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At least 811 records · Page 45Linked to original sources
PubMed1981

In vivo lipid peroxidation: measurement via exhaled pentane and protection by vitamin E.

Lipid peroxidation occurs in animal tissue when antioxidant protective systems are lacking. Among the protective systems in animals are the biological antioxidant vitamin E and selenium-glutathione peroxidase, a decomposer of peroxides. Lipid peroxidation also occurs when a variety of chemical oxidants are introduced into a animal. The most recently developed technique for measurement of lipid peroxidation in vivo is the analysis of expired air for volatile hydrocarbon products of lipid hydroperoxide decomposition. Pentane is derived from the major fatty acids of the animal body, those of the omega 6-un-saturated fatty acid family, while ethane is derived from omega 3-unsaturated fatty acids. The technique of measuring volatile hydrocarbons has been used by a number of investigators to show increased lipid peroxidation in animals fed diets deficient in antioxidant nutrients and in animals exposed to ozone or injected with iron, halogenated hydrocarbons, or peroxides. Evidence that volatile hydrocarbons are produced during lipid peroxidation, the similarities of results obtained by different investigators who have measured lipid peroxidation by volatile hydrocarbon production, and the relative effects of nutritional and chemical treatments on production of volatile hydrocarbons by laboratory animals or humans are reviewed.

Fatty Acids, Unsaturated↗
PubMed1994

Nitric oxide regulation of superoxide and peroxynitrite-dependent lipid peroxidation. Formation of novel nitrogen-containing oxidized lipid derivatives.

Superoxide (O2-.), nitric oxide (.NO), and their reaction product peroxynitrite (ONOO-) have all been shown to independently exert toxic target molecule reactions. Because these reactive species are often generated in excess during diverse inflammatory and other pathologic circumstances, we assessed the influence of .NO on membrane lipid peroxidation induced by O2-., H2O2, and .OH derived from xanthine oxidase (XO) and by ONOO-. Experimental conditions in lipid oxidation systems were adjusted to yield different rates of delivery of .NO, relative to rates of O2-. and H2O2 generation, by infusion of either .NO or via .NO released from S-nitroso-N-acetylpenicillamine or S-nitrosoglutathione. Peroxidation of phosphatidylcholine liposomes was assessed by formation of thiobarbituric acid-reactive products and by liquid chromatography-mass spectrometry. Liposomes exposed to XO-derived reactive species in the presence of .NO exhibited both stimulation and inhibition of lipid peroxidation, depending on the ratio of the rates of reactive oxygen species production and .NO introduction into reaction systems. Nitric oxide alone did not induce lipid peroxidation. Linolenic acid emulsions peroxidized by XO-derived reactive species showed similar dose-dependent regulation of lipid peroxidation by .NO. Mass spectral analysis of oxidation products showed formation of nitrito-, nitro-, nitrosoperoxo-, and/or nitrated lipid oxidation adducts, demonstrating that .NO serves as a potent terminator of radical chain propagation reactions. Electron spin resonance (ESR) analysis of incubation mixtures provided no evidence for formation of paramagnetic iron-lipid-nitric oxide complexes in reaction systems. Peroxynitrite-dependent lipid peroxidation, which predominantly occurs by metal-independent mechanisms, was also inhibited by .NO. Peroxynitrite-mediated benzoate hydroxylation was partially inhibited by .NO, inferring reaction between .NO and ONOOH. It is concluded that .NO can both stimulate O2-./H2O2/.OH-induced lipid oxidation and mediate oxidant-protective reactions in membranes at higher rates of .NO production, with the prooxidant versus antioxidant outcome critically dependent on relative concentrations of individual reactive species. Prooxidant reactions of .NO will occur after O2-. reaction with .NO to yield potent secondary oxidants such as ONOO- and the antioxidant effects of .NO a consequence of direct reaction with alkoxyl and peroxyl radical intermediates during lipid peroxidation, thus terminating lipid radical chain propagation reactions.

Hydroxyl Radical↗
PubMed1994

Interactions of human blood plasma with hydrogen peroxide and hypochlorous acid.

Activated neutrophils produce both hydrogen peroxide (H2O2) and hypochlorous acid (HOCl). Previous work has shown that HOCl depletes antioxidants, modifies proteins, and forms fatty acid chlorohydrins but does not cause significant lipid peroxidation in human plasma. Because activated phagocytes have been claimed to stimulate lipid peroxidation in plasma, we examined the effects of H2O2 and HOCl alone and in combination on plasma constituents. Hydrogen peroxide at concentrations below 0.5 mmol/L had little effect, but 1 to 2 mmol/L H2O2 caused loss of ascorbic acid and protein thiol groups, an effect potentiated by preincubation of the plasma with sodium azide to inhibit catalase. H2O2 caused no detectable lipid peroxidation or loss of alpha-tocopherol in plasma, but some depletion of ubiquinol occurred. The combination of HOCl and H2O2 caused more lipid peroxidation than either agent alone. Peroxidation was not inhibited by the metal chelators ethylenediaminetetraacetic acid and deferoxamine or by the singlet O2/hydroxyl radical scavenger histidine. We hypothesize that the phagocyte-derived H2O2 and HOCl could interact in the microenvironment of the activated leukocyte to induce lipid peroxidation of plasma lipoproteins or cell membranes (or both).

Antioxidants↗
PubMed1993

Influence of palm oil or its tocotrienol-rich fraction on the lipid peroxidation potential of rat liver mitochondria and microsomes.

The effect of palm oil, a widely used vegetable oil, rich in tocotrienols, on peroxidation potential of rat liver was examined. Long-term feeding of rats with palm oil as one of the dietary components significantly reduced the peroxidation potential of hepatic mitochondria and microsomes. As compared to hepatic mitochondria isolated from rats fed control or corn oil-rich diet, those from palm oil-fed group showed significantly less susceptibility to peroxidation induced by ascorbate and NADPH. However, in microsomes, only NADPH-induced lipid peroxidation was significantly reduced in rats fed palm oil rich-diet. Though the accumulation of thiobarbituric acid reactive substances during ascorbate-induced lipid peroxidation in mitochondria from rats fed corn oil-rich diet supplemented with tocotrienol-rich fraction (TRF) of palm oil was similar to that of control rats, the initial rate of peroxidation was much slower than those from control or corn oil fed diets. Our in vitro studies as well as analyses of co-factors related to peroxidation potential indicated that the observed decrease in palm oil-fed rats may be due to increased amount of antioxidants in terms of tocotrienol as well as decrease in the availability of substrates for peroxidation.

Animals↗
PubMed1996

Mouse liver microsomal metabolism of chloral hydrate, trichloroacetic acid, and trichloroethanol leading to induction of lipid peroxidation via a free radical mechanism.

Metabolism of chloral hydrate (CH) by male B6C3F1 mouse liver microsomes (control-microsomes) generated free radical intermediates that resulted in endogenous lipid peroxidation, forming malondialdehyde (MDA), formaldehyde (FA), acetaldehyde (ACT), acetone, and propionaldehyde. Because MDA, FA, and ACT are tumorigens, endogenous formation of lipid peroxidation products via a free radical mechanism may be responsible for hepatocellular tumorigenicity of CH to the B6C3F1 mice. Trichloroacetic acid (TCA) and trichloroethanol (TCE), the primary metabolites of CH, also generated free radicals and induced lipid peroxidation. Lipid peroxidation from TCA equaled that induced by CH, whereas that from TCE was 3- to 4-fold lower, suggesting that metabolism of CH to TCA may be the predominant pathway leading to lipid peroxidation. Metabolism of CH, TCA, and TCE by liver microsomes of mice pretreated with pyrazole (pyrazole-microsomes) yielded lipid peroxidation products at a level 2- to 3-fold higher than those from liver microsomes of untreated mice. In addition, CH-induced lipid peroxidation catalyzed by control-microsomes and pyrazole-microsomes was reduced significantly by 2,4-dichloro-6-phenylphenoxyethylamine, a general cytochrome P450 inhibitor. Thus, our study suggests that cytochrome P450 is the enzyme catalyzing the metabolic activation of CH and its metabolites (TCA and TCE) leading to lipid peroxidation, and that CYP2E1 may be the major isozyme responsible. This latter conclusion was supported by results using human lymphoblastoid cells expressing cytochrome P4502E1, which metabolized CH to reactants inducing mutations, whereas the parental cell line was inactive.

Allopurinol↗
PubMed1998

Hydrogen peroxide inhibits giant cell tumor and osteoblast metabolism in vitro.

This study investigates the efficacy of using hydrogen peroxide as adjuvant therapy after extended local curettage for benign giant cell tumors of bone. Hydrogen peroxide is used clinically as a chemical adjuvant for removal of residual tumor cells, presumably by effervescent cleansing with minimal damage to surrounding soft tissue and bone cells. This investigation examined the effects of hydrogen peroxide on giant cell tumor cells and osteoblasts grown in culture. Fresh fragments of histologically confirmed giant cell tumor tissue (six patients) and trabecular bone (one patient) were excised. Cells obtained from the fragments were grown in culture. Confluent cell cultures were exposed to saline (control) or hydrogen peroxide (0.1-1000 mm) for 2 minutes, and incubation was continued for 12, 24, or 48 hours without hydrogen peroxide. Protein content, deoxyribonucleic acid content, tartrate resistant acid phosphatase activity, and alkaline phosphatase activity were measured in the cell layers. The medium from the final 12 hours of each incubation period was used to evaluate lactate production. Cell lysis or death occurred after exposing giant cell tumor cells and osteoblasts to 100 mm and 30 mm hydrogen peroxide, respectively, concentrations substantially lower than the 3% (880 mm) hydrogen peroxide commonly used clinically. These results support the theory of using a minimal concentration of hydrogen peroxide as a chemical adjuvant in the surgical treatment of giant cell tumors of bone.

Adult↗
PubMed1996

Continuous monitoring of hydroperoxide-induced peroxidation in human erythrocytes by low-level chemiluminescence.

We studied the effect of cumene hydroperoxide, t-butyl hydroperoxide, and hydrogen peroxide on intact healthy human erythrocytes (15 g hemoglobin/dl) using chemiluminescence to monitor peroxidation. We measured the chemiluminescence spectrum, the process of hemolysis, the pH shift, and absorbance spectrum during the incubation with chemicals producing oxidative stress. Maximum chemiluminescence was reached with cumene hydroperoxide at about 50 min, but with t-butyl hydroperoxide at 100 min. The effect of organic hydroperoxide was concentration dependent, whereas the effect of hydrogen peroxide was independent of concentration. Peroxides induced hemolysis after 30 min. The pH shift to alkaline was observed in the first 20-min period. Incubation with organic hydroperoxides induced a decrease in absorption at 580, 545, and 345 nm. Hydrogen peroxide induced a decrease in the same period of time but this returned to the normal range by 120 min. There was no change in absorption at 420 nm with any of the peroxidative agents. Our results suggest that low-level chemiluminescence is a useful model for studying hydroperoxide-induced peroxidation in human erythrocytes.

Antioxidants↗
PubMed1993

Roles of catalase and cytochrome c in hydroperoxide-dependent lipid peroxidation and chemiluminescence in rat heart and kidney mitochondria.

A recent report (Radi et al., J. Biol. Chem. 266:22028-22034, 1991) showed that rat heart mitochondria contain catalase. The protective role of mitochondrial catalase was tested by exposing heart or kidney mitochondria and mitoplasts to two oxidants (H2O2) or tert-butyl hydroperoxide, t-BOOH), estimating lipid peroxidation (as thiobarbituric acid-reactive substances, TBARS) and overall oxidative stress (as chemiluminescence). Additional controls included heart and kidney preparations from aminotriazole-treated (catalase-depleted) rats. Both oxidants increased TBARS in catalase-free preparations to similar extents over their respective controls (between 200 to 350%). In catalase-containing preparations, H2O2 lipid peroxidation increased by only 40 to 96% over controls. Similar qualitative results were obtained when measuring chemiluminescence. The catalytic role of cytochrome c in mitochondrial lipid peroxidation was investigated by exposing either control or cytochrome-c-depleted kidney mitoplasts (catalase free) to either H2O2 or t-BOOH. Hydrogen-peroxide-dependent mitochondrial lipid peroxidation varied with cytochrome c concentration, remaining close to controls when cytochrome c concentration decreased by 66%, even though there was no catalase present. Tert-butyl hydroperoxide-dependent lipid peroxidation was less affected by cytochrome c remaining 2.3-fold above controls under the same conditions, suggesting that organic peroxides are more likely to remain in the less polar membrane environment being decomposed by heme or nonheme iron imbedded in the inner mitochondrial membrane. Chemiluminescence was less affected by cytochrome c depletion. Comparing control and cytochrome-c-deficient mitochondria, chemiluminescence was 1.7-fold and 2.8-fold higher when control preparations were challenged with t-BOOH or H2O2, respectively.

Animals↗
PubMed2002

Effect of acetaminophen on the myeloperoxidase-hydrogen peroxide-nitrite mediated oxidation of LDL.

Myeloperoxidase, in the presence of hydrogen peroxide and nitrite, promotes the lipid peroxidation of low density lipoprotein (LDL); the modified lipoprotein is then capable of being readily endocytosed by macrophages. Since acetaminophen has been shown to inhibit the leukocyte myeloperoxidase antimicrobial system and is, under certain experimental conditions, an antioxidant, the effect of acetaminophen on the myeloperoxidase-hydrogen peroxide-nitrite mediated oxidation of LDL was examined. The content of LDL lipid hydroperoxides after incubation with 50 nM myeloperoxidase, 100 microM nitrite and a hydrogen peroxide generating system for 6 h was reduced by approx. 80% in the presence of 25-250 microM acetaminophen. The production of thiobarbituric acid-reactive substances was also inhibited by acetaminophen to a similar extent. Acetylsalicylic acid (25-100 microM) did not inhibit LDL lipid peroxidation mediated by the myeloperoxidase enzyme system. LDL, treated with myeloperoxidase, hydrogen peroxide and nitrite for 14 h, was metabolized by macrophages to a much greater extent than native LDL. The presence of acetaminophen prevented the modification of LDL; the lipoprotein was metabolized by macrophages to the same extent as was native LDL. These results demonstrate that acetaminophen is a potent inhibitor of the myeloperoxidase-hydrogen peroxide-nitrite mediated modification of LDL.

Acetaminophen↗
PubMed2002

Comparison of peroxide value methods used for semihard cheeses.

The objective was to evaluate alternatives to the peroxide value method of choice in the dairy industry, the method issued by the International Dairy Federation. Furthermore, the study evaluated the feasibility of alternative solvents for extracting lipids and subsequent peroxide value determinations. Packaged cheeses were stored under illuminated display at 4 degrees C to obtain samples with various peroxide contents but with uniform gross composition. The hydroperoxide contents were measured during 3 weeks of storage by applying two lipid extraction methods, Folch and Bureau of Dairy Industry (BDI) extractions, and three different hydroperoxide extraction solutions [chloroform/methanol (7:3, v/v), hexane/2-propanol/methanol (5:7:2, v/v/v), and methanol/decanol/hexane (3:2:1, v/v/v)], prior to standard colorimetric measurements. Extraction yields of fat from Havarti cheeses using the Folch and BDI extraction methods were approximately 109 and 61%, respectively, of the yields obtained by the International Dairy Federation gravimetric reference method. Although differences in fat extraction yields were compensated for, significantly higher peroxide values resulted from the Folch extraction method than from the BDI extraction method. The peroxide values obtained by the three methods were all in the same range, and pronounced linear correlations between peroxide contents determined using the three solutions were noted (r (2) in the range of 0.951-0.983). Peroxide value levels were not significantly different in samples stored in the dark or exposed to light.

2-Propanol↗
PubMed2005

Peroxide release into saliva from five different home bleaching systems in vivo.

PURPOSE: This study determined hydrogen peroxide release into the oral cavity during use of different home bleaching products and compared them with accepted safe levels. METHODS: Determination of peroxide in saliva was performed with peroxidase, phenol and 4-aminoantipyrin in a photometric method. Upper jaw incisors were bleached with individual trays charged with 350 mg Opalescence 10%, Opalescence 15% (OP) and Vivastyle (V). Additionally, Whitestrips (WS) designed for upper or lower jaw were used. All systems were adopted by five subjects for 30 minutes on different days. Whole saliva was collected at 2-minute intervals during the first 10 minutes of bleaching and every 5 minutes thereafter. RESULTS: Highest release of peroxide was found for all products in the saliva sample collected initially after application of the bleaching agent. Total amount of peroxide released into saliva during 30-minute bleaching period was 0.78+/-0.45 for Opalescence 10% and 1.52+/-0.44 mg for Opalescence 15%. Significantly more peroxide was released from Vivastyle (2.67+/-1.03 mg) and from Whitestrips (upper: 3.25+/-5,65, lower: 2.09+/-0.34 mg). A significantly smaller fraction of the charged peroxides was released into saliva from individual trays than from Whitestrips during the 30-minute use time. From the peroxide loaded in the trays or strips the following fractions were released during the application period: Opalescence 10% (6.4+/-3.7%), Opalescence 15% (8+/-2.4%), Vivastyle (18.6+/-8.5%), upper Whitestrips (30.4+/-4.9), lower Whitestrips (27.4+/-4.4%). In terms of amount/kg body weight the bleaching systems led to a single exposure of 0.013-0.056 mg/kg which is distinctly less than the maximum safe daily dose of 0.26 mg/kg/day if calculated for a small person (58 kg/128 lbs).

Carbamide Peroxide↗
PubMed1998

Tooth bleaching using peroxide-containing agents: current status of safety issues.

During the last 10 years, at-home tooth bleaching using peroxide-containing agents has quickly become well accepted. It is one of the most popular cosmetic dental procedures for whitening teeth. Although there are few disputes regarding their efficacy, concerns and debates have continued regarding the safety of peroxide-containing tooth bleaching agents. Potential carcinogenicity and genotoxicity of the peroxides used in bleaching agents are the two most persistent and controversial issues. This article reviews and discusses available information on carcinogenicity and genotoxicity of hydrogen peroxide and the potential risks associated with the use of peroxide-containing bleaching agents. Clinical studies reported after the 1996 international symposium on responses of oral tissues to peroxide-containing bleaching agents are also reviewed. Overall evidence supports the conclusion that the proper use of peroxide-containing at-home tooth bleaching agents is safe. However, potential adverse effects may occur in inappropriate applications, abuses, or the use of inappropriate products. At-home tooth bleaching should be monitored by dental professionals to maximize the benefits while minimizing potential risks.

Animals↗
PubMed2005

Quantitative analysis of hydrogen peroxide by 1H NMR spectroscopy.

A technique utilizing 1H NMR spectroscopy has been developed to measure the concentration of hydrogen peroxide from 10(-3) to 10 M. Hydrogen peroxide produces a peak at around 10-11 ppm, depending upon the interaction between solvent molecules and hydrogen peroxide molecules. The intensity of this peak can be monitored once every 30 s, enabling the measurement of changes in hydrogen peroxide concentration as a function of time. 1H NMR has several advantages over other techniques: (1) applicability to a broad range of solvents, (2) ability to quantify hydrogen peroxide rapidly, and (3) ability to follow reactions forming and/or consuming hydrogen peroxide as a function of time. As an example, this analytical technique has been used to measure the concentration of hydrogen peroxide as a function of time in a study of hydrogen peroxide decomposition catalyzed by iron(III) tetrakispentafluorophenyl porphyrin.

Journal Article↗
PubMed1981

The cooperative interaction between vitamin E and vitamin C in suppression of peroxidation of membrane phospholipids.

The time course of peroxidation of rat liver microsomes by FeSO4 in the presence of ascorbate showed a delay in the onset of peroxidation compared to the time course when NADPH replaced ascorbate as the electron donor. The delay was consistent with an antioxidant function of ascorbate, possibly mediated through endogenous vitamin E. In order to further investigate the cooperation between ascorbate and vitamin E in suppressing lipid peroxidation, a liposomal system containing polyunsaturated phospholipids was used. Peroxidation was initiated by ferrous iron at pH 5, where spontaneous oxidation of Fe2+ did not occur and the antioxidant properties of ascorbic acid could be characterized independently of its pro-oxidant properties as a reducer of Fe3+. Ascorbic acid alone at concentrations of 30--100 microM delayed peroxidation by 20 min and at higher concentrations prevented peroxidation for 60 min. Physiological levels of vitamin E decreased peroxidation at early time points but the vitamin was apparently consumed during the course of the incubation. The presence of both vitamin C and vitamin E produced suppression of peroxidation at early time points (0--20 min) which was approximately the sum of the individual inhibitions. At longer time points, however, the mixture of antioxidants was much more effective than the sum of both vitamins alone. This suggests that interaction between these antioxidants yields and enhanced delivery of antioxidant protection.

Animals↗
PubMed1989

Lipid peroxidation of human granulocytes (PMN) and monocytes by iron complexes.

Because the phagocytic function of non-stimulated human polymorphonuclear granulocytes (PMN) is impaired after incubation with either polynuclear Fe(III) or Fe(II), we decided to study lipid peroxidation of PMN and monocytes by these iron complexes. Lipid peroxidation was assessed by measuring thiobarbituric acid reactive substances and fluorescent compounds. In this study we report that monocytes, isolated in the standard way (EDTA-mediated detachment), release significantly more thiobarbituric acid reactive substances after incubation with iron than PMN. Monocytes, however, isolated without EDTA release the same amount after incubation with iron as PMN. The iron complexes shown to impair phagocyte function also stimulated the peroxidation of membrane lipids. Ascorbic acid in high concentrations enhanced iron-induced lipid peroxidation. Lipid peroxidation induced by ferrous ascorbate (1:20) could be inhibited by catalase, the iron chelators deferoxamine and transferrin, and the hydroxyl radical scavenger thiourea. Mononuclear complexes (ferric citrate 1:20) did not impair granulocyte function and did not induce lipid peroxidation. Our results suggest that impaired phagocyte function in patients with iron overload may be due to non-transferrin bound iron-mediated peroxidation of membrane lipids. However, the lowest amount of ferrous ascorbate (1:20) capable of inducing lipid peroxidation (50 microM) was significantly higher than that which impaired phagocyte function (10 microM).

Ferric Compounds↗
PubMed1977

Stimulative effects of chelating agents, 2,2'-bipyridine and 1,10-phenanthroline, on lipid peroxidation in rat liver microsomes.

Well known lipid peroxidation inhibitors, 1,10-phenanthroline and 2,2'-bipyridine, stimulated microsomal NADPH- and ascorbic acid-dependent lipid peroxidation when low concentrations of these chelating agents were added to incubation mixture. The stimulatory effects of the chelating agents on lipid peroxidation were enhanced when ferrous ion was added together with the chelating agents to the mixture at a molar ratio of 1:1. Ethylenediaminetetraacetic acid (EDTA) had no stimulatory effect on lipid peroxidation. Ferrous ion-EDTA complex increased lipid peroxidation by only 20-30%, which was lower than that obtained by addition of the same concentration of ferrous ion alone. On the other hand, manganese and calcium ions, which are also inhibitors of lipid peroxidation, had no ability to stimulate lipid peroxidation even in the presence of extra ferrous ions. Changes in the lipid peroxidation by chelating agents affected the apparent activity of ethylmorphine N-demethylation.

2,2'-Dipyridyl↗
PubMed1992

[Calcium channel blockers inhibit human low-density lipoprotein peroxidation induced by oxygen free radicals in vitro].

Previous studies have shown that calcium-antagonists may reduce the development of experimental atherosclerosis, and that nifedipine may slow progression of coronary atherosclerosis in man. The mechanisms responsible for this effect are still unclear. It has been recently proposed that oxygen-free radicals can induce peroxidation of human low-density lipoproteins (LDL), and that peroxidized LDL may be an atherogenic stimulus. Chemical modified LDL are internalized by macrophages via specific cell surface receptor that was termed the scavenger receptor, and could induce foam cells transformation in vivo. Previous studies on other systems have shown that calcium-antagonists may effectively inhibit oxygen radical-induced lipid peroxidation. These drugs, though differing widely in their chemical structure, are lipophilic to various degrees and presumably would concentrate in the lipid domain of the phospholipid-rich membranes. Therefore, the aim of the present study was to investigate whether calcium-channel blockers may reduce human LDL peroxidation. Purified human LDL were exposed to oxygen radicals generated by xanthine-xanthine oxidase (18 hours) after a pre-incubation (30 min) in presence of different concentrations of nifedipine, diltiazem and verapamil. Peroxidation was measured from malonyldialdehyde production. The results show that calcium-antagonists prevent LDL peroxidation. Thus, calcium-antagonists may reduce peroxidation of human LDL in vitro, at clinically relevant concentrations. These data suggest that reduced formation of atherogenic peroxidized LDL may be an additional mechanism for the anti-atherosclerotic effects of calcium-antagonists in vivo.

Arteriosclerosis↗
PubMed1997

Peroxidative activity of human Cu,Zn-superoxide dismutase.

In addition to the usual superoxide dismutation activity, Cu,Zn-superoxide dismutase (SOD) has a peroxidative function that utilizes its own dismutation product, H2O2 as a substrate. The peroxidative activity of human Cu,Zn-SOD was studied by using a chromogen, 2,2'-azinobis-(3-ethylbenzthiazoline-6-sulfonate) (ABTS) which reacts with OH radicals to form ABTS+. The optimal pH for the peroxidative activity of human Cu,Zn-SOD was 7.6-9.5. The peroxidative activity retained about 50% of the maximum activity when exposed at 40 degrees C for 5 min. The peroxidative activity showed a typical Michaelis-Menten kinetics for ABTS and H2O2 whose K(m) values were 16 microM and 9.3 mM, respectively. The peroxidative activity of human Cu,Zn-SOD was inhibited about 60% by the copper chelator, diethyldithiocarbamate (DDC) at 10 microM while the dismutation activity was not inhibited under a similar condition. We found that there are differences in the effects of temperature and DDC on the dismutation and peroxidative activities of human Cu,Zn-SOD. These results suggest that the amino acid residues which affect the activities of this enzyme may be different between dismutation and peroxidation.

Benzothiazoles↗