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At least 73 records · Page 4Linked to original sources
PubMed1996

Spectrophotometric determination of hydrogen peroxide: catalase activity and rates of hydrogen peroxide removal by erythrocytes.

A new method of hydrogen peroxide determination for the measurement of catalase activity and rates of hydrogen peroxide removal by erythrocytes was described. Hydrogen peroxide was determined by converting it to the indamine dye with a water-soluble ironporphyrin and measuring the absorbance at 590 nm. This method was applied to the assay of catalase in hemolysates from human, rat and mouse blood. The activities obtained were in agreement with those obtained by other methods including UV method. The present method was also applied to the determination of rates of hydrogen peroxide removal by intact erythrocytes from human subjects, rats and mice. Data suggested that normal erythrocytes have substantial capacity to remove extracellular hydrogen peroxide. From the measurement of catalase activity in erythrocytes treated with 3-amino-1,2,4-triazole and rates of hydrogen peroxide removal by the erythrocytes, it is deduced that rate constants related to the hemoglobin content (k/g Hb) for hydrogen peroxide removal by catalase in normal and acatalasemic erythrocytes are 42.0 +/- 6.0 and 8.0 +/- 3.0, respectively.

Amitrole↗
PubMed1990

Increased levels of lipid peroxides in aged rat brain as revealed by direct assay of peroxide values.

Lipid peroxide concentrations in brain tissues of young and aged rats were determined by a direct method for measuring peroxide values. Three different brain regions were analyzed for lipid peroxides. The peroxide levels increased in all three regions of aged as compared to those of young rats, while lipid peroxides in plasma appeared to be stable along with age. Lipid peroxides in cerebrum and cerebellum increased 1.6-2.0 times in aged brains compared with young ones, and about 3-fold in the brain stem. Increased levels of lipid peroxides in aged brains seem not merely due to increased pools of precursor polyene fatty acids, but rather due to altered protection systems for lipid peroxidase formation.

Aging↗
PubMed2000

The effect of dietary treatment on erythrocyte lipid peroxidation, superoxide dismutase, glutathione peroxidase, and serum lipid peroxidation in patients with type 2 diabetes mellitus.

OBJECTIVES: The aim of the present study was to investigate the effect of dietary treatment on serum and erythrocyte lipid peroxidation and erythrocyte antioxidative enzyme activity of patients with Type 2 diabetes. DESIGN AND METHODS: A total of 30 patients with newly diagnosed as Type 2 diabetes were enrolled to the study. A total of 30 healthy subjects served as controls. Diabetic patients were given standard dietary treatment that was composed of 50% to 55% carbohydrate and 30% fat for 2 months. No diet was applied for controls. For both groups serum and erythrocyte lipid peroxidation and erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were obtained at first and at the end of 2 months. RESULTS: Diabetic patients had higher serum and erythrocyte lipid peroxidation than those of controls before dietary treatment(p < 0.05). However, there was no absolute differences in erythrocyte SOD and GSH-Px (p > 0.05). At the end of 2 months of dietary treatment, while diabetics had still higher glucose and erythrocyte lipid peroxidation than controls (p < 0.05), serum lipid peroxidation, erythrocyte SOD, and GSH-Px levels did not differ significantly from those of controls (p > 0.05). In diabetic patients, after 2 months of dietary treatment, whereas serum and erythrocyte lipid peroxidation decreased, erythrocyte SOD and GSH-Px activities showed significant increase (p < 0.05). CONCLUSIONS: Our results showed significant alteration in serum and erythrocyte lipid peroxidation and erythrocyte antioxidant enzyme status of patients with Type 2 diabetes by dietary treatment. However, whether such alterations have clinical importance for diabetic patients needs further investigation.

Adult↗
PubMed1995

Cloning and characterization of the katB gene of Pseudomonas aeruginosa encoding a hydrogen peroxide-inducible catalase: purification of KatB, cellular localization, and demonstration that it is essential for optimal resistance to hydrogen peroxide.

Pseudomonas aeruginosa is an obligate aerobe that is virtually ubiquitous in the environment. During aerobic respiration, the metabolism of dioxygen can lead to the production of reactive oxygen intermediates, one of which includes hydrogen peroxide. To counteract the potentially toxic effects of this compound, P. aeruginosa possesses two heme-containing catalases which detoxify hydrogen peroxide. In this study, we have cloned katB, encoding one catalase gene of P. aeruginosa. The gene was cloned on a 5.4-kb EcoRI fragment and is composed of 1,539 bp, encoding 513 amino acids. The amino acid sequence of the P. aeruginosa katB was approximately 65% identical to that of a catalase from a related species, Pseudomonas syringae. The katB gene was mapped to the 71- to 75-min region of the P. aeruginosa chromosome, the identical region which harbors both sodA and sodB genes encoding both manganese and iron superoxide dismutases. When cloned into a catalase-deficient mutant of Escherichia coli (UM255), the recombinant P. aeruginosa KatB was expressed (229 U/mg) and afforded this strain resistance to hydrogen peroxide nearly equivalent to that of the wild-type E. coli strain (HB101). The KatB protein was purified to homogeneity and determined to be a tetramer of approximately 228 kDa, which was in good agreement with the predicted protein size derived from the translated katB gene. Interestingly, KatB was not produced during the normal P. aeruginosa growth cycle, and catalase activity was greater in nonmucoid than in mucoid, alginate-producing organisms. When exposed to hydrogen peroxide and, to a greater extent, paraquat, total catalase activity was elevated 7- to 16-fold, respectively. In addition, an increase in KatB activity caused a marked increase in resistance to hydrogen peroxide. KatB was localized to the cytoplasm, while KatA, the "housekeeping" enzyme, was detected in both cytoplasmic and periplasmic extracts. A P. aeruginosa katB mutant demonstrated 50% greater sensitivity to hydrogen peroxide than wild-type bacteria, suggesting that KatB is essential for optimal resistance of P. aeroginosa to exogenous hydrogen peroxide.

Aerobiosis↗
PubMed2001

Comparison of the efficacy and safety of a combination topical gel formulation of benzoyl peroxide and clindamycin with benzoyl peroxide, clindamycin and vehicle gel in the treatments of acne vulgaris.

BACKGROUND: Topical clindamycin and benzoyl peroxide have each demonstrated clinical efficacy in the treatment of acne vulgaris. When used in combination, they promise greater efficacy than either individual agent used alone and the combined use of benzoyl peroxide with topical antibacterial has been shown to decrease the emergence of antibacterial resistant species. OBJECTIVE: The objective was to determine the efficacy and safety of a combination benzoyl peroxide plus clindamycin in a gel formulation compared with each of its 2 active constituents in gel vehicle, and gel vehicle given alone in the treatment of acne vulgaris. METHODS: In this 10-week, multicenter, double-blind trial, 480 patients with moderate to moderately severe acne were randomized to receive twice-daily treatment with 5% benzoyl peroxide plus 1% clindamycin, 5% benzoyl peroxide, 1% clindamycin, or vehicle. RESULTS: Significantly greater reductions in the number of inflammatory and total lesions were demonstrated in patients using combination therapy compared with those using any of its 3 individual components. Likewise, both physicians' and patients' global evaluations showed significantly greater improvements with the combination therapy than with its individual components. The most frequent adverse effect, dry skin, occurred to a similar extent in the combination and benzoyl peroxide treatment groups. CONCLUSION: The improved efficacy obtained with the combination therapy was accompanied by a tolerability profile similar to that of benzoyl peroxide alone, making this new combination product an alternative antimicrobial therapy for acne vulgaris.

Acne Vulgaris↗
PubMedDate not supplied

Effect of paraquat intoxication and ambroxol treatment on hydrogen peroxide production and lipid peroxidation in selected organs of rat.

Paraquat (Pq) is a herbicide which is very toxic to all animals and to man. It generates free radicals and leads to acute or chronic lung injury and usually to death. So far, the role of lipid peroxidation of cell membranes in the mechanism of its toxicity has not been proved satisfactorily and therefore in the present study we examined the concentration of hydrogen peroxide (H2O2) and various lipid peroxidation products (LPP) such as conjugated dienes (CD), lipid hydroperoxides (LH), malonyldialdehyde (MDA) and Schiff bases in selected organs of the rat given a single intraperitoneal dose 35 mg kg-1 Pq. We also evaluated the influence of a mucolytic and probably antioxidant drug, ambroxol, on Pq-induced changes in the concentration of H2O2 and LPP. Paraquat increased the hepatic concentration of H2O2, CD, LH and MDA by approximately fourfold. Though the dose of Pq was nearly twice the LD50 dose, we did not notice any changes in the concentration of these substances in the critical organ, lung or heart and kidney. Ambroxol alleviated the increase of H2O2 in the liver but did not reduce the concentration of LPP. Moreover, the drug administered alone induced lipid peroxidation in the liver. Our results indicate that Pq dose not induce H2O2 production and lipid peroxidation in the lung but it increases the concentration of H2O2 and LPP in the liver. Ambroxol inhibits the Pq-induced increase in the concentration of H2O2 in the liver without protecting it against lipid peroxidation. Moreover, the drug alone may act as a pro-oxidant.

Ambroxol↗
PubMed1995

Role of cytochrome b5 in NADH-dependent microsomal reduction of ferric complexes, lipid peroxidation, and hydrogen peroxide generation.

The NADH-dependent microsomal electron transfer system consists of NADH-cytochrome b5 reductase and cytochrome b5, which donates reducing equivalents to fatty acyl desaturase, cytochrome P450, and other reactions. A study was carried out to investigate the interaction of NADH with several ferric complexes and to evaluate the role of cytochrome b5 in these interactions. NADH-dependent microsomal lipid peroxidation was stimulated by ferric-ATP, ferric-histidine, and ferric-ammonium sulfate, but not by ferric-EDTA. Anti-cytochrome b5 IgG produced a concentration-dependent inhibition of lipid peroxidation catalyzed by all three ferric complexes. Addition of purified cytochrome b5 to the microsomes increased the rate of lipid peroxidation with all three ferric complexes. Lipid peroxidation in control and the cytochrome b5-fortified microsomes was not sensitive to superoxide dismutase, catalase, or DMSO and was completely inhibited by trolox and propylgallate. Ferric-EDTA stimulated NADH-dependent microsomal production of H2O2 and NADH consumption. Anti-cytochrome b5 IgG had only a small inhibitory effect on this stimulation by ferric-EDTA. NADH supported microsomal reduction of ferric complexes in the order ferric-ATP > ferric-histidine approximately ferric-ammonium sulfate > ferric-EDTA. Anti-cytochrome b5 IgG inhibited, whereas added cytochrome b5 stimulated, the reduction of ferric-ATP, ferric-histidine, and ferric-ammonium sulfate, whereas reduction of ferric-EDTA was not affected by these additions. Ferric-ATP, at high concentrations, was more effective than ferric-histidine or ferric-ammonium sulfate in stimulating lipid peroxidation and in becoming reduced by NADH-dependent microsomal electron transport; anti-cytochrome b5 IgG was less inhibitory and added b5 was less stimulatory at 50 microM ferric-ATP compared to 5 microM ferric-ATP or 50 microM ferric-histidine or 50 microM ferric-ammonium sulfate. It is concluded that cytochrome b5 is required for reduction of low and high concentrations of ferric-histidine and ferric-ammonium sulfate and low concentrations of ferric-ATP and for the lipid peroxidation catalyzed by these ferric complexes. The reductase, not cytochrome b5, is involved in interaction with ferric-EDTA. Higher concentrations of ferric-ATP can also interact with the reductase, as well as with cytochrome b5.

Animals↗
PubMed1992

Ferric(III) ions inhibits copper(II)/hydrogen peroxide-catalyzing lipid peroxidation in human erythrocyte membranes.

1. Effect of ferric ions (Fe3+) on the lipid peroxidation catalyzed by copper ions (Cu2+) and hydrogen peroxide (H2O2) was studied in human erythrocyte membranes. 2. The formation of thiobarbituric acid-reactive products elicited by CuCl2/H2O2 was inhibited by FeCl3 in a concentration-dependent manner; 0.25 mM FeCl3 were enough to cause 50% inhibition of the formation of peroxides. 3. The inhibitory effect of FeCl3 is not due to competition against Cu2+. 4. FeCl3 inhibited the initiation, but did not inhibit the propagation of Cu2+/H2O2-catalyzing lipid peroxidation. 5. In the heat- or trypsin-treated erythrocyte membranes, FeCl3 had no inhibitory effect on Cu2+/H2O2-catalyzing lipid peroxidation. 6. Sodium azide, an inhibitor of catalase, had no effect on the inhibitory effect of FeCl3. 7. These results suggest that a protein factor(s), which is not catalase, is involved in the inhibition of Cu2+/H2O2-catalyzing lipid peroxidation by Fe3+.

Copper↗
PubMed2002

Lipid peroxidation induced by indomethacin with horseradish peroxidase and hydrogen peroxide: involvement of indomethacin radicals.

Some of the side-effects of using indomethacin (IM) involve damage to the gastric mucosa and liver mitochondria. On the other hand, neutrophils infiltrate inflammatory sites to damage the tissues through the generation of reactive oxygen species by myeloperoxidase. The stomach and intestine have large amounts of peroxidase. These findings suggest that peroxidases are involved in tissue damage induced by IM. To clarify the basis for the tissue damage induced by IM in the presence of horseradish peroxidase (HRP) and H2O2 (HRP-H2O2), lipid peroxidation was investigated. When IM was incubated with liver microsomes in the presence of HRP-H2O2 and ADP-Fe3+, lipid peroxidation was time-dependent. Catalase and desferrioxamine almost completely inhibited lipid peroxidation, indicating that H2O2 and iron are necessary for lipid peroxidation. Of interest, superoxide dismutase strongly inhibited lipid peroxidation, and it also inhibited the formation of bathophenanthroline-Fe2+, indicating that reduction of the ferric ion was due to superoxide (O2-). ESR signals of IM radicals were detected during the interaction of IM with HRP-H2O2. However, the IM radical by itself did not reduce the ferric ion. These results suggest that O2- may be generated during the interaction of IM radicals with H2O2. Ferryl species, which are formed during the reduction of iron by O2-, probably are involved in lipid peroxidation.

Animals↗
PubMed1999

Lipid peroxidation induced by the Cu,Zn-superoxide dismutase and hydrogen peroxide system.

Cu,Zn-superoxide dismutase (SOD) can catalyze hydroxyl radical generation using H2O2 as a substrate. Lipid peroxidation induced by the Cu,Zn-SOD and H2O2 system was investigated. When linoleic acids micelles or phosphatidylcholine liposomes were incubated with Cu,Zn-SOD and H2O2, lipid peroxidation was gradually increased in a time-dependent manner. The extent of lipid peroxidation was proportional to Cu,Zn-SOD and H2O2 concentrations. Hydroxyl radical scavengers and copper chelator inhibited lipid peroxidation induced by the Cu,Zn-SOD and H2O2 system. These results suggest that lipid peroxidation is mediated by the Cu,Zn-SOD and H2O2 system via the generation of hydroxyl radicals by a combination of the peroxidative reaction of Cu,Zn-SOD and the Fenton-like reaction of free copper released from oxidatively damaged SOD.

Copper↗
PubMed1977

Studies on vitamin E and selenium deficiency in young pigs. II. The hydrogen peroxide hemolysis test and the measure of red cell lipid peroxides as indices of vitamin E and selenium status.

The usefulness of the hydrogen peroxide hemolysis test and the measure of red cell lipid peroxides as indices of vitamin E and selenium deficiency in swine has been evaluated. Results indicated that although the hydrogen peroxide hemolysis test may be of some indication of the vitamin E status, it is not a reliable index of vitamin E deficiency in swine, at least on an individual basis. In contrast, the measure of red cell lipid peroxides can be considered a reliable test for vitamin E deficiency in swine. The hydrogen peroxide hemolysis test and the red cell lipid peroxides were not significantly affected by selenium deficiency.

Animals↗
PubMed1987

Effect of succinate on mitochondrial lipid peroxidation. 1. Comparative studies on ferrous ion and ADP . Fe/NADPH-induced peroxidation.

Lipid peroxidation in isolated rat liver mitochondria, mitoplast, and mitochondrial inner membrane fragments was induced either by ferrous ions, or in an NADPH-dependent process by complexing with adenine nucleotides (ADP or ATP) iron. The Fe2+-induced lipid peroxidation is nonenzymic when inner membrane fragments are used, while the differences in the inhibitory effect of Mn2+ ions and the stimulatory effect of the ionophore A-23187 in mitochondria and inner membrane fragments suggest an enzymic mechanism for ferrous ion-induced lipid peroxidation in intact mitochondria. Contrary to this the ADP/Fe/NADPH-dependent lipid peroxidation is an enzymic process both in mitochondria and inner membrane preparations. We have shown that cytochrome P450 is involved in the ADP/Fe/NADPH-induced lipid peroxidation. Succinate, a known inhibitor of NADPH-dependent lipid peroxidation, inhibited the Fe2+-induced process also, and there was no difference in this effect when inner membrane preparations, mitochondria, or mitoplasts were used.

Adenosine Diphosphate↗
PubMed1979

Reaction between peroxidized phospholipid and protein: II. Molecular weight and phosphorus content of albumin after reaction with peroxidized cardiolipin.

Peroxidized cardiolipin (diphosphatidylglycerol) reacts covalently with albumin. Incubation of albumin with increasing amounts of peroxidized cardiolipin produces a gradual increase in molecular size. Incubation with a small amount of peroxidized cardiolipin (molar ratio of cardiolipin/albumin 21) produces a mixture of complexes that differs considerably with respect to the number of cardiolipin molecules bound per molecule of albumin. With larger amounts of peroxidized cardiolipin (molar ratios of cardiolipin/albumin 54 and 114), the complexes formed seem to be of a more uniform type since the numbers of cardiolipin molecules bound per molecule of albumin are similar. No polymerization occurs for reactions in which up to at least 15 moles of cardiolipin have become bound per mole of albumin, and 20--25 moles may be found with only very little polymerization. Only when the ratio of peroxidized cardiolipin to albumin was increased to a high value of 314 did polymerization occur. The present findings show that extensive covalent binding of peroxidized cardiolipin to albumin can occur without intermolecular crosslinking of the protein.

Albumins↗
PubMed1997

Treatment of acne with a combination clindamycin/benzoyl peroxide gel compared with clindamycin gel, benzoyl peroxide gel and vehicle gel: combined results of two double-blind investigations.

BACKGROUND: It has previously been shown that a combination of erythromycin and benzoyl peroxide is superior to either ingredient when used alone in the treatment of acne. A clindamycin/benzoyl peroxide combination gel might have an advantage over erythromycin/benzoyl peroxide gel because the former does not require refrigeration after it is dispensed. OBJECTIVE: Our purpose was to determine the efficacy and safety of a combination clindamycin/benzoyl peroxide gel when compared with benzoyl peroxide, clindamycin, or vehicle gels. METHODS: In two double-blind, randomized, parallel, vehicle-controlled trials, patients were treated for 11 weeks with once-nightly application of one of the above preparations. Evaluations were performed at 2, 5, 8, and 11 weeks and included lesion counts and assessment of global responses and irritant effects. RESULTS: A total of 334 patients completed the study. All three active preparations were significantly superior to the vehicle in global improvement and in reducing inflammatory lesions and noninflammatory lesions. The combination gel was significantly superior to the two individual agents in global improvement and reduction of inflammatory lesions and also to the clindamycin gel in reducing noninflammatory lesions. There was no significant difference in tolerance to the active gels versus the vehicle gel. CONCLUSION: In the treatment of acne, topical clindamycin/benzoyl peroxide combination gel is well tolerated and superior to either individual ingredient.

Acne Vulgaris↗
PubMed1983

Hydrogen peroxide excretion by oral streptococci and effect of lactoperoxidase-thiocyanate-hydrogen peroxide.

Approved type strains of Streptococcus sanguis, S. mitis, S. mutans, and S. salivarius were grown under aerobic and anaerobic conditions. The rate of hydrogen peroxide excretion, oxygen uptake, and acid production from glucose by washed-cell suspensions of these strains were studied, and the levels of enzymes in cell-free extracts which reduced oxygen, hydrogen peroxide, or hypothiocyanite (OSCN-) in the presence of NADH or NADPH were assayed. The effects of lactoperoxidase-thiocyanate-hydrogen peroxide on the rate of acid production and oxygen uptake by intact cells, the activity of glycolytic enzymes in cell-free extracts, and the levels of intracellular glycolytic intermediates were also studied. All strains consumed oxygen in the presence of glucose. S. sanguis, S. mitis, and anaerobically grown S. mutans excreted hydrogen peroxide. There was higher NADH oxidase and NADH peroxidase activity in aerobically grown cells than in anaerobically grown cells. NADPH oxidase activity was low in all species. Acid production, oxygen uptake, and, consequently, hydrogen peroxide excretion were inhibited in all the strains by lactoperoxidase-thiocyanate-hydrogen peroxide. S. sanguis and S. mitis had a higher capacity than S. mutans and S. salivarius to recover from this inhibition. Higher activity in the former strains of an NADH-OSCN oxidoreductase, which converted OSCN- into thiocyanate, explained this difference. The change in levels of intracellular glycolytic intermediates after inhibition of glycolysis by OSCN- and the actual activity of glycolytic enzymes in cell-free extracts in the presence of OSCN- indicated that the primary target of OSCN- in the glycolytic pathway was glyceraldehyde 3-phosphate dehydrogenase.

Depression, Chemical↗
PubMed2004

Vital bleaching with a thin peroxide gel: the safety and efficacy of a professional-strength hydrogen peroxide whitening strip.

BACKGROUND: Use of higher peroxide concentrations for professional at-home vital bleaching often balances two factors in patient compliance: whitening and tolerability. Development of a polyethylene strip coated with a very thin (0.10-millimeter) layer of 14 percent hydrogen peroxide gel (Crest Whitestrips Supreme, Procter & Gamble, Cincinnati)--which represents an increase in concentration and a decrease in amount of gel--was believed to allow for greater at-home whitening with little additional oral soft-tissue exposure to peroxide. METHODS: The authors conducted a randomized, double-blind, two-week clinical trial with 38 adults to evaluate the safety and efficacy of twice-daily use of the thin, concentrated bleaching gel strip versus the effects of a control product (Crest Whitestrips, Procter & Gamble). The two products differed only in concentration (14 percent versus 6 percent) and gel layer thickness (0.10 mm versus 0.20 mm). The authors measured efficacy from digital images using the Commission Internationale de l'Eclairage L*a*b* color scale. They assessed safety via subject interviews and clinical examination and compared treatments using analysis of covariance. RESULTS: Relative to baseline color, both strip groups exhibited significant (P < .001) improvement in yellowness, brightness and composite color change. Between-group comparisons after two weeks demonstrated significant (P < .003) color improvement for the experimental strip relative to the control. Both products were well-tolerated generally. Despite the concentration differences, clinical examination of each group showed a similar low level (11 percent) of "minor oral irritation." CONCLUSION: Use of the thin 14 percent hydrogen peroxide gel strip resulted in greater whitening, including 42 to 49 percent greater improvement in tooth color and faster whitening onset than that seen with a 6 percent hydrogen peroxide whitening strip, without clinical evidence of increased oral-tissue irritation. CLINICAL IMPLICATIONS: Use of whitening strips with a thin, concentrated layer of hydrogen peroxide gel may represent a useful approach for professionally directed at-home vital bleaching.

Adolescent↗
PubMed2003

Apoptotic-resistance of the human osteosarcoma cell line HS-Os-1 to irradiation is converted to apoptotic-susceptibility by hydrogen peroxide: a potent role of hydrogen peroxide as a new radiosensitizer.

In our previous study, we demonstrated that the radioresistance of the human osteosarcoma cell line HS-Os-1, was considered to arise, at least in part, from the low level of ROS formation following irradiation, which in turn may have resulted from the strong scavenging ability of the cells for free radicals, including hydroxyl radicals. Following the study, we found that addition of 1 or 10 mM hydrogen peroxide induced ROS formation, oxidative DNA damage, dysfunction of the mitochondrial membrane potential, and early apoptotic changes in the human osteosarcoma cell line HS-Os-1. We therefore speculated that combined use of irradiation and hydrogen peroxide might exert an additive effect for apoptotic-resistant tumors such as the human osteosarcoma cell line HS-Os-1, in terms of preservation of the radiation-induced hydroxyl radical production supported by the intracellular ROS formation that is induced by exogenous hydrogen peroxide addition. Therefore, in this study, we examined the effect of various doses of irradiation on the existence of 0.1 mM hydrogen peroxide in the culture medium. We found that irradiation with 10 or 20 Gy, under the condition of the presence of 0.1 mM hydrogen peroxide, induced ROS formation, oxidative DNA damage, dysfunction of the mitochondrial membrane potential, and early apoptotic changes in the human osteosarcoma cell line HS-Os-1, though ROS formation and oxidative DNA damage were scarcely seen in response to irradiation of up to 30 Gy, as was shown in our previous study. We therefore concluded that the combined modality of irradiation and such a low concentration of hydrogen peroxide (0.1 mM) is potentially applicable in clinical radiotherapy for many kinds of apoptotic-resistant neoplasms in terms of achieving both local control and improving survival benefit of patients.

Annexin A5↗
PubMed1989

The inhibition of lipid peroxidation by disulfiram prevents the killing of cultured hepatocytes by allyl alcohol, tert-butyl hydroperoxide, hydrogen peroxide and diethyl maleate.

Disulfiram is a potent antioxidant that prevented the peroxidation of microsomal phospholipids induced by ADP/Fe3+ at concentrations as low as 1 microM. However, disulfiram had a biphasic action when used to assess the role of lipid peroxidation in the killing of cultured hepatocytes by an acute oxidative stress. At a relatively low concentration (10 microM), the antioxidant activity of disulfiram predominated, and there was protection against the killing of the hepatocytes by allyl alcohol, tert-butyl hydroperoxide, hydrogen peroxide, and diethyl maleate. As the concentration of disulfiram was increased above 10 microM, the extent of protection progressively decreased. Thus, with higher concentrations of disulfiram, there was a second action whose consequence is to obscure the protective effect of the lower doses. With the agents studied, this additional and as yet undefined action of disulfiram leads to the killing of the hepatocytes by a mechanism that is unrelated to the peroxidation of lipids. This biphasic action of disulfiram must be appreciated in any attempt to use this compound to assess the role of lipid peroxidation in toxic cell injury.

1-Propanol↗