Desferal (desferoxamine mesylate) was investigated as a contrast-enhancing
agent for tumor and abscess imaging with 67Ga-citrate. Tumor studies were
performed in mice with Cloudman S-91 melanoma. Abscess studies were performed
with a subcutaneous abscess model in rabbits. When Desferal is administered 16
to 18 hours after injection of 67Ga, rapid blood clearance of 67 Ga occurs with
only slight (tumor) or no (abscess) loss of activity from the lesion. Retention
in other organs is variable. Tumor-to-blood ratios are improved eightfold in
tumor and fourfold in abscess in studies performed with single Desferal
injections of 150 mg/kg. Blood and total body clearance studies in rabbits
reveal that maximum Desferal effect is achieved in the 17 to 50 mg/kg dose range
and that only minimal improvement occurs at higher doses.
- Language of Publication
- English
- Unique Identifier
- 79180979
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- MeSH Heading (Major)
- Abscess|ME/*RI; Deferoxamine|*AA/BL/ME; Gallium Radioisotopes|*DU/ME;
Melanoma|ME/*RI
- MeSH Heading
- Animal; Drug Interactions; Image Enhancement; Mice; Neoplasms,
Experimental|ME/RI; Rabbits; Time Factors; Tissue Distribution
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0033-8419
- Country of Publication
- UNITED STATES
Record 2 from database: MEDLINE
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- Title
- Antineuroblastoma activity of desferoxamine in human cell lines.
- Author
- Blatt J; Stitely S
- Address
-
- Source
- Cancer Res, 1987 Apr, 47:7, 1749-50
- Abstract
- That ferritin, an iron storage protein, can be produced by neuroblastoma
cells raises the possibility that iron may have some role in promoting tumor
cell growth. To explore this possibility, we studied the effects of
desferoxamine, a compound which chelates iron, on viability of CHP 126 and CHP
100, two human neuroblastoma cell lines. Cells (5 X 10(4)) were incubated with
graded amounts of desferoxamine or ferrioxamine, an iron-saturated analogue of
desferoxamine. Within 5 days of exposure to 60 microM desferoxamine,
approximately 90% of cells from each of these cell lines were dead. This effect
was dose dependent, was not seen with ferrioxamine, and could be prevented by
coincubation with greater than stoichiometric amounts of ferric citrate. As
determined by binding of OK-T9, desferoxamine also resulted in increased
expression of receptors for transferrin, an iron transport protein.
Desferoxamine had only minimal effects on viability of several non-neuroblastoma
cell lines. These results suggest that iron is required for growth of
neuroblastoma and that desferoxamine has potent, specific, antineuroblastoma
activity in vitro.
- Language of Publication
- English
- Unique Identifier
- 87130756
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- MeSH Heading (Major)
- Antineoplastic Agents|*; Deferoxamine|*TO; Neuroblastoma|*PA
- MeSH Heading
- Cell Line; Cell Survival|DE; Human; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0008-5472
- Country of Publication
- UNITED STATES
Record 3 from database: MEDLINE
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- Title
- Effect of iron and desferoxamine on cell growth and in vitro ferritin
synthesis in human hepatoma cell lines.
- Author
- Hann HW; Stahlhut MW; Hann CL
- Address
- Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111.
- Source
- Hepatology, 1990 Apr, 11:4, 566-9
- Abstract
- To investigate the effects of iron supplementation on hepatoma cell growth,
cells from a human hepatoma cell line, PLC/PRF/5, were grown in RPMI 1640
supplemented with 0, 10 and 20 micrograms/ml of FeSO4 and harvested weekly. At
the end of 6 wk culture, cell mass measured 9.6, 14.7 and 13.2 gm, respectively.
Amounts of ferritin from these cell masses were 0 (undetectable), 0.89 and 2.27
micrograms/gm of cells. To study the effects of iron deprivation of hepatoma
cells, three human hepatoma cell lines (PLC/PRF/5, Hep G2 and Hep 3B) were
incubated in tissue culture medium mixed with graded amounts of an
iron-chelating agent, desferoxamine, for 48 to 96 hr at 37 degrees C with 5%
CO2. Over 50% cell death in PLC/PRF/5 cells and 30% to 50% cell death in Hep G2
and Hep 3B cells were observed 48 to 72 hr after exposure to desferoxamine.
Addition of ferric citrate partially reversed the cytotoxic effect of
desferoxamine. On the other hand, viability of control cells, human diploid cell
line (WI 38), was not affected by desferoxamine. Even after 96 hr exposure to
desferoxamine, cell death was only 2% to 4%. These results suggest that (a) iron
enhances tumor cell growth, (b) iron induces increased ferritin synthesis by
tumor cells in vitro and (c) iron depletion causes tumor cell death but has
little effect on normal human diploid cells. These findings should be considered
when designing treatment of patients with hepatoma. Iron oversupply in patients
with cancer might enhance tumor growth and adversely affect cancer therapy. Iron
chelation with desferoxamine might have a place in the treatment of patients
with hepatoma in conjunction with other anticancer agents.
- Language of Publication
- English
- Unique Identifier
- 90228900
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- MeSH Heading (Major)
- Antineoplastic Agents|*; Carcinoma, Hepatocellular|ME/*PA; Deferoxamine|*PD;
Ferritin|*BI; Iron|*PD; Liver Neoplasms|ME/*PA
- MeSH Heading
- Cell Division|DE; Cell Survival|DE; Human; Support, Non-U.S. Gov't; Support,
U.S. Gov't, P.H.S.; Tumor Cells, Cultured|DE/ME/PA
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0270-9139
- Country of Publication
- UNITED STATES
Record 4 from database: MEDLINE
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- Title
- Suppression of delayed type hypersensitivity by desferoxamine.
- Author
- Sahasrabudhe DM; Dusel J; Jedlika S
- Address
- Cancer Center, University of Rochester School of Medicine and Dentistry, New
York.
- Source
- J Immunother, 1991 Apr, 10:2, 112-9
- Abstract
- Desferoxamine, a chelating agent, inhibits proliferation of T cells in
vitro. We reasoned that it may also suppress T-cell-mediated immune responses in
vivo. The effect of desferoxamine on delayed type hypersensitivity reaction to
dinitrofluorobenzene was evaluated in Balb/c mice. We report that desferoxamine
inhibits sensitization and elicitation of skin test reactivity and that the
immunosuppressive effect of desferoxamine is transient. While its mechanism of
action remains to be determined, it may be a potentially useful
immunosuppressive agent.
- Language of Publication
- English
- Unique Identifier
- 91255147
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- MeSH Heading (Major)
- Deferoxamine|AD/*PD; Hypersensitivity, Delayed|*/IM
- MeSH Heading
- Animal; Cell Division|DE; Dinitrofluorobenzene|IM; Ferric Compounds|PD;
Immunosuppression; Mice; Mice, Inbred BALB C; Support, Non-U.S. Gov't; Support,
U.S. Gov't, P.H.S.; T-Lymphocytes|CY/IM
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 1053-8550
- Country of Publication
- UNITED STATES
Record 5 from database: MEDLINE
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- Title
- Determination of desferoxamine and a major metabolite by high-performance
liquid chromatography. Application to the treatment of aluminium-related
disorders.
- Author
- Kruck TP; Kalow W; McLachlan DR
- Address
-
- Source
- J Chromatogr, 1985 May, 341:1, 123-30
- Abstract
- A high-performance liquid chromatography method is described that permits
separation and quantification of desferoxamine, a major metabolite, the
iron(III) and the aluminum(III) chelates of desferoxamine. This method now
facilitates pharmacokinetic studies on desferoxamine and derivatives designed to
study side-effects and metabolite patterns in patients undergoing treatment.
- Language of Publication
- English
- Unique Identifier
- 85261771
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- MeSH Heading (Major)
- Aluminum|BL/*PO; Chelating Agents|BL/*TU; Deferoxamine|*AN/BL/TU/UR
- MeSH Heading
- Alzheimer Disease|BL; Chromatography, High Pressure Liquid; Female; Human;
Kinetics; Middle Age; Spectrophotometry, Ultraviolet; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0021-9673
- Country of Publication
- NETHERLANDS
Record 6 from database: MEDLINE
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- Title
- Altered biodistribution of gallium-67 in a patient with aluminum toxicity
treated with desferoxamine.
- Author
- Brown SJ; Slizofski WJ; Dadparvar S
- Address
- Department of Radiation Oncology and Nuclear Medicine, Hahnemann University
Hospital, Philadelphia, Pennsylvania 19102.
- Source
- J Nucl Med, 1990 Jan, 31:1, 115-7
- Abstract
- Markedly altered biodistribution of [67Ga]citrate was observed in a
66-yr-old hemodialysis patient imaged at 48 hr postinjection. A review of the
patient's hospital records revealed toxic serum levels of aluminum, treated with
the chelating agent desferoxamine. Based on what is known about the biologic
interactions between gallium, aluminum, transferrin, and desferoxamine, we
believe that both toxic serum aluminum levels and desferoxamine therapy may
cause altered biodistribution on [67Ga]citrate scintigraphy.
- Language of Publication
- English
- Unique Identifier
- 90111855
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- MeSH Heading (Major)
- Aluminum|*AE; Citrates|*DU/PK; Deferoxamine|*TU; Gallium Radioisotopes|*DU
- MeSH Heading
- Aged; Case Report; Drug Interactions; Hemodialysis; Human; Kidney Failure,
Chronic|TH; Male; Tissue Distribution
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0161-5505
- Country of Publication
- UNITED STATES
Record 7 from database: MEDLINE
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- Title
- Synthesis of indium-labeled antibody-chelate conjugates for radioassays.
- Author
- Gokce A; Nakamura RM; Tubis M; Wolf W
- Address
-
- Source
- Int J Nucl Med Biol, 1982, 9:2, 85-95
- Abstract
- A method has been developed to achieve rapid and reproducible complexation
of indium to transferrin at pH 7.4. The system consists of nitrilotriacetic acid
(NTA) as the intermediate carrier ligand, whose function is to allow the 113m In
ion, in a solution in Tris buffer, pH 7.4, to be transferred rapidly to the
specific binding sites on transferrin. Just as in the case of iron, this
complexation requires the presence of a synergistic ion such as bicarbonate. The
present system can be used to allow the binding of 113mIn to transferrin when
coupled to an antibody. This method has been tested by studying the conjugation
of an antibody, the IgG fraction of goat anti-rabbit-IgG, with either
transferrin or desferoxamine, using glutaraldehyde as the coupling agent.
Optimization in terms of total protein concentration and glutaraldehyde levels
lead to products where the specific metal binding capacity of the transferrin
moiety remains unchanged, and where the antibody retains 70% of its antigenic
activity. The present system can be considered an extension of the ELISA
techniques and can be used to determine, by a terminal 113mIn labeling
technique, the level of specific binding of an antibody to its antigen.
- Language of Publication
- English
- Unique Identifier
- 82264575
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- MeSH Heading (Major)
- IgG|*; Indium|*DU; Radioisotopes|*DU; Transferrin|*
- MeSH Heading
- Animal; Binding Sites, Antibody; Deferoxamine; Glutaral; Human; Hydrogen-Ion
Concentration; Isotope Labeling; Nitrilotriacetic Acid; Radioimmunoassay;
Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0047-0740
- Country of Publication
- UNITED STATES
Record 8 from database: MEDLINE
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- Title
- Accidental iron poisoning in childhood. Six cases including one fatality.
- Author
- Greenblatt DJ; Allen MD; Kock Weser J
- Address
-
- Source
- Clin Pediatr (Phila), 1976 Sep, 15:9, 835-8
- Abstract
- Between 1962 and 1973, six children were admitted to the Massachusetts
General Hospital because of accidental iron poisoning. Intoxication was
life-threatening in two children whose serum iron concentrations exceeded their
iron binding capacities. One of these patients died despite intensive supportive
care and desferoxamine therapy. Although iron poisoning appears to be relatively
uncommon, it can produce life-threatening and fatal intoxication in children.
- Language of Publication
- English
- Unique Identifier
- 76256275
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- MeSH Heading (Major)
- Iron|BL/*PO/UR
- MeSH Heading
- Case Report; Child, Preschool; Deferoxamine|TU; Female; Heart Arrest|CO;
Human; Infant; Male; Pulmonary Edema|CO; Support, U.S. Gov't, P.H.S.;
Tracheotomy
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0009-9228
- Country of Publication
- UNITED STATES
Record 9 from database: MEDLINE
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- Title
- Low lung capacity and hypoxemia in children with thalassemia major.
- Author
- Cooper DM; Mansell AL; Weiner MA; Berdon WE; Chetty Baktaviziam A; Reid L;
Mellins RB
- Address
-
- Source
- Am Rev Respir Dis, 1980 Apr, 121:4, 639-46
- Abstract
- We evaluated lung function in 17 children with thalassemia major in stable
condition receiving blood transfusions at regular intervals and subcutaneous
desferoxamine daily. Total lung capacity (TLC) was below 2 SD of normal values
for height in 7 of the 17 children and arterialized capillary PO2 was below the
normal range in 15. We studied lung mechanics in 4 children with reduced TLC and
found static and dynamic compliance below 2 SD of normal values for height in 3,
and lung recoil at TLC above normal values and specific upstream conductance
(Gus/TLC) above 2 SD of normal values in all 4. Although these alterations in
lung function have been described in patients with pulmonary fibrosis, we found
no fibrosis in autopsy specimens of lung from 8 other patients with thalassemia.
The rate constant of carbon monoxide diffusion (kCO) was above the predicted
mean in 14 of 15 children. These findings can be explained by a decrease in the
growth of airspace relative to the vascular bed and major airways during
childhood.
- Language of Publication
- English
- Unique Identifier
- 80218412
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- MeSH Heading (Major)
- Anoxemia|*PP; Lung|PA/*PP; Thalassemia|PA/*PP
- MeSH Heading
- Adolescence; Blood Gas Analysis; Child; Esophagus|PP; Human; Lung Volume
Measurements; Maximal Expiratory Flow Rate; Oxygen|BL; Partial Pressure;
Pulmonary Diffusing Capacity; Support, U.S. Gov't, P.H.S.; Total Lung Capacity
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0003-0805
- Country of Publication
- UNITED STATES
Record 10 from database: MEDLINE
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- Title
- Desferoxamine blocks IL 2 receptor expression on human T lymphocytes.
- Author
- Carotenuto P; Pontesilli O; Cambier JC; Hayward AR
- Address
-
- Source
- J Immunol, 1986 Apr, 136:7, 2342-7
- Abstract
- Thymidine uptake by PHA-stimulated human lymphocytes is reduced in the
presence of 100 microM or greater concentrations of the iron-chelating agent
desferoxamine (DF). We assessed expression of IL 2 receptor, 4F2 and Ia
antigens, IL 2 production, and cell cycle progression by blood mononuclear cells
(MNC) stimulated by PHA in the presence or absence of DF to determine whether
the lack of T cell proliferation was a manifestation of inhibition of an earlier
activation event. Tac antigen expression on PHA-stimulated MNC was inhibited by
DF throughout 8 days of culture, and those cells which were positive had a low
density of Tac antigen as compared with controls without DF. Expression of other
activation antigens, 4F2 and Ia, was not impaired by DF. The supernatants of the
DF-containing and control cultures contained equivalent IL 2 activity, as
measured on the HT-2 cell line. Cell cycle analysis of these cultures shows that
the addition of DF at the beginning of culture blocks most cells from undergoing
G0 to G1 transition, whereas later addition of DF arrests the progression of the
T cell blasts through the cell cycle. Separation of cells cultured with PHA and
DF into Tac and Tac- subsets showed that progression from G0 to G1 was
restricted to the former subset. These results suggest that interference with IL
2 receptor expression might contribute to the block in mitogen-induced
proliferation caused by DF.
- Language of Publication
- English
- Unique Identifier
- 86141831
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- MeSH Heading (Major)
- Deferoxamine|*PD; Interleukin-2|BI/*ME; Receptors, Antigen, T-Cell|*DE;
Receptors, Immunologic|*DE; T-Lymphocytes|CL/CY/IM/*ME
- MeSH Heading
- Antigens, Surface|AN; Cell Cycle|DE; Human; Lymphocyte Transformation|DE;
Phenotype; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Thymidine|ME
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0022-1767
- Country of Publication
- UNITED STATES
Record 11 from database: MEDLINE
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- Title
- Transferrin in FRTL5 cells: regulation of its receptor by mitogenic agents
and its role in growth.
- Author
- Lombardi A; Tramontano D; Braverman LE; Ingbar SH
- Address
- Charles A. Dana Research Institute, Beth Israel Hospital, Boston,
Massachusetts.
- Source
- Endocrinology, 1989 Aug, 125:2, 652-8
- Abstract
- Transferrin, a serum iron-binding protein, delivers iron to the cell after
binding to specific receptors on the cell surface and is an important component
of culture medium for virtually all cell lines, including the FRTL5 line of rat
thyroid follicular cells. Therefore, we undertook studies in FRTL5 cells to
examine the regulation of the transferrin receptor, the effects of transferrin
on growth and differentiated functions, and the interactions of transferrin with
several mitogenic pathways. FRTL5 cells possess one class of saturable
transferrin receptors (Ka, 0.7 x 10(9) M-1). Binding of 125I-labeled transferrin
was highest in actively growing cells and declined progressively, reaching
minimal values when confluence was achieved. Removal of transferrin from culture
medium caused a rapid increase in transferrin binding. TSH, acting within 5 min,
induced a modest increase in transferrin binding, due to a
cycloheximide-resistant increase in binding sites. Binding of transferrin after
a 24-h incubation was also increased by other mitogenic agents, (Bu)2cAMP,
forskolin (FK), insulin, insulin-like growth factor-I (IGF-I), and the phorbol
ester TPA. Transferrin alone stimulated growth only minimally, but enhanced the
mitogenic effect of TSH, (Bu)2cAMP, and FK, all of which act through the cAMP
pathway. In contrast, transferrin did not alter the cAMP-independent mitogenic
effects of insulin and IGF-I. Transferrin did not affect TSH-induced cAMP
generation. Desferoxamine, an iron chelator, inhibited the mitogenic effects of
all of the agents tested. Desferoxamine had no significant effect on TSH-induced
cAMP accumulation. We conclude that FRTL5 cells contain saturable receptors for
transferrin whose abundance varies with the rate of cell replication.
Transferrin down-regulates its own receptors, while stimulation of growth by
various mitogens is accompanied by increased binding of transferrin. Transferrin
enhances the mitogenic effect of the cAMP-dependent mitogens, TSH, (Bu)2cAMP,
and FK, without modifying basal or stimulated cAMP generation. In contrast,
transferrin fails to affect the mitogenic responses to IGF-I and insulin, which
are cAMP independent. Iron is required for the mitogenic response to various
mitogens, especially those that are cAMP dependent.
- Language of Publication
- English
- Unique Identifier
- 89325152
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- MeSH Heading (Major)
- Mitogens|*PD; Receptors, Transferrin|*DE/ME; Transferrin|ME/PD/*PH
- MeSH Heading
- Animal; Bucladesine|PD; Cell Differentiation|DE; Cell Division|DE; Cell
Line; Cells, Cultured; Cyclic AMP|ME; Deferoxamine|PD; Insulin|PD; Insulin-Like
Growth Factor I|PD; Rats; Support, U.S. Gov't, P.H.S.; Tetradecanoylphorbol
Acetate|PD; Thyroid Gland|CY/DE/UL; Thyrotropin|PD
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0013-7227
- Country of Publication
- UNITED STATES
Record 12 from database: MEDLINE
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- Title
- Hepatocyte injury resulting from the inhibition of mitochondrial respiration
at low oxygen concentrations involves reductive stress and oxygen activation.
- Author
- Niknahad H; Khan S; OBrien PJ
- Address
- Faculty of Pharmacy, University of Toronto, Ontario, Canada.
- Source
- Chem Biol Interact, 1995 Oct, 98:1, 27-44
- Abstract
- By correlating lactate/pyruvate ratios and ATP levels, cytotoxicity induced
by the mitochondrial respiratory inhibitors or hypoxia:reoxygenation injury can
be attributed not only to ATP depletion but also to reductive stress and oxygen
activation. Thus hypoxia, cyanide or antimycin markedly increases reductive
stress, non-heme Fe release and H2O2 formation in hepatocytes. Cytotoxicity was
partly prevented with the ferric chelator desferoxamine, the xanthine oxidase
inhibitor oxypurinol and the hydrogen peroxide scavenger glutathione. No lipid
peroxidation could be detected and phenolic anti-oxidants had little effect.
However, polyphenolic antioxidants or the superoxide dismutase mimics TEMPO or
TEMPOL partly prevented cytotoxicity. Furthermore, increasing the hepatocyte
NADH/NAD ratio with NADH generating compounds such as ethanol, glycerol, or
beta-hydroxybutyrate markedly increased cytotoxicity (prevented by
desferoxamine) and further increased the intracellular release of non-heme iron.
Cytotoxicity could be prevented by glycolytic substrates (eg. fructose,
dihydroxyacetone, glyceraldehyde) or the NADH utilising substrates acetoacetate
or acetaldehyde which decreased the reductive stress and prevented intracellular
iron release. These results suggest that liver injury resulting from
insufficient respiration involves reductive stress which releases intracellular
Fe, converts xanthine dehydrogenase to xanthine oxidase and causes mitochondrial
oxygen activation. The cell's antioxidant defences are compromised and ATP
catabolism contributes to oxygen activation.
- Language of Publication
- English
- Unique Identifier
- 96080343
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- MeSH Heading (Major)
- Liver|*CY/ME; Mitochondria, Liver|DE/*ME; Oxygen Consumption|*/DE
- MeSH Heading
- Adenosine Triphosphate|ME; Animal; Antimycin A|AA/PD; Antioxidants|PD; Cell
Death|DE; Cell Hypoxia; Cyanides|PD; Ethanol|PD; Hydrogen Peroxide|ME; Iron|ME;
Lactates|ME; Male; NAD|ME; Oxidation-Reduction; Pyruvates|ME; Rats; Rats,
Sprague-Dawley; Reactive Oxygen Species|ME; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0009-2797
- Country of Publication
- IRELAND
Record 13 from database: MEDLINE
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- Title
- Hepatocyte toxicity of mechlorethamine and other alkylating anticancer
drugs. Role of lipid peroxidation.
- Author
- Khan S; Ramwani JJ; OBrien PJ
- Address
- Faculty of Pharmacy, University of Toronto, Ontario, Canada.
- Source
- Biochem Pharmacol, 1992 May, 43:9, 1963-7
- Abstract
- The alkylating anticancer drugs, mechlorethamine (HN2), chlorambucil,
cyclophosphamide, carmustine and lomustine readily induced cytotoxicity in
isolated rat hepatocytes. Hepatocyte glutathione (GSH) was depleted rapidly
following addition of the drugs. Lipid peroxidation ensued following GSH
depletion and before cytotoxicity occurred. Furthermore, cytotoxicity was
delayed by the antioxidants butylated hydroxyanisole (BHA) and alpha-tocopherol,
the ferric iron chelator desferoxamine or the radical trap
4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl (TEMPO) even when added 10 min
later. HN2 was much less toxic to hepatocytes under nitrogen and caused much
less lipid peroxidation than under aerobic conditions. Cytotoxicity induced by
HN2 was also prevented by choline, suggesting that a choline carrier is
responsible for HN2 uptake in the hepatocytes. Various sulfur compounds acted as
antidotes for HN2 cytotoxicity. Thiosulfate was still effective when added 30
min after HN2. Depletion of GSH in the hepatocytes markedly increased their
susceptibility to HN2. However, BHA, desferoxamine or TEMPO protected these
hepatocytes from HN2. This suggests that antioxidants could prove useful in
preventing the increased risk of hepatotoxicity if GSH-depleting agents are used
to overcome tumor resistance to nitrogen mustards.
- Language of Publication
- English
- Unique Identifier
- 92281562
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- MeSH Heading (Major)
- Alkylating Agents|*TO; Lipid Peroxidation|*; Liver|*DE/ME;
Mechlorethamine|AI/*TO
- MeSH Heading
- Animal; Antioxidants|PD; Butylated Hydroxyanisole|PD; Cell Death|DE; Cyclic
N-Oxides|PD; Deferoxamine|PD; Glutathione|ME; Male; Malondialdehyde|AN; Rats;
Rats, Inbred Strains; Vitamin E|PD
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0006-2952
- Country of Publication
- ENGLAND
Record 14 from database: MEDLINE
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- Title
- Conjugated desferoxamine attenuates hepatic microvascular injury following
ischemia/reperfusion.
- Author
- Drugas GT; Paidas CN; Yahanda AM; Ferguson D; Clemens MG
- Address
- Division of Pediatric Surgery, Johns Hopkins University School of Medicine,
Baltimore, MD 21205.
- Source
- Circ Shock, 1991 Jun, 34:2, 278-83
- Abstract
- Iron-dependent oxy radicals have been implicated in reperfusion injury.
Although the iron chelator desferoxamine (DFO) is beneficial, its hemodynamic
effects and short vascular retention limit its use in vivo. We tested whether
DFO conjugated to a high-molecular-weight starch might ameliorate in vivo
hepatic microvascular injury without adverse side effects following 120 min of
ischemia. Prior to reperfusion, conjugated DFO (100 mg/kg), vehicle (Veh), or
saline (I/R) was administered. After 90 min of reperfusion, blood was collected
for serum transaminase determination (ALT; U/liter), and fluorescein-albumin was
injected to label perfused microvessels, which were quantified in frozen
sections by a point-count technique. Tissue edema was estimated by wet to dry
weight ratios (W/D). Reperfusion results in hepatocyte injury (rise in ALT and
W/D) and a 30% loss of perfused microvessels. Intravenous administration of
conjugated DFO produces no significant change in systemic hemodynamics, whereas
both ALT and tissue edema were decreased by approximately 50%. Moreover,
perfused microvessels were restored virtually to nonischemic control levels.
Enhanced perfusion and attenuated cell injury with DFO suggest that
microvascular failure and resultant cell death are mediated, at least in part,
by iron-dependent mechanisms in reperfusion.
- Language of Publication
- English
- Unique Identifier
- 92035373
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- MeSH Heading (Major)
- Deferoxamine|*PD; Liver Circulation|*DE; Starch|*AA
- MeSH Heading
- Animal; Blood Vessels|PA; Ischemia|PA; Male; Microcirculation|DE; Rats;
Rats, Inbred Strains; Reperfusion; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0092-6213
- Country of Publication
- UNITED STATES
Record 15 from database: MEDLINE
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- Title
- Free radicals may contribute to oxidative skeletal muscle fatigue.
- Author
- Barclay JK; Hansel M
- Address
- School of Human Biology, University of Guelph, Ont., Canada.
- Source
- Can J Physiol Pharmacol, 1991 Feb, 69:2, 279-84
- Abstract
- We used mouse soleus in vitro (n = 30) and canine gastrocnemius-plantaris
preparations (n = 20) pump-perfused at the animal's blood pressure to establish
if free radicals contribute to fatigue in oxidative skeletal muscle. The soleus
from each leg contracted for 200 ms (70 Hz) once every minute for 60 min in
Hepes buffer gassed with 100% oxygen at 27 degrees C. When contracting in Hepes
alone, both muscles fatigued at 0.9 mN/mm2.min over the 60 min. The addition of
purines to the bath increased the rate to 1.4 mN/mm2.min and the addition of
xanthine oxidase to generate free radicals increased the rate again to 1.9
mN/mm2.min. Thus free radicals appeared to attenuate oxidative skeletal muscle
function. Each canine muscle contracted isometrically at 4 Hz for 30 min and
then rested for 45 min before contracting for a second 30 min at 4 Hz. In each
experiment, we infused saline at 0.76 mL/min into resting muscle and at 1.91
mL/min during the first contraction period. During the remainder of the
experiment, we infused, at the same rates, saline (n = 4), 10 microM dimethyl
sulfoxide (DMSO) (n = 4) to identify the effect of scavenging hydroxyl radicals,
1 mM allopurinol to establish the effect of blocking xanthine oxidase (n = 4),
or 200 microM desferoxamine to determine the effect of chelating iron (n = 4).
With saline, the fatigue rate over the 30 min of contractions increased from 5.0
0.2 to 6.3 0.5 N/kg.min from the first to the second stimulation period. The
fatigue rate was slower in the second period with each of the three experimental
substances (DMSO, 5.9 0.8 to 3.2 0.3; allopurinol, 7.3 1.1 to 4.6 0.6;
desferoxamine, 6.8 0.8 to 4.4 0.8 N/kg.min). The fatigue rate was the same as
control when DMSO was infused only during the second contraction period.
Therefore, free radicals appeared to contribute to fatigue in oxidative skeletal
muscle.
- Language of Publication
- English
- Unique Identifier
- 91275049
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- MeSH Heading (Major)
- Fatigue|*ME; Muscles|BS/EN/*ME
- MeSH Heading
- Animal; Dogs; Free Radical Scavengers; Free Radicals; Hindlimb|PH; In Vitro;
Isometric Contraction|PH; Mice; Muscle Contraction|PH; Oxidation-Reduction;
Oxygen Consumption|PH; Regional Blood Flow|PH; Xanthine Oxidase|ME
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0008-4212
- Country of Publication
- CANADA
Record 16 from database: MEDLINE
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- Title
- Mechanism of hemoglobin-induced protection against endotoxemia in rats: a
ferritin-independent pathway.
- Author
- Otterbein L; Chin BY; Otterbein SL; Lowe VC; Fessler HE; Choi AM
- Address
- Division of Pulmonary and Critical Care, Johns Hopkins University School of
Medicine, Baltimore, Maryland 21205, USA.
- Source
- Am J Physiol, 1997 Feb, 272:2 Pt 1, L268-75
- Abstract
- Hemoglobin (Hb) induces heme oxygenase-1 (HO-1), which catalyzes the
breakdown of heme to bilirubin, and ferritin. Rats pretreated with Hb have been
shown to survive lethal doses of lipopolysaccharide (LPS; see L. Otterbein, S.
L. Sylvester, and A. M. Choi. Am. J. Respir. Cell Mol. Biol. 13: 595-601, 1995).
The physiological basis of this increased survival and the mechanism(s) involved
in the protection against LPS by Hb are unknown. Here we investigated 1) the
effects of Hb on the hemodynamic and biochemical parameters of LPS-induced
tissue injury and 2) the mechanism(s) by which Hb conferred protection against
shock and tissue injury. Hb-treated rats maintained normal mean arterial blood
pressure, whereas control rats experienced cardiovascular collapse after a
lethal dose of LPS. Hepatic and renal functions, peripheral white blood cells,
serum lactate dehydrogenase, and phosphate also remained normal after LPS in
Hb-treated rats. Hb also attenuated LPS-induced neutrophil alveolitis and tumor
necrosis factor-alpha levels. Pretreatment with both desferoxamine, which, like
ferritin, can bind iron, and with exogenous apoferritin failed to protect
against LPS. In contrast, treatment with Hb plus desferoxamine, which induced
HO-1 but not ferritin, did protect against LPS. Treatment with iron-dextran,
which induced ferritin but not HO-1, did not protect against LPS. We conclude
that Hb pretreatment reduces the inflammatory and physiological consequences of
LPS and that the Hb-induced protection against LPS is dependent on HO-1 and not
ferritin induction.
- Language of Publication
- English
- Unique Identifier
- 97216006
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- MeSH Heading (Major)
- Endotoxemia|*PC/PP; Ferritin|GE/*PH; Hemoglobins|*PD
- MeSH Heading
- Animal; Blood Pressure|DE; Enzyme Induction; Heme Oxygenase
(Decyclizing)|GE/ME; Inflammation|PC/PP; Lipopolysaccharides|PD; Male; Rats;
Rats, Sprague-Dawley; Reference Values; RNA, Messenger|ME; Shock, Septic|MO/PC;
Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Tumor Necrosis Factor|AN
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0002-9513
- Country of Publication
- UNITED STATES
Record 17 from database: MEDLINE
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- Title
- Preparation of 67Ga-labelled human IgG and its Fab fragments using
desferoxamine as chelating agent.
- Author
- Motta Hennessy C; Eccles SA; Dean C; Coghlan G
- Address
-
- Source
- Eur J Nucl Med, 1985, 11:6-7, 240-5
- Abstract
- Human IgG and its Fab fragments were chosen as a model system for studying
the desferoxamine (DF) coupling reaction using glutaraldehyde or carbodiimide at
various concentrations. The labelling of the IgG-DF conjugates with 67Ga proved
to be highly efficient and reproducible. The labelling efficiency in relation to
storage time of the conjugate was analysed over a 1-month period by
Sephadex-G-50 chromatography. Gel-filtration analysis on Sephacryl S-300 showed
that, following the coupling procedure, a high proportion (more than 80%) of the
conjugate remained monomeric. Immunoelectrophoresis on agar plates demonstrated
that the antibody immunoreactivity was preserved. The biodistribution in mice of
the 67Ga-DF-IgG conjugates was comparable to that of the conventional
radiopharmaceutical, 125I-HSA. Conditions were established for the coupling of
DF to two rat IgG2b monoclonal antibodies M10/76 and 11/160, that are specific
for the Hooded rat sarcomata MC 24 and HSN respectively; the immunoreactivity of
these conjugates was tested by a cell-binding assay. The data indicate that
monoclonal-antibody/DF conjugates prepared with the bifunctional reagent
glutaraldehyde maintain their capacity for binding to their tumour-associated
antigens.
- Language of Publication
- English
- Unique Identifier
- 86081879
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- MeSH Heading (Major)
- Antibodies, Monoclonal|*DU; Deferoxamine|*; Gallium Radioisotopes|*/DU;
IgG|*; Immunoglobulins, Fab|*
- MeSH Heading
- Animal; Chelating Agents; Chromatography, Gel; Human; Immunoelectrophoresis;
Isotope Labeling|MT; Mice; Rats
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0340-6997
- Country of Publication
- GERMANY, WEST
Record 18 from database: MEDLINE
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- Title
- Pulmonary clearance of three aerosolized solutes in oleic acid-induced lung
injury.
- Author
- Huchon GJ; Montgomery AB; Lipavsky A; Hoeffel JM; Murray JF
- Address
- UniversitÆe RenÆe Descartes, Clinique de Pneumophtisiologie, HÈopital
LÂaennec, Paris, France.
- Source
- J Appl Physiol, 1988 Mar, 64:3, 1171-8
- Abstract
- We studied the effects of oleic acid (OA) on pulmonary clearance of three
aerosolized radioactive solutes: 99mTc-diethylenetriamine pentaacetate
(99mTc-DTPA), 67Ga-desferoxamine (67Ga-DFOM), and 111In-transferrin (111In-TF).
Either 0.09 ml/kg OA or an equivalent volume of 0.9% NaCl (controls) was
administered intravenously to 48 anesthetized, paralyzed dogs. Each animal
received one aerosolized solute either 60 min after (protocol A) or 30 min
before (protocol B) the infusion of OA or NaCl. In protocol A clearances of all
three solutes were similar in OA and control animals. In contrast, in protocol B
clearances of all three solutes increased significantly during OA infusion;
during the next 60 min clearances of 99mTc-DTPA and 67Ga-DFOM returned to
control values but 111In-TF remained increased. We conclude that 1) in
OA-induced permeability edema pulmonary clearance of aerosolized solutes is
increased when the aerosol is delivered 30 min before but not 60 min after
injury, and 2) increased clearance persists only for large molecules, presumably
because smaller molecules cross injured epithelium quickly and completely. These
phenomena are best explained by a nonhomogeneous distribution of OA-induced
injury.
- Language of Publication
- English
- Unique Identifier
- 88213228
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- MeSH Heading (Major)
- Lung|DE/*ME/RI; Oleic Acids|*PD; Pulmonary Edema|*ME
- MeSH Heading
- Aerosols; Analysis of Variance; Animal; Capillary Permeability; Comparative
Study; Deferoxamine|DU; Dogs; Extracellular Space|ME; Gallium Radioisotopes|DU;
Indium Radioisotopes|DU; Organometallic Compounds|DU; Oxygen|BL; Pentetic
Acid|DU; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Technetium|DU;
Time Factors; Transferrin|DU
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 8750-7587
- Country of Publication
- UNITED STATES
Record 19 from database: MEDLINE
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- Title
- Oxygen consumption in Plasmodium berghei-infected murine red cells: a direct
spectrophotometric assay in intact erythrocytes.
- Author
- Deslauriers R; Moffatt DJ; Smith IC
- Address
-
- Source
- Biochim Biophys Acta, 1986 May, 886:3, 319-26
- Abstract
- A spectrophotometric assay has been devised to measure oxygen consumption
non-invasively in intact murine red cells parasitized by Plasmodium berghei. The
method uses oxyhemoglobin in the erythrocytes both as a source of oxygen and as
an indicator of oxygen consumption. Spectra of intact cells show broad peaks and
sloping baselines due to light-scattering. In order to ascertain the number of
varying components in the 370-450 nm range, the resolution of the spectra was
enhanced using Fourier transforms of the frequency domain spectra. Calculation
of oxygen consumption was carried out for two-component systems (oxyhemoglobin,
deoxyhemoglobin) using absorbances at 415 and 431 nm. Samples prepared from
highly parasitized mice (greater than 80% parasitemia, 5% hematocrit) showed
oxygen consumption rates of (4-8) X 10(-8) microliter/cell per h. This rate was
not attributable to the presence of white cells or reticulocytes. The rate of
oxygen consumption in the erythrocytes is shown to be modulated by various
agents: the respiratory inhibitors NaN3 and KCN (1 mM) reduced oxygen
consumption 2-3-fold; salicylhydroxamic acid (2.5 mM) caused a 20% reduction in
rate and 10 mM NaN3, completely blocked deoxygenation. Antimalarial drugs and
metal-chelating agents were also tested. Chloroquine, EDTA and desferal
(desferoxamine mesylate) did not decrease the deoxygenation rate of hemoglobin
in parasitized cells. Quinacrine, quinine and primaquine reduced the rate of
formation of deoxyhemoglobin but also produced substantial quantities of
methemoglobin. The lipophilic chelator, 5-hydroxyquinoline, decreased the rate
of deoxygenation one-third. The spectrophotometric assay provides a convenient
means to monitor oxygen consumption in parasitized red cells, to test the
effects of various agents thereon, and potentially to explore possible
mechanisms for oxygen utilization.
- Language of Publication
- English
- Unique Identifier
- 86216302
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- MeSH Heading (Major)
- Malaria|*BL; Plasmodium berghei|*ME
- MeSH Heading
- Animal; Antimalarials|PD; Azides|PD; Chelating Agents|PD; Comparative Study;
Erythrocytes|PS; Male; Mice; Oxygen Consumption|DE; Oxyhemoglobins|AN; Potassium
Cyanide|PD; Rats; Spectrophotometry; Time Factors
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0006-3002
- Country of Publication
- NETHERLANDS
Record 20 from database: MEDLINE
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- Title
- Gastric injury induced by ethanol and ischemia-reperfusion in the rat.
Differing roles for lipid peroxidation and oxygen radicals.
- Author
- Smith GS; Mercer DW; Cross JM; Barreto JC; Miller TA
- Address
- Department of Surgery, University of Texas Medical School, USA.
- Source
- Dig Dis Sci, 1996 Jun, 41:6, 1157-64
- Abstract
- This study determined the role that oxygen-derived free radicals played in
the production of gastric injury in rats challenged orally with concentrated
ethanol or subjected to vascular compromise. In the ethanol study, rats were
pretreated with a variety of free radical scavengers or enzyme inhibitors prior
to exposing the stomach to 100% ethanol. At sacrifice, the degree of macroscopic
damage to the glandular gastric mucosa was quantified. In separate studies, the
effects of ethanol on gastric mucosal levels of enaldehydes (malondialdehyde and
4-hydroxynonenal) were examined as an index of lipid peroxidation. Superoxide
dismutase and catalase pretreatment were without benefit in reducing injury in
our ethanol model, excluding potential contributory roles for the superoxide
anion or hydrogen peroxide, respectively. Dimethyl sulfoxide and desferoxamine
were likewise without protective capabilities, eliminating a role for the
hydroxyl radical. Allopurinol, a xanthine oxidase inhibitor, provided no
protection under acute conditions, even though partial protection was noted when
administered chronically. Further, enaldehyde levels were not increased over
control levels in alcohol-exposed mucosa, indicating no enhanced lipid peroxide
formation. In contrast, in animals in which ischemia to the stomach was induced
followed by reperfusion, marked gastric injury was observed in combination with
enhanced enaldehyde levels. Prevention of enaldehyde formation by a
21-aminosteroid concomitantly prevented injury induced by ischemia-reperfusion.
These findings support the conclusion that ischemia-reperfusion injury to the
stomach is an oxygen-derived free radical process whereas ethanol-induced injury
clearly involved some other process. Although allopurinal was partially
protective against ethanol damage when administered chronically, observations in
other models of injury suggest that this action is independent of its inhibitory
effect on xanthine oxidase.
- Language of Publication
- English
- Unique Identifier
- 96258871
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- MeSH Heading (Major)
- Ethanol|*TO; Gastric Mucosa|BS/*DE/ME/*PA; Lipid Peroxidation|*; Reperfusion
Injury|ME/*PA
- MeSH Heading
- Allopurinol|PD; Animal; Antioxidants|PD; Catalase|PD; Deferoxamine|PD;
Dimethyl Sulfoxide|PD; Free Radicals|ME; Pregnatrienes|PD; Rats; Rats,
Sprague-Dawley; Superoxide Dismutase|PD
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0163-2116
- Country of Publication
- UNITED STATES
Record 21 from database: MEDLINE
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- Title
- Relationship of bacterial growth phase to killing of Listeria monocytogenes
by oxidative agents generated by neutrophils and enzyme systems.
- Author
- Bortolussi R; Vandenbroucke Grauls CM; van Asbeck BS; Verhoef J
- Address
- Department of Pediatrics, Dalhousie University, Halifax, Nova Scotia,
Canada.
- Source
- Infect Immun, 1987 Dec, 55:12, 3197-203
- Abstract
- Listeria monocytogenes, a gram-positive motile bacterium which can cause
severe bacterial infection in humans, is considered to be pathogenic by virtue
of its ability to resist intracellular killing. Since the mechanism of
intracellular survival is poorly understood, we assessed the sensitivity of L.
monocytogenes to several potent antibacterial products. Phorbol myristate
acetate (PMA)-stimulated polymorphonuclear cells (PMNs) produced extracellular
antibacterial products which were inhibited completely by catalase, suggesting a
role for oxidative agents in this process. L. monocytogenes in logarithmic (log)
growth phase resisted PMA-stimulated PMN extracellular products significantly
more than L. monocytogenes in stationary (stat) growth phase or Escherichia coli
(three strains) in either phase of growth. The role of oxidative agents was
studied further by using xanthine oxidase-xanthine, glucose oxidase-glucose, and
myeloperoxidase enzyme systems to generate hydroxyl radical (.OH), hydrogen
peroxide (H2O2), and hypochlorous acid (OCl-), respectively. L. monocytogenes in
log phase resisted the antibacterial products of these enzyme systems under
conditions which produced superoxide (O2-) and H2O2 at concentrations similar to
those produced extracellularly by PMA-stimulated PMNs, while stat-growth-phase
L. monocytogenes and E. coli in either phase of growth were susceptible.
Antibacterial activity could be blocked or inhibited by exogenous catalase (for
all oxygen radical-generating systems), mannitol, or desferoxamine (for xanthine
oxidase-xanthine) and alanine (for myeloperoxidase), suggesting that .OH and
OCl- were responsible for this activity. Log-phase L. monocytogenes had 2.5-fold
higher bacteria-associated catalase activity, as compared with stat-phase L.
monocytogenes. These experiments, therefore, suggest that log-phase L.
monocytogenes resists oxidative antibacterial agents by producing sufficient
catalase to inactivate these products. This may contribute to the ability of L.
monocytogenes to survive intracellularly.
- Language of Publication
- English
- Unique Identifier
- 88057619
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- MeSH Heading (Major)
- Listeria monocytogenes|DE/*GD/IM; Neutrophils|*IM; Oxygen|*TO
- MeSH Heading
- Blood Bactericidal Activity; Catalase|ME; Extracellular Space; Free
Radicals; Glucose Oxidase|ME; Hydrogen Peroxide|BI; Hydroxides; Monocytes|PH;
Peroxidase|PH; Superoxides|BI; Support, Non-U.S. Gov't; Tetradecanoylphorbol
Acetate|PD; Xanthine Oxidase|PH
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0019-9567
- Country of Publication
- UNITED STATES
Record 22 from database: MEDLINE
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- Title
- Superoxide mediates the toxicity of paraquat for Chinese hamster ovary
cells.
- Author
- Bagley AC; Krall J; Lynch RE
- Address
-
- Source
- Proc Natl Acad Sci U S A, 1986 May, 83:10, 3189-93
- Abstract
- The roles of superoxide and H2O2 in the cytotoxicity of paraquat were
assessed in Chinese hamster ovary cells. Neither catalase nor superoxide
dismutase inhibited the loss of ability to form colonies when added to the
medium. When introduced into the cells, superoxide dismutase but not catalase
inhibited the toxicity of paraquat. That superoxide dismutase acted by its known
catalytic action is shown by the loss of inhibition when the enzyme was
inactivated by H2O2 before being introduced into the cells. The lack of
inhibition by catalase, by dimethyl sulfoxide, and by desferoxamine suggests
that the toxicity is not mediated by a reaction between H2O2 and superoxide to
engender the hydroxyl radical. Exposure of Chinese hamster ovary cells to
paraquat may be a suitable means to determine the effects of superoxide anion in
cultured cells and the ways in which cells can resist this toxic action.
- Language of Publication
- English
- Unique Identifier
- 86205862
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- MeSH Heading (Major)
- Paraquat|*TO; Superoxides|*TO
- MeSH Heading
- Animal; Catalase|AD/ME; Cell Line; Cell Survival|DE; Female; Hamsters;
Ovary; Superoxide Dismutase|AD/ME; Support, Non-U.S. Gov't; Support, U.S. Gov't,
P.H.S.
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0027-8424
- Country of Publication
- UNITED STATES
Record 23 from database: MEDLINE
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- Title
- Lungs in thalassaemia major patients receiving regular transfusion.
- Author
- Tai DY; Wang YT; Lou J; Wang WY; Mak KH; Cheng HK
- Address
- Dept of Respiratory Medicine, Tan Tock Seng Hospital, Singapore.
- Source
- Eur Respir J, 1996 Jul, 9:7, 1389-94
- Abstract
- Progressive tissue iron deposition from multiple blood transfusions is
common in beta-thalassaemia and pulmonary iron deposition may result in
parenchymal damage. The objectives of this study were to: 1) determine the
predominant pulmonary dysfunction in patients with thalassaemia major; and 2)
demonstrate that parenchymal disease, if present, is at the level of the
alveolocapillary membrane. Fourteen thalassaemia major patients (13 nonsmokers)
receiving regular blood transfusion and without any history of chronic
respiratory disease were recruited. Pulmonary function tests and
echocardiography were performed before the scheduled transfusions. Three
patients with the most restricted lung function were selected for high
resolution computerized tomography (CT) of the lungs. One patient had an
obstructive pattern with a forced expiratory volume in one second as percentage
of forced vital capacity (FEV1/FVC) of 71%. Four patients demonstrated a
restrictive pattern, as defined by total lung capacity (TLC) less than 80%
predicted with normal FEV1/FVC%. Twelve patients had pulmonary transfer factors
for carbon monoxide (TL,CO) below 80% pred, even after correction for the
anaemia, indicating parenchymal disease. Eight of these 12 patients had
alveolocapillary membrane defect, as demonstrated by a gas transfer factor of
the pulmonary membrane (Tm) less than 80% pred. Mean resting arterial oxygen
saturation was 95 2 (range 92-98) %. Eleven patients had oxygen desaturation of
5% or more during exercise on a bicycle ergometer, consistent with interstitial
lung disease. There was no clinical or echocardiographic evidence of heart
failure. Percentage predicted TLC was inversely correlated with age (r = -0.547;
p = 0.043). Both percentage predicted TLC and TL,CO were not correlated with
iron burden or desferoxamine ratio. High resolution CT in the three selected
patients showed no evidence of pulmonary fibrosis. We conclude that thalassaemia
major patients have a predominant restrictive lung dysfunction with pulmonary
parenchymal disease and alveolocapillary membrane block. The restrictive and
interstitial lung disease could not be accounted for by iron loading or
pulmonary fibrosis in our patients.
- Language of Publication
- English
- Unique Identifier
- 96433668
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- MeSH Heading (Major)
- beta-Thalassemia|CO/*PP/TH; Blood Transfusion|*AE; Lung Diseases|DI/*ET/PP
- MeSH Heading
- Adolescence; Blood-Air Barrier|PH; Echocardiography; Exercise Test; Female;
Human; Iron Overload|DI; Lung|RA; Male; Respiratory Function Tests; Spirometry
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0903-1936
- Country of Publication
- DENMARK
Record 24 from database: MEDLINE
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- Title
- Involvement of nitric oxide in nitroprusside-induced hepatocyte
cytotoxicity.
- Author
- Niknahad H; OBrien PJ
- Address
- Faculty of Pharmacy, University of Toronto, Ontario, Canada.
- Source
- Biochem Pharmacol, 1996 Apr, 51:8, 1031-9
- Abstract
- Sodium nitroprusside (SNP) cytotoxicity towards rat hepatocytes was
accompanied by peroxynitrite formation, lipid peroxidation, inhibition of
glycolysis, cyanide (CN) release, partial inhibition of hepatocyte respiration,
and ATP depletion. Antioxidants and desferoxamine prevented both cytotoxicity
and lipid peroxidation induced by SNP. The CN antidote thiosulfate or the CN
trapping agents dihydroxyacetone and glyceraldehyde increased SNP metabolism,
SNP-induced peroxynitrite formation, cytotoxicity, and lipid peroxidation. On
the other hand, addition of non-toxic concentrations of CN to hepatocytes
prevented SNP metabolism and SNP-induced lipid peroxidation and cytotoxicity.
SNP depleted hepatocyte GSH immediately upon addition, and GSH-depleted
hepatocytes were more susceptible to SNP. The results of this study suggest that
nitric oxide rather than CN mediates SNP cytotoxicity in isolated cells.
- Language of Publication
- English
- Unique Identifier
- 97020446
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- MeSH Heading (Major)
- Liver|*DE/ME; Nitric Oxide|*ME; Nitroprusside|*PD/TO
- MeSH Heading
- Animal; Cell Survival; Cells, Cultured; Lipid Peroxidation; Male;
Nitrates|ME; Rats; Rats, Sprague-Dawley; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0006-2952
- Country of Publication
- ENGLAND
Record 25 from database: MEDLINE
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- Title
- Non-proteolytic activation of latent human neutrophil collagenase and its
role in matrix destruction in periodontal diseases.
- Author
- Sorsa T; Saari H; Konttinen YT; Suomalainen K; Lindy S; Uitto VJ
- Address
- Department of Medical Chemistry, University of Helsinki, Finland.
- Source
- Int J Tissue React, 1989, 11:4, 153-9
- Abstract
- Collagenases are known to be associated with tissue destruction in chronic
inflammatory diseases such as periodontal diseases and rheumatoid arthritis.
Collagenases are secreted by circulating inflammatory cells (polymorphonuclear
leukocytes and monocytes), resident mesenchymal cells and epithelial cells in
latent forms, which can be activated by proteases and compounds reacting with
protein thiol groups. We have studied here the effects of oxygen-derived free
radicals (ODFR) on latent human neutrophil collagenase. Also, in order to
elucidate the cellular sources of collagenases, the ability of human gingival
crevicular fluid (GCF) collagenases both from adult periodontitis (AP) and
localized juvenile periodontitis (LJP) patients to degrade soluble interstitial
collagen types I and II was studied. ODFR generated by the xanthine
oxidase/hypoxanthine system in the presence of trace amounts of iron and EDTA
activated latent neutrophil collagenase to an equal extent as the known
activators phenylmercuric chloride and gold thioglucose. ODFR activation was
inhibited by desferoxamine and mannitol as well as by superoxide dismutase and
catalase. Clear differences in the susceptibility of collagen types I and II to
AP and LJP GCF collagenases were observed. AP GCF collagenase degraded type I
and II collagens at equal rates, resembling the substrate-specificity of human
neutrophil collagenase. LJP GCF collagenase degraded type I collagen
considerably faster than type II collagen, which was only negligibly degraded.
This corresponds to the substrate specificity of fibroblast collagenase.
Zymographic evaluation of gelatinolytic proteases showed the presence of 90 and
68 kD gelatinases in both AP and LJP GCF. Non-proteolytic means apparently
provide a potent activation pathway of neutrophil collagenase in vivo and the
hydroxyl radical was identified to be one of the potent activating
oxidants.(ABSTRACT TRUNCATED AT 250 WORDS)
- Language of Publication
- English
- Unique Identifier
- 90236600
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- MeSH Heading (Major)
- Extracellular Matrix|*ME; Microbial Collagenase|*BL/IP/PH; Neutrophils|*EN;
Oxygen|*PD; Periodontal Diseases|*EN/ME
- MeSH Heading
- Body Fluids|EN; Collagen|ME; Electrophoresis, Polyacrylamide Gel; Enzyme
Activation; Free Radicals; Gingiva|EN; Human; Molecular Weight; Support,
Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0250-0868
- Country of Publication
- SWITZERLAND
Record 26 from database: MEDLINE
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- Title
- Elucidation of antioxidant activity of alpha-lipoic acid toward hydroxyl
radical.
- Author
- Matsugo S; Yan LJ; Han D; Trischler HJ; Packer L
- Address
- Department of Molecular and Cell Biology, University of California at
Berkeley 94720-3200.
- Source
- Biochem Biophys Res Commun, 1995 Mar, 208:1, 161-7
- Abstract
- The photosensitive organic hydroperoxide, NP-III, which produces hydroxyl
radicals on illumination by UVA light, was used to examine the antioxidant
activity of alpha-lipoic acid and its derivatives toward hydroxyl radical.
Apolipoprotein (apo-B) of human low density lipoprotein (LDL) and bovine serum
alubumin (BSA) were irradiated with UVA in the presence of NP-III and
alpha-lipoic acid. The oxidation of BSA and the apo-B protein of LDL by NP-III
was completely suppressed by alpha-lipoic acid. ESR studies using
dimethylpyrroline oxide (DMPO) as a spin trapping reagent also revealed that in
the presence of alpha-lipoic acid, the DMPO-OH adduct produced from the
irradiation of NP-III and DMPO completely disappeared. DMPO-OH quenching
experiments were performed in the presence or absence of desferoxamine but no
change in the signal intensity was found. Hence, the quenching activity of
alpha-lipoic acid is not due to its chelating activity toward transition metals
(ferrous ions). The results lead us to conclude that alpha-lipoic acid is an
efficient hydroxyl radical quencher owing to the disulfide bond in the
dithiolane ring.
- Language of Publication
- English
- Unique Identifier
- 95194401
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- MeSH Heading (Major)
- Antioxidants|*/PD; Apolipoproteins B|*DE/RE; Hydroxyl Radical|*; Serum
Albumin, Bovine|*DE/RE; Thioctic Acid|*/PD
- MeSH Heading
- Cyclic N-Oxides; Electron Spin Resonance Spectroscopy; Human; Kinetics;
Naphthalenes; Radiation-Sensitizing Agents; Salicylic Acids; Spin Labels;
Ultraviolet Rays
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0006-291X
- Country of Publication
- UNITED STATES
Record 27 from database: MEDLINE
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- Title
- Modulating hypoxia-induced hepatocyte injury by affecting intracellular
redox state.
- Author
- Khan S; OBrien PJ
- Address
- Faculty of Pharmacy, University of Toronto, Ont., Canada.
- Source
- Biochim Biophys Acta, 1995 Nov, 1269:2, 153-61
- Abstract
- Hypoxia-induced hepatocyte injury results not only from ATP depletion but
also from reductive stress and oxygen activation. Thus the NADH/NAD ratio was
markedly increased in isolated hepatocytes maintained under 95% N2/5% CO2 in
Krebs-Henseleit buffer well before plasma membrane disruption occurred.
Glycolytic nutrients fructose, dihydroxyacetone or glyceraldehyde prevented
cytotoxicity, restored the NADH/NAD ratio, and prevented complete ATP depletion.
However, the NADH generating nutrients sorbitol, xylitol, glycerol and
beta-hydroxybutyrate enhanced hypoxic cytotoxicity even though ATP depletion was
not affected. On the other hand, NADH oxidising metabolic intermediates
oxaloacetate or acetoacetate prevented hypoxic cytotoxicity but did not affect
ATP depletion. Restoring the cellular NADH/NAD ratio with the artificial
electron acceptors dichlorophenolindophenol and Methylene blue also prevented
hypoxic injury and partly restored ATP levels. Ethanol which further increased
the cellular NADH/NAD ratio increased by hypoxia also markedly increased
toxicity whereas acetaldehyde which restored the normal cellular NADH/NAD ratio,
prevented toxicity even though hypoxia induced ATP depletion was little affected
by ethanol or acetaldehyde. The viability of hypoxic hepatocytes is therefore
more dependent on the maintenance of normal redox homeostasis than ATP levels.
GSH may buffer these redox changes as hypoxia caused cell injury much sooner
with GSH depleted hepatocytes. Hypoxia also caused an intracellular release of
free iron and cytotoxicity was prevented by desferoxamine. Furthermore,
increasing the cellular NADH/NAD ratio markedly increased the intracellular
release of iron. Hypoxia-induced hepatocyte injury was also prevented by
oxypurinol, a xanthine oxidase inhibitor. Polyphenolic antioxidants or the
superoxide dismutase mimic, TEMPO partly prevented cytotoxicity suggesting that
reactive oxygen species contributed to the cytotoxicity. The above results
suggests that hypoxia induced hepatocyte injury results from sustained reductive
stress and oxygen activation.
- Language of Publication
- English
- Unique Identifier
- 96087038
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- MeSH Heading (Major)
- Cell Hypoxia|*PH; Liver|*CY/DE/*ME
- MeSH Heading
- Acetaldehyde|PD; Adenosine Triphosphate|ME; Animal; Antioxidants|PD;
Calcium|PD; Cell Death; Cell Survival; Cells, Cultured; Chelating Agents|PD;
Deferoxamine|PD; Ethanol|PD; Free Radical Scavengers|PD; Lactates|ME; Models,
Biological; NAD|ME; Oxidation-Reduction; Phenols|PD; Polymers|PD; Pyruvates|ME;
Rats; Rats, Sprague-Dawley
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0006-3002
- Country of Publication
- NETHERLANDS
Record 28 from database: MEDLINE
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- Title
- Scavenging of reactive oxygen species as the mechanism of drug action.
- Author
- Robak J; Marcinkiewicz E
- Address
- Department of Pharmacology, Medical College of Jagiellonian University,
KrakÆow, Poland.
- Source
- Pol J Pharmacol, 1995 Mar, 47:2, 89-98
- Abstract
- Reactive oxygen species (ROS) are generated when oxygen is supplied in
excess and/or its reduction is insufficient. The best explored ROS are
superoxide anions, hydroxyl radicals and hydrogen peroxide. The first two are
free radicals. ROS are harmful for the living cells and are implicated in a
variety of pathological processes and diseases. Drugs used in the treatment of
these states are either stimulators of endogenous defense mechanisms against ROS
or inhibitors of ROS formation. Six groups of anti-ROS substances have been
described in this paper. 1) Antioxidant substances used in substitutive therapy
such as enzymes (e.g. superoxide dismutase), substances containing thiol groups
and vitamins (A, E, P, C). 2) Chelating agents (e.g. desferoxamine), which lower
the level of prooxidative transition metal ions. 3) Inhibitors of superoxide
ions generation by stimulated cells or xanthine oxidase. Such mechanism of
action was described for xanthine oxidase inhibitor-allopurinol. 4) Superoxide
scavengers. Many known drugs were investigated for this activity, but the best
documentation was presented for flavonoids. 5) Substances which eliminate
hydrogen peroxide, mainly glutathione and its precursors. 6) Scavengers of
hydroxyl radicals. Studies of the above activity were conducted mainly using an
unspecific method--estimation of malondialdehyde generated during the action of
hydroxyl radicals on lipids or on desoxyribose. Inhibition of malondialdehyde
formation was described for many drugs of plant and synthetic origin.
- Language of Publication
- English
- Unique Identifier
- 96296419
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- MeSH Heading (Major)
- Free Radical Scavengers|AE/*ME; Reactive Oxygen Species|AE/CL/*ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 1230-6002
- Country of Publication
- POLAND
Record 29 from database: MEDLINE
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- Title
- The uptake of ascorbic acid into human umbilical vein endothelial cells and
its effect on oxidant insult.
- Author
- Ek A; Ström K; Cotgreave IA
- Address
- Division of Toxicology, Karolinska Institute, Stockholm, Sweden.
- Source
- Biochem Pharmacol, 1995 Oct, 50:9, 1339-46
- Abstract
- Intracellular reduced ascorbate (AA) levels in confluent cultures of human
umbilical vein endothelial (HUVE) cells, grown under conventional conditions,
were shown to be very low, ranging between undetectable, < 0.1 nmol/mg
protein, and 0.3 nmol/mg protein. Reduced ascorbate was accumulated into the
endothelial cells from M199 culture medium in time- and concentration-dependent
manners, and was saturated at medium concentrations related to the normal plasma
concentrations of the antioxidant (i.e. between 50 microM and 100 microM). Cells
derived from different individuals demonstrated considerable inter-individual
variation in these AA uptake parameters. The uptake of AA was sensitive to
temperature and the presence of the structural analogue isoascorbate in the
medium, indicating the involvement of an active transport mechanism. A role for
the glucose transporter is, however, not indicated, as AA uptake was not
sensitive to phloretin, an inhibitor of the cellular glucose transporter, nor
greatly enhanced by depletion of glucose from the medium. Incubation of HUVE
cells with dehydroascorbate (DHAA) caused a dose-dependent, but transient
increase in intracellular AA. This indicates that HUVE cells are both competent
in the uptake and intracellular reduction of oxidised ascorbate, and may
resecrete AA into the medium. Indeed, reduced ascorbate in the medium was shown
to be preferentially maintained in the presence of cells. The uptake of AA was
not sensitive to the presence of DHAA in the medium, perhaps indicating
different transporters for reduced and oxidised forms of ascorbate in these
human cells. Pre-loading HUVE cells with AA was shown to protect control cells
only weakly from the acute, sub-lethal toxicity of H2O2 generated by xanthine
oxidase (1 U/mL or 10 U/mL). Protection was optimal at intracellular levels of
3-4 nmol AA/mg protein, with higher concentrations lacking a protective effect.
Additionally, the presence of the iron chelator, desferoxamine, significantly
protected GSH-depleted HUVE cells only in response to the peroxide, but did not
potentiate the protective action of intracellular AA in either control or GSH-depleted cells. This indicates that ascorbate-driven
redox-cycling of the
Fe2ﱗ does not hamper the intracellular protective function of ascorbate during
hydrogen peroxide-derived oxidative stress. These results are discussed in terms
of the central role of endothelial cells in the distribution of AA to the
tissues of the body, the use of the HUVE cell system for model studies of the
toxicity of oxidants in the human endothelium, and the balance between the
antioxidant and pro-oxidant actions of AA.
- Language of Publication
- English
- Unique Identifier
- 96080268
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- MeSH Heading (Major)
- Ascorbic Acid|*PK; Endothelium, Vascular|*ME; Hydrogen Peroxide|*TO;
Oxidative Stress|*PH
- MeSH Heading
- Cells, Cultured; Culture Media; Dehydroascorbic Acid|ME/PK; Human;
Intracellular Fluid|ME; Iron|ME; Monosaccharide Transport Proteins|ME;
Oxidation-Reduction; Support, Non-U.S. Gov't; Umbilical Veins|ME
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0006-2952
- Country of Publication
- ENGLAND
Record 30 from database: MEDLINE
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- Title
- Aluminum levels and stores in patients with total hip endoprostheses from
TiAIV or TiAINb alloys.
- Author
- Dittert DD; Warnecke G; Willert HG
- Address
- Abteilung Pathologie I, UniversitÂatsklinik, GÂottingen, Germany.
- Source
- Arch Orthop Trauma Surg, 1995, 114:3, 133-6
- Abstract
- Aluminum ranks as a potentially hazardous agent. Pathologic findings in
different organs show that it can accumulate in brain, muscle, liver and bone.
Therefore, we investigated whether patients with cementless total hip
endoprostheses made out of titanium alloys containing aluminum are at risk. In
order to determine the complete aluminum body loading in patients who have had
their hip replacement for a long period of time (mean 58 months), we mobilized
possible stores of aluminum with desferoxamine (DFO). Electrothermal atomic
absorption spectroscopy was used to quantify the level of aluminum in serum and
urine before and after DFO treatment. A serum aluminum value of 10 micrograms/l
or less is internationally accepted as safe. The average serum aluminum level in
this study was 14.2 micrograms/l, which is slightly above the limit, but clearly
below those levels which can lead to disease (> 50 micrograms/l). No relevant
storage of aluminum was found. This latter finding is more important since
chronically elevated aluminum levels lead to cellular deposits, which affect the
cellular biochemistry. The values before and after DFO mobilization did not
differ substantially, indicating that aluminum in alloys for biomaterials can be
regarded as safe as far as the risk of aluminum release in vivo is concerned.
Histologic studies of bone from the bone-metal interface also showed no deposits
of local aluminum release.
- Language of Publication
- English
- Unique Identifier
- 95344894
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- MeSH Heading (Major)
- Aluminum|BL/*ME/UR; Biocompatible Materials|*ME; Hip Prosthesis|*IS;
Titanium|*ME
- MeSH Heading
- Adult; Aged; Bone and Bones|ME/PA; Deferoxamine|AD/DU; Female; Human; Male;
Middle Age; Prognosis; Prosthesis Design; Spectrophotometry, Atomic Absorption;
Time Factors
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0936-8051
- Country of Publication
- GERMANY
Record 31 from database: MEDLINE
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- Title
- Reactive oxygen species as regulators of human neutrophil and fibroblast
interstitial collagenases.
- Author
- Saari H; Sorsa T; Lindy O; Suomalainen K; Halinen S; Konttinen YT
- Address
- IVth Department of Medicine, Helsinki University Central Hospital, Finland.
- Source
- Int J Tissue React, 1992, 14:3, 113-20
- Abstract
- The effects of various reactive oxygen species on latent human neutrophil
and fibroblast-type interstitial collagenases were studied. Latent human
neutrophil collagenases (proMMP-8) was efficiently activated by hypochlorous
acid and hydrogen peroxide and less efficiently by the serine proteinases
trypsin and chymotrypsin. Human plasmin and plasma kallikrein did not activate
latent human neutrophil collagenase. The activation of latent human neutrophil
collagenase by hypochlorous acid and hydrogen peroxide corresponded to the
activation obtained with the other known non-proteolytic activators
phenylmercuric chloride and gold thioglucose. The activation by hydrogen
peroxide was inhibited by mannitol and desferoxamine, suggesting a localized
Fenton-type reaction to be responsible for the generation of hydroxyl radical
and/or hydroxyl radical-like reactive oxygen pathway of neutrophil
procollagenase does not involve plasmin and plasma kallikrein, which are
efficient proteolytic activators of latent fibroblast-type procollagenase
(proMMP-1). Fibroblast procollagenase was also slightly activated by
hypochlorous acid and gold thioglucose. Thus neutrophil procollagenase seems to
prefer non-proteolytic means of activation and reactive oxygen species can be
regarded as potent activators in vivo. Synovial-fluid neutrophils from
rheumatoid arthritis patients were found to release collagenase in 30% active
form when compared to same patients' peripheral blood neutrophils, which
released collagenase in completely latent form. This may indicate that the
triggering of neutrophil at the site of inflammation in vivo involves initial
oxidative activation of collagenase upon the degranulation process.
- Language of Publication
- English
- Unique Identifier
- 93077254
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- MeSH Heading (Major)
- Collagenases|*ME; Neutrophils|*EN; Reactive Oxygen Species|*ME
- MeSH Heading
- Comparative Study; Fibroblasts|EN; Human; Support, Non-U.S. Gov't; Synovial
Fluid|CY
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0250-0868
- Country of Publication
- SWITZERLAND
Record 32 from database: MEDLINE
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- Title
- The mechanism of cytogenetic genotoxicity of exogenous glutathione in V-79
cells in vitro--implication of hydrogen peroxide and general traits of oxidative
chromosome damage.
- Author
- Thust R
- Address
- Institute of Pathological Anatomy, Medical Academy of Erfurt, German
Democratic Republic.
- Source
- Cell Biol Toxicol, 1988 Jun, 4:2, 241-57
- Abstract
- The mechanism of cytogenetic genotoxicity (clastogenicity, induction, cell
cycle delay) of 10(-3) M glutathione in V79-E cells, as described by Thust and
Bach (1985), was studied in detail by using different treatment conditions. It
was found that 1-cystine is the essential cofactor in the incubation system.
Catalase, but not superoxide dismutase, abolished the genotoxic effect, and the
iron chelator desferoxamine, as well as the hydroxyl radical scavenger mannitol,
diminished the activity. It is suggested that glutathione, in combination with
V79-E cells and cystine, forms a hydrogen peroxide-generating system which
provokes the adverse effects. Glutathione as well as 1-cysteine and
2-mercaptopropionylglycine, which were checked for comparison, show a "paradoxic
genotoxicity," i.e., at 10(-2) M the effects return almost to the level of
controls. Concentration dependence and other criteria of cytogenetic
genotoxicity observed with glutathione show obvious similarities to those of
other oxidatively acting agents and reveal striking differences to the
cytogenetic effects of "typical" genotoxins.
- Language of Publication
- English
- Unique Identifier
- 89167840
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- MeSH Heading (Major)
- Glutathione|*TO
- MeSH Heading
- Animal; Cell Cycle|DE; Cells, Cultured; Chromosome Aberrations|DE;
Dose-Response Relationship, Drug; Guinea Pigs; Mutagenicity Tests; Rats
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0742-2091
- Country of Publication
- UNITED STATES
Record 33 from database: MEDLINE
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- Title
- Are ethane and pentane evolution and thiobarbituric acid reactivity specific
for lipid peroxidation in erythrocyte membranes? [published erratum appears in
Scand J Clin Lab Invest 1993 Apr;53(2):201]
- Author
- Pitkänen OM
- Address
- Children's Hospital, University Central Hospital, Helsinki, Finland.
- Source
- Scand J Clin Lab Invest, 1992 Sep, 52:5, 379-85
- Abstract
- Peroxidation of human erythrocyte membranes was followed in vitro with head
space analysis of ethane and pentane and a thiobarbituric acid assay in a
standardized system liberating free oxygen radicals. Simultaneously, the
decrease of the membrane palmitic, linoleic, arachidonic and docosahexaenoic
acid was monitored. The recoveries of the peroxidation products of the red cell
ghost preparations were compared with those obtained by peroxidation of pure
fatty acids. Experiments using purified fatty acids revealed that ethane was
preferentially produced from docosahexaenoic and linolenic, and pentane from
linoleic and arachidonic acids. Thiobarbituric acid-reactive material (TBAR) was
produced from each unsaturated fatty acid tested, but the amount was dependent
on the number of carbon chain double bonds. During peroxidation of the
erythrocyte ghosts, 72% of ethane and 51% pentane were produced during the first
12 h of incubation, whereas TBAR was produced at a constant rate throughout the
36-h test period. Hydrocarbon and TBAR production were similarly inhibited by
desferoxamine (at p less than 0.005 and p less than 0.0001, respectively). The
total recoveries of ethane, pentane and TBAR exceeded the amount expected by
7.8-, 1.4- and 5.5-fold, respectively. It was concluded that measurement of
pentane is a reliable method to monitor lipid peroxidation during oxidative
damage of the erythrocyte membrane.
- Language of Publication
- English
- Unique Identifier
- 92383503
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- MeSH Heading (Major)
- Erythrocyte Membrane|*ME; Ethane|*BL; Lipid Peroxidation|*; Pentanes|*BL;
Thiobarbiturates|*BL
- MeSH Heading
- Fatty Acids|BL; Free Radicals; Human; Kinetics; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE
- ISSN
- 0036-5513
- Country of Publication
- ENGLAND
Record 34 from database: MEDLINE
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- Title
- Detailed characterization of experimental acute alcoholic pancreatitis.
- Author
- Nordback IH; Olson JL; Chacko VP; Cameron JL
- Address
- Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, Md
21205-2196.
- Source
- Surgery, 1995 Jan, 117:1, 41-9
- Abstract
- BACKGROUND. With the ex vivo perfused c
