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PubMed2000

Hydrogen peroxide induces midzonal heat shock protein 72 and apoptosis in sinusoidal endothelial cells of hypoxic rat liver.

OBJECTIVE: To investigate the heat shock protein (HSP) 72 expression and apoptosis induced by hydrogen peroxide in hypoxic rat liver. DESIGN: Prospective control study using the isolated rat liver. SETTING: Animal research facility. SUBJECTS: Fasted, pathogen-free specific, male Sprague-Dawley rats. INTERVENTIONS: A low-flow hypoxia model was made by reducing an afferent pressure from 10 to 2.5 cm H2O, and by perfusing the isolated rat liver for 2 hrs. MEASUREMENT AND MAIN RESULTS: We investigated the hydrogen peroxide production by using the 2'-7' dichlorofluorescein image, the induction of HSP 72 by using immunohistochemistry, and apoptosis by using terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end-labeling method in the low flow hypoxic rat liver. In low-flow hypoxia, hydrogen peroxide production, HSP 72 expression, and apoptosis were induced in the midzone of rat liver. Prevalence of HSP 72 expression was higher in the sinusoidal endothelial cells (SEC) than in the hepatocytes. All apoptotic cells were SEC with expression of HSP 72. Hydrogen peroxide was derived from hepatocytes. Pretreatment with the specific xanthine oxidase inhibitor, sodium(-)-8-(3-methoxy-phenylsulfinylphenyl) pyrazolo [1,5-a]-1,3,5-triazine-4-olate monohydrate significantly attenuated hydrogen peroxide production, HSP 72 expression, and apoptosis of SEC in the midzone. CONCLUSION: Xanthine oxidase-dependent hydrogen peroxide induces midzonal and SEC-dominant HSP 72 expression and apoptosis in hypoxic rat liver.

Animals↗
PubMed1988

Ocular response to hydrogen peroxide.

A controlled, randomized, double-masked study was conducted on eight human subjects to determine the threshold level of hydrogen peroxide, which is toxic when introduced into the eye via a high water content (75%; Durasoft 4) hydrogel contact lens. Subjective comfort, conjunctival hyperemia, corneal and conjunctival epithelial staining, and corneal oxygen uptake were assessed in response to 5-min wear of lenses that were presoaked in isotonic saline solutions of physiologic pH containing 0, 25, 50, 100, 200, 400, and 800 parts per million (ppm) hydrogen peroxide. Higher levels of hydrogen peroxide were associated with greater discomfort (p less than 0.05) and increased conjunctival hyperemia (p less than 0.001). The highest level of hydrogen peroxide tested (800 ppm) did not induce significant corneal or conjunctival epithelial staining or alter the corneal aerobic response. We conclude that residual concentrations of hydrogen peroxide in contact lens care systems should not exceed 100 ppm. Practitioners can use these data to estimate the level of residual hydrogen peroxide to which a patient may have been exposed upon lens application after neutralization.

Adult↗
PubMed2005

The role of placental oxidative stress and lipid peroxidation in preeclampsia.

UNLABELLED: Preeclampsia is a complex multisystem disorder exclusively seen in human species that is characterized by hypertension and proteinuria. This disorder has the highest maternal and fetal morbidity and mortality of all pregnancy-related complications. Growing evidence suggests that placental oxidative stress is involved in the etiopathogenesis of preeclampsia. Reduced perfusion as a result of abnormal placentation leads to ischemia reperfusion injury to the placenta. Placental oxidative stress, which results from the ischemia reperfusion injury, is being increasingly reported to be involved in the etiopathogenesis of preeclampsia. It has been proposed as a promoter of lipid peroxidation and the endothelial cell dysfunction that is commonly seen in this condition. Although preeclampsia is characterized by increased lipid peroxidation and diminished antioxidant capacity, there is no consensus regarding causality of lipid peroxidation in preeclampsia. In this article, we address the question of the biologic association of lipid peroxidation and preeclampsia. Lipid peroxidation and leukocyte activation may play a pivotal role in endothelial cell dysfunction. We also review the different factors that have been proposed to cause endothelial cell dysfunction in preeclampsia, trials investigating the role of antioxidant supplementation in preeclampsia, and the lack of consensus among the trials. Additional longitudinal studies are necessary to determine if the various oxidative stress biomarkers estimated early in pregnancy can be narrowed to a single marker for predicting preeclampsia. TARGET AUDIENCE: Obstetricians & Gynecologists, Family Physicians. LEARNING OBJECTIVES: After completion of this article, the reader should be able to recall that placental oxidative stress is involved in the etiopathogenesis of preeclampsia, state that placental oxidative stress results from ischemic reperfusion injury, and explain that ischemic reperfusion injury is a promoter of lipid peroxidation and endothelial cell dysfunction seen in preeclampsia.

Antioxidants↗
PubMed2002

Resistance to hydrogen peroxide in Helicobacter pylori: role of catalase (KatA) and Fur, and functional analysis of a novel gene product designated 'KatA-associated protein', KapA (HP0874).

Helicobacter pylori infection elicits an aggressive inflammatory response that the bacterium is able to resist by virtue of its well-adapted antioxidant defence mechanisms. Catalase (KatA) appears to be a key enzyme in this resistance. Upstream of katA, a low-affinity ferric uptake regulator (Fur)-box has been identified. Downstream of katA, an ORF (HP0874) with no known function has also been identified. Non-polar isogenic mutants of katA, fur and HP0874 were constructed by allelic exchange. The impact of these mutations on the catalase activities and bacterial viability following exposure to hydrogen peroxide was studied. Concurrently, the effect of variation in the iron content of the media used to grow the cells was determined. The data showed that catalase-deficient isolates of H. pylori were hypersensitive to hydrogen peroxide, whereas wild-type cells could resist approximately approximately 100 mM hydrogen peroxide. Fur-deficient mutants and cells grown on low-iron-containing medium showed a distinct reduction in catalase activity and increased sensitivity to hydrogen peroxide. The data suggest a direct or indirect effect of Fur and iron on the activity of catalase. HP0874-deficient mutants showed no reduction in catalase activity but showed an increased sensitivity to hydrogen peroxide. That is, the protein encoded by HP0874 appears to have a role in resistance to hydrogen peroxide not directly related to catalase activity. This is the first report of a functional relationship of the product of this ORF. There is evidence of protein-protein interaction between KatA and the product encoded by HP0874, and the name 'KatA-associated protein' (KapA) is proposed.

Arabidopsis Proteins↗
PubMed1983

Hydrogen peroxide release from eosinophils: quantitative, comparative studies of human and guinea pig eosinophils.

Eosinophils play an important role in host defense against parasitic infection, employing both oxidative and nonoxidative systems to effect damage. The active oxygen product, hydrogen peroxide, either alone or in combination with the enzyme eosinophil peroxidase, may damage parasites. These studies use a sensitive fluorometric assay to document the release of hydrogen peroxide from guinea pig peritoneal exudate eosinophils and human peripheral blood eosinophils. Guinea pig eosinophils released 0.13 +/- 0.02 (n = 10) nmol H2O2/10(5) eos/5 min under resting conditions which were markedly increased when stimulated by phorbal myristate acetate (PMA, 1 microgram/ml) [4.80 +/- 0.50 (19) nmol H2O2/10(5) eos/5 min], preopsonized zymosan [2.40 +/- 0.17 (4) nmol H2O2/10(5) eos/5 min], or latex beads [1.14 +/- 0.26 (5) nmol H2O2/10(5) eos/5 min]. Normal human peripheral blood eosinophils had greater resting release of hydrogen peroxide [0.34 +/- 0.05 (8) nmol H2O2/10(5) eos/5 min], but were less effectively stimulated by PMA [3.12 +/- 0.57 (9) nmol H2O2/10(5) eos/5 min], preopsonized zymosan [0.78 +/- 0.16 (8) nmol H2O2/10(5) eos/5 min] or latex beads [0.69 +/- 0.32 (6) nmol H2O2/10(5) eos] (p less than or equal to 0.05). Hydrogen peroxide release was markedly enhanced by the presence of exogenous glucose and was linearly dependent upon cell number when the soluble stimulus PMA was used. Particle-stimulated hydrogen peroxide was not necessarily enhanced by increases in the particle:cell ratio. The demonstration of the release of large amounts of hydrogen peroxide from eosinophils is further support for the concept that eosinophils play an active role in host defense.

Animals↗
PubMed1993

Quantification of hydrogen peroxide generation by Granuflex (DuoDERM) Hydrocolloid Granules and its constituents (gelatin, sodium carboxymethylcellulose, and pectin).

The hydrogen peroxide generating capacity of Granuflex Hydrocolloid Granules and its constituents (porcine gelatin, sodium carboxymethylcellulose and pectin) was examined using the scopoletin-horseradish peroxidase assay in the presence and absence of catalase. Oxygen purging reduced the formation of hydrogen peroxide by 77-96%. The total concentrations of hydrogen peroxide detected were 1.9 x 10(-6), 1.2 x 10(-6) and 2.3 x 10(-6) mol/l for Granuflex, pectin and gelatin (using 0.5% w/v), respectively, after 48 h incubation in a phosphate buffer, pH 7.4, at 37 degrees C. No hydrogen peroxide was formed by sodium carboxymethylcellulose. The results indicate that hydrogen peroxide generation by Granuflex may be ascribed to its gelatin and pectin components, but not to the sodium carboxymethylcellulose. The release of low levels of hydrogen peroxide into the wound environment could conceivably contribute both to the inflammatory phase and to fibroblast proliferation, and hence to the granulation phase of wound healing.

Animals↗
PubMed1992

A double-blind evaluation of topical isotretinoin 0.05%, benzoyl peroxide gel 5% and placebo in patients with acne.

A double-blind, randomized study comparing isotretinoin gel (Isotrex), its vehicle base, and benzoyl peroxide was performed on 77 patients with mild to moderate acne vulgaris. The effect of treatment was assessed by acne grade and lesion count. The vehicle base had no effect, but both active groups produced significant improvements. Benzoyl peroxide and isotretinoin significantly reduced non-inflamed lesions at 4 (P < 0.05), 8 (P < 0.01), 12 (P < 0.01) weeks. Benzoyl peroxide had a more rapid effect on inflamed lesions, their being significant reductions at 4, 8 and 12 weeks (P < 0.01), whereas with isotretinoin there was a significant improvement at 12 weeks (P < 0.01). In addition, compared to placebo, both active treatments significantly reduced inflamed and non-inflamed lesions. Acne grade had improved significantly in the benzoyl peroxide group by 4 weeks (P < 0.01) and in the isotretinoin group by 8 weeks (P < 0.05). No significant change in haematological or biochemical parameters occurred. An irritant dermatitis occurred equally with both treatments but was well tolerated by the patients. This data confirms the clinical benefit of benzoyl peroxide in acne. The initial effect of isotretinoin on non-inflamed lesions in this study suggests that the prime mode of action is on comedone formation or separation whereas benzoyl peroxide has an effect on both comedones and inflammation.

Acne Vulgaris↗
PubMed1991

Cyclosporin-A-induced lipid peroxidation in human liver microsomes and its influence on cytochrome P-450.

The present in vitro study using human liver tissue was performed to investigate the effect of cyclosporin A on lipid peroxidation and cytochrome P-450 concentration in isolated liver microsomes. Incubations were either carried out with cyclosporin A concentrations of 10, 30, 100 and 300 micrograms ml-1 for 1 h or for different time periods (15, 30, 60 and 90 min) with cyclosporin A 300 micrograms ml-1. Lipid peroxidation was monitored measuring the amount of malondialdehyde. In additional experiments the effect of reduced and oxidized glutathione (1 mM) on cyclosporin-A-induced lipid peroxidation in human liver microsomes was studied. Cyclosporin A caused a significant dose and time-dependent increase of the lipid peroxidation product malondialdehyde. At the highest cyclosporin A concentration (300 micrograms ml-1) malondialdehyde production increased 5-fold in comparison to corresponding control values. Incubations for different time periods resulted in a 5-fold net increase of malondialdehyde formation after 90 min. In the presence of reduced glutathione, cyclosporin-A-induced lipid peroxidation was significantly inhibited. Furthermore, cyclosporin-A-induced microsomal lipid peroxidation was accompanied by a significant dose-dependent decline of the microsomal cytochrome P-450 content. At a cyclosporin A concentration of 300 micrograms ml-1, cytochrome P-450 content was decreased to 49% in comparison to control values. In the presence of reduced glutathione, cyclosporin A decreased the cytochrome P-450 concentration only to 79% (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Cyclosporine↗
PubMed2005

Decontamination assessment of Bacillus anthracis, Bacillus subtilis, and Geobacillus stearothermophilus spores on indoor surfaces using a hydrogen peroxide gas generator.

AIMS: To evaluate the decontamination of Bacillus anthracis, Bacillus subtilis, and Geobacillus stearothermophilus spores on indoor surface materials using hydrogen peroxide gas. METHODS AND RESULTS: Bacillus anthracis, B. subtilis, and G. stearothermophilus spores were dried on seven types of indoor surfaces and exposed to > or =1000 ppm hydrogen peroxide gas for 20 min. Hydrogen peroxide exposure significantly decreased viable B. anthracis, B. subtilis, and G. stearothermophilus spores on all test materials except G. stearothermophilus on industrial carpet. Significant differences were observed when comparing the reduction in viable spores of B. anthracis with both surrogates. The effectiveness of gaseous hydrogen peroxide on the growth of biological indicators and spore strips was evaluated in parallel as a qualitative assessment of decontamination. At 1 and 7 days postexposure, decontaminated biological indicators and spore strips exhibited no growth, while the nondecontaminated samples displayed growth. CONCLUSIONS: Significant differences in decontamination efficacy of hydrogen peroxide gas on porous and nonporous surfaces were observed when comparing the mean log reduction in B. anthracis spores with B. subtilis and G. stearothermophilus spores. SIGNIFICANCE AND IMPACT OF THE STUDY: These results provide comparative information for the decontamination of B. anthracis spores with surrogates on indoor surfaces using hydrogen peroxide gas.

Bacillaceae↗
PubMed1982

Peroxide-induced conformational transitions of peanut storage protein (arachin).

Several effects of peroxides on protein have been described in the literature. Some of the effects have been ascribed to alterations in protein conformation but this has never been examined directly. This paper described responses of peanut storage globulin (arachin) to rancid oil and hydrogen peroxide as measured by electrophoretic mobility, antigenicity and circular dichroism of the globulin. Rancid oil and 3% hydrogen peroxide had little effect on these properties but 30% hydrogen peroxide increased the mobility, abolished the antigenicity and reduced the ordered structural modes of the protein. The results indicated that changes in protein conformation do not occur after contact with organoleptically rancid oil or dilute peroxides but do occur with concentrated peroxides.

Arachis↗
PubMed1991

Plaque-growth inhibiting effect of chewing gum containing urea hydrogen peroxide.

The plaque-reducing effect of a chewing gum containing hydrogen peroxide was assessed. 12 dental hygienist students participated in a double-blind 3 x randomly crossed-over study. During the 4-day test periods, from Monday to Friday, no oral hygiene measures were allowed other than chewing 2 pieces of gum for approximately 10 min 5 x daily. The 800 mg pieces of gum were V6+regular (V6+) containing 0.4 g sorbitol and 6.3 mg hydrogen peroxide, V6 placebo gum (PLAC) containing 0.45 g sorbitol and no hydrogen peroxide, and only the gum base (GB) as a negative control. The quantity of plaque was assessed using the plaque index and the visible plaque index, and by scraping "all" plaque off the teeth in half the mouth during 2.5 min for determination of plaque wet weight. With all 3 measurements, chewing of the hydrogen peroxide-releasing gum (V6+) resulted in significantly lower plaque increments, from Monday to Friday, than chewing of the gum base (P less than 0.05). Chewing of the V6 placebo gum (PLAC) resulted in plaque scores which differed from neither those recorded after use of the hydrogen peroxide releasing (V6+) nor the placebo (GB) gums. The observed plaque-growth inhibiting effect of the hydrogen peroxide-releasing chewing gum in the present study was found to be of limited clinical significance.

Chewing Gum↗
PubMedDate not supplied

UV-dependent quinolone-induced human erythrocyte membrane lipid peroxidation: studies on the phototoxicity of Y-26611, a new quinolone derivative.

Quinolone antibacterial drugs are widely used as oral therapeutic agents. However, in some patients they cause ultraviolet (UV)-dependent dermatitis. Using lipid peroxidation as an index of phototoxicity, we studied the effects of a new quinolone derivative, Y-26611 together with ofloxacin, sparofloxicin and lomefloxacin on washed human erythrocyte suspensions. Irradiation of erythrocytes with UV-A or UV-B for 60 min. in the presence of Y-26611 (30-600 micrograms/ml) strong dose dependent lipid peroxidation, up to 17.01 nmoles/ml was induced. Under identical conditions, lipid peroxidation induced by up to 600 micrograms/ml ofloxacin, sparofloxacin or lomefloxacin were 0.94, 3.36 and 2.98 nmoles/ml respectively. The lipid peroxidation was entirely dependent on both UV as well as the drug. The lipid peroxidation responses to drug+UV could completely be inhibited by sodium azide (hydroxyl radical, HO. and single oxygen, 1O2 scavenger) or by phenyl N-tert-butylnitrone (PBN, HO. and superoxide anion radical, O2- scavenger). It is likely that reactive oxygen species generated by interaction between UV-sensitized drug molecules and oxygen molecules mediate erythrocyte membrane lipid peroxidation. The method used in this study is rapid and convenient for screening drugs for UV-dependent cytotoxicity.

4-Quinolones↗
PubMed1995

Role of Ca2+ on endotoxin-sensitivity by galactosamine challenge: lipid peroxide formation and hepatotoxicity in zymosan-primed mice.

This study was investigated to clarify the role of intracellular Ca2+ following endotoxin treatment (1 mg/kg, intraperitoneally) to D-galactosamine-sensitized mice (400 mg/kg, intraperitoneally), and to observe lipid peroxide levels, an index of hepatotoxicity, in endotoxin/galactosamine (Ga1N)-challenged mice under activation of macrophages, especially Kupffer cells, by zymosan. The liver lipid peroxide level and serum glutamic pyruvic transminase activity in mice 18 hr after administration of endotoxin/Ga1N were markedly higher than those in mice treated only with endotoxin. In spite of an increase in lipid peroxide formation, there was little or no effect of Ga1N administration on xanthine oxidase and superoxide dismutase activities in mice given endotoxin. However, the injection of verapamil (10 mg/kg, subcutaneously) markedly decreased lipid peroxide levels in liver of endotoxin/Ga1N-injected mice. In the mice given a Ca(2+)-deficient diet, lipid peroxide level in liver after endotoxin/Ga1N injection was markedly decreased compared to that in mice fed a normal diet. Administration of dexamethasone (200 micrograms/kg, intraperitoneally) in mice 1 hr before treatment with endotoxin/Ga1N did not induce lipid peroxide formation. Administration of endotoxin to Ga1N-treated mice resulted in a higher level of liver cytosolic free Ca2+ ([Ca2+]i) than that in endotoxin-treated mice. On the other hand, Ca(2+)-ATPase activity in liver plasma membrane in the endotoxin/Ga1N-treated mice was markedly decreased as compared with endotoxin alone. On the contrary, the Ca(2+)-ATPase activity in liver mitochondria was higher in endotoxaemic mice treated with GA1N than in mice given endotoxin alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine Transaminase↗
PubMed1999

Inhibition of lipid peroxidation by pindolol.

Among beta-blockers, including atenolol, metaproterenol, pindolol and propranolol, only pindolol strongly inhibited lipid peroxidation induced by xanthine oxidase-hypoxanthine in the presence of adenosine-5'-phosphate-Fe3+. In the reaction system, superoxide predominantly reduced iron because superoxide dismutase strongly prevented the iron reduction. However, pindolol had no effect on the superoxide-dependent iron reduction. Adding superoxide dismutase immediately stopped the lipid peroxidation, indicating that superoxide is closely connected with forming the initiator of xanthine oxidase-hypoxanthine-induced lipid peroxidation. On the other hand, pindolol also inhibited lipid peroxidation, whereas it did not react with superoxide, indicating that it inhibited xanthine oxidase-hypoxanthine-induced lipid peroxidation by an independent mechanism of superoxide. Pindolol sharply scavenged 2,2'-azino-bis-(3-ethylbenzothiazoline-6-sulfonate) radical cations, but the ability of pindolol to scavenge peroxyl radicals of 2,2'-azobis(2-amidinopropane)-dihydrochloride and 2,2'-diphenyl-p-picrylhydrazyl radicals was low. In addition, pindolol did not scavenge hydroxyl radicals at physiologically significant concentrations. These results suggest that the ability of pindolol to inhibit lipid peroxidation was due to scavenging carbon-centered radicals rather than peroxyl radicals.

Adenosine Diphosphate↗
PubMed2006

Lipid-protein modifications during ascorbate-Fe2+ peroxidation of photoreceptor membranes: protective effect of melatonin.

The rod outer segment (ROSg) membranes are essentially lipoprotein complexes. Rhodopsin, the major integral protein of ROSg, is surrounded by phospholipids highly enriched in docosahexaenoic acid (22:6 n3). This fluid environment plays an important role for conformational changes after photo-activation. Thus, ROSg membranes are highly susceptible to oxidative damage. Melatonin synthesized in the pineal gland, retina and other tissues is a free radical scavenger. The principal aim of this work was to study the changes in the ROSg membranes isolated from bovine retina submitted to nonenzymatic lipid peroxidation (ascorbate-Fe2+ induced), during different time intervals (0-180 min). Oxidative stress was monitored by increase in the chemiluminescence and fatty acid alterations. In addition we studied the in vitro protective effect of 5 mm melatonin. The total cpm originated from light emission (chemiluminescence) was found to be lower in those membranes incubated in the presence of melatonin. The docosahexaenoic acid content decreased considerably when the membranes were exposed to oxidative damage. This reduction was from 35.5 +/- 2.9% in the native membranes to 12.65 +/- 1.86% in those peroxidized during 180 min. In the presence of 5 mm melatonin we observed a content preservation of 22:6 n3 (23.85 +/- 2.77%) at the same time of peroxidation. Simultaneously the alterations of membrane proteins under oxidative stress were studied using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Loss of protein sulfhydryl groups and increased incorporation of carbonyl groups were utilized as biomarkers of protein oxidation. In membranes exposed to Fe2+ -ascorbate, we observed a decrease of protein thiols from 50.9 +/- 3.38 in native membranes to 1.72 +/- 2.81 nmol/mg of protein after 180 min of lipid peroxidation associated with increased incorporation of carbonyl groups into proteins from 7.20 +/- 2.50 to 12.50 +/- 1.12 nmol/mg of protein. In the SDS-PAGE we observed a decrease in the content of all the proteins, mainly rhodopsin, as a consequence of peroxidation. Melatonin, prevent both lipid peroxidation and protein oxidation.

Animals↗
PubMed2000

Safety issues relating to the use of hydrogen peroxide in dentistry.

Hydrogen peroxide is used widely in professionally and self-administered products. Hydrogen peroxide is a highly reactive substance which can damage oral soft tissues and hard tissues when present in high concentrations and with exposures of prolonged duration. This report provides an overview of health issues relating to the use of hydrogen peroxide, with an emphasis on safety with prolonged exposure to low concentrations of peroxide products. There is good evidence for the safety of hydrogen peroxide when used at low concentrations on a daily basis over extended periods of time, in self-administered oral health care products such as dentifrices and mouthrinses. These low concentrations neither damage oral hard or soft tissues, nor do they pose a significant risk of adverse long-term effects. Caution should be exercised with the increasingly higher concentration peroxide products used for 'walking' or 'power' bleaching due to the possibility of chemical irritation of oral soft tissues with injudicious use. The volumes of material and application times should be controlled carefully. Thorough education of patients is particularly important with self-applied gels because of the lack of professional supervision with such products. Such education is part of the duty of care of the dentist who supplies bleaching gels for at-home use.

Anti-Infective Agents, Local↗
PubMed1997

Polyhydroxylated C60, fullerenol, a novel free-radical trapper, prevented hydrogen peroxide- and cumene hydroperoxide-elicited changes in rat hippocampus in-vitro.

The role of polyhydroxylated C60 (fullerenol), a novel free-radical trapper, in prevention of hydrogen peroxide- and cumene hydroperoxide-elicited damage was studied in hippocampal slices from the rat in-vitro. The interactions of polyhydroxylated C60, adenosine and 6,7-dinitroquinoxaline-2,3-dione (DNQX) were also compared. Hydrogen peroxide (0.006-0.02%) and cumene hydroperoxide (0.5-1.0 mM) both reversibly reduced the amplitudes of CA1-evoked population spikes in the hippocampal slices. Deferoxamine (1 mM) had little effect on the population spikes. Deferoxamine (1 mM) significantly prevented the hydrogen peroxide (0.006%) elicited inhibition of the population spikes. Polyhydroxylated C60 (0.1 mM) significantly prevented hydrogen peroxide- or cumene hydroperoxide-elicited reduction of the population spikes and also prevented the effects of hydrogen peroxide and cumene hydroperoxide on paired-pulse facilitation in the hippocampal slice. Adenosine reduced the amplitude of population spikes and promoted paired-pulse facilitation in the CA1 region of the hippocampus. Polyhydroxylated C60 did not alter either of the effects of adenosine on the population spikes. DNQX reduced the amplitude of the population spikes in the CA1 region but did not affect the ratio of paired-pulse facilitation. Fullerenol did not alter either effect of DNQX on the population spikes. These results suggested that polyhydroxylated C60 prevented hydrogen peroxide- and cumene hydroperoxide-elicited damage in the hippocampuss slices. These effects might be associated with the free-radical scavenging activity of polyhydroxylated C60.

Adenosine↗
PubMed1994

Effects of peroxides on susceptibilities of Escherichia coli and Mycobacterium smegmatis to isoniazid.

Escherichia coli strains were previously found to be susceptible to the antituberculosis drug isonicotinic acid hydrazide (isoniazid [INH]) when they carried certain mutations that also sensitize them to peroxides: a deletion in oxyR, a redox-sensitive regulator of hydrogen peroxide-inducible genes, or mutations in both katG and ahpCF, OxyR-regulated genes encoding hydroperoxidase I, and an alkyl hydroperoxide reductase. To test whether INH, like peroxides, activates OxyR, the effect of INH on OxyR regulation was examined. Primer extension assays showed that transcription of the OxyR-regulated oxyS gene was not significantly induced by INH in wild-type cells, indicating that INH does not activate OxyR. However, the INH-susceptible katG ahpCF mutant strain was found to have constitutively high levels of oxyS transcription. This suggested that the lack of peroxidase expression in these strains allows endogenous oxidants to accumulate, and this leads not only to constitutive OxyR activation but also to INH susceptibility. Consistent with this concept, hydrogen peroxide or cumene hydroperoxide potentiated the INH susceptibilities of wild-type cells, while the antioxidant ascorbic acid protected the susceptible katG ahpCF mutant strain from INH. Superoxide radicals, generated by paraquat, did not enhance the INH susceptibilities of wild-type cells. Hydrogen peroxide also potentiated the INH susceptibilities of susceptible and resistant (katG mutant) Mycobacterium smegmatis strains. Our results suggest that INH is converted to a more active drug by reaction with peroxides and that the INH susceptibilities of enterobacteria and mycobacteria are mechanistically related.

Ascorbic Acid↗