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PubMed2002

Increased antioxidant potential of combined topical vitamin E and C against lipid peroxidation of eicosapentaenoic acid in pig skin induced by simulated solar radiation.

PURPOSE: To study the protective effect of topically applied vitamin E (TOC), vitamin C (ASC), or a combination of both, against the lipid peroxidation of eicosapentaenoic acid (EPA) induced by simulated solar radiation (SSR). MATERIAL AND METHODS: EPA (25 nmol cm(-2)) was topically applied to pig skin explants, followed by increasing doses of TOC and ASC, either alone or combined. Epidermal lipid peroxidation was assessed after 15 min of exposure to SSR (resulting in a UVA and UVB dose of 18 and 3 kJ m(-2), respectively). SSR-induced changes in the levels of TOC and ASC were determined in the stratum cornaeum and the viable epidermis. RESULTS: SSR exposure of EPA-treated pig skin resulted in a twofold increase in epidermal lipid peroxidation (p <0.005) which was reduced by topically applied TOC or ASC 60 min before SSR exposure (p <0.05). Compared with TOC (5 nmol cm(-2)), a 400-fold higher ASC dose was needed and only TOC provided complete protection against the lipid peroxidation of EPA. The levels of both TOC and ASC clearly increased in both skin compartments by increasing the applied dose of these two compounds (p <0.05). In contrast to ASC, TOC was consumed by up to 55-70% during SSR exposure (p <0.05). Compared with separate application, combined TOC and ASC efficiently protected against lipid peroxidation of EPA at doses that were five and 200 times lower, respectively. In the presence of low ASC doses, 70-100% of epidermal TOC was regenerated during SSR exposure (p <0.05). CONCLUSIONS: Topically applied TOC and ASC protect against SSR-induced lipid peroxidation of EPA. The synergism between TOC and ASC resulted in a more efficient protection at substantially lower doses of both antioxidants. Co-supplementation of EPA with TOC and/or ASC might improve the beneficial biological effects of EPA.

Administration, Topical↗
PubMed2005

Induction of radical scavenging ability and suppression of lipid peroxidation in rat liver microsomes following whole-body, low-dose X-irradiation.

PURPOSE: To investigate changes in radical scavenging ability and lipid peroxidation in liver microsomal membranes and cooperative suppression of lipid peroxidation by microsomal and cytosolic radical scavengers, 24 h after whole-body, low-dose X-irradiation of rats. MATERIALS AND METHODS: Male Wistar rats were irradiated with 1-50 cGy of X-rays. Liver microsomal radical scavenging ability was determined using the trapping ability of 1,1-diphenyl-2-picrylhydrazyl (DPPH), a stable free radical. Microsomal alpha-tocopherol (Vit.E) content was determined using an electrochemical detector. Microsomal glutathione peroxidase (GPx) activity was determined as the consuming rate of NADPH. Microsomal lipid peroxidation was determined by the thiobarbituric acid method. RESULTS: Low molecular weight radical scavenging ability of rat liver microsomes increased 24 h after whole-body, low-dose X-irradiation when alpha-tocopherol was included, showing a maximum level at 5-10 cGy. Microsomal GPx activity also increased 24 h after 5 cGy irradiation. The lipid peroxidation level in microsomes decreased, showing a maximal suppression at 5 cGy. High-dose irradiation-induced microsomal lipid peroxidation was strongly suppressed cooperatively by microsomal and cytosolic antioxidants induced by low-dose irradiation. CONCLUSION: Low doses of radiation induce increases in liver microsomal antioxidants, which in turn result in enhanced suppression of microsomal lipid peroxidation cooperatively with cytosolic antioxidants induced by low-dose irradiation.

Animals↗
PubMed1986

The oxidation of benzo[a]pyrene mediated by lipid peroxidation in irradiated synthetic diets.

The effect of gamma-irradiation (1000-4000 Gy) on the formation of lipid peroxides and on the oxidation of the environmental carcinogen benzo[a]pyrene (BP) has been studied in mixtures of starch/fat and BP which were used as models for natural foods. When mixtures containing polyunsaturated fats (mackerel oil and cod-liver oil which contain relatively large proportions of C20:5 and C22:6) were exposed to gamma-irradiation, large concentrations of lipid peroxide were formed and a concomitant oxidation of BP to mutagenic and toxic BP quinones took place. The rate of BP oxidation was closely related to the extent of peroxidation of the lipids in the starch mixtures and was dependent on the dose of gamma-irradiation and the presence of air. Mackerel oil also underwent peroxidation during the storage of both irradiated and unirradiated starch/mackerel oil/BP mixtures and this resulted in a significant oxidation of the BP present in these samples. Antioxidants such as vitamin E and BHA inhibited both lipid peroxidation and BP oxidation resulting from gamma-irradiation. These results demonstrate that the species generated during the peroxidation of unsaturated fats in foodstuffs can react with polycyclic aromatic hydrocarbons such as BP and convert them into active mutagenic and toxic products. This has important toxicological implications, particularly as the consumption of polyunsaturated fat in the Western world is increasing and gamma-irradiation may soon be widely used for food sterilization.

Benzo(a)pyrene↗
PubMed2000

Resveratrol inhibition of lipid peroxidation.

To define the molecular mechanism(s) of resveratrol inhibition of lipid peroxidation we have utilized model systems that allow us to study the different reactions involved in this complex process. Resveratrol proved (a) to inhibit more efficiently than either Trolox or ascorbate the Fe2+ catalyzed lipid hydroperoxide-dependent peroxidation of sonicated phosphatidylcholine liposomes; (b) to be less effective than Trolox in inhibiting lipid peroxidation initiated by the water soluble AAPH peroxyl radicals; (c) when exogenously added to liposomes, to be more potent than alpha-tocopherol and Trolox, in the inhibition of peroxidation initiated by the lipid soluble AMVN peroxyl radicals; (d) when incorporated within liposomes, to be a less potent chain-breaking antioxidant than alpha-tocopherol; (e) to be a weaker antiradical than alpha-tocopherol in the reduction of the stable radical DPPH*. Resveratrol reduced Fe3+ but its reduction rate was much slower than that observed in the presence of either ascorbate or Trolox. However, at the concentration inhibiting iron catalyzed lipid peroxidation, resveratrol did not significantly reduce Fe3+, contrary to ascorbate. In their complex, our data indicate that resveratrol inhibits lipid peroxidation mainly by scavenging lipid peroxyl radicals within the membrane, like alpha-tocopherol. Although it is less effective, its capacity of spontaneously entering the lipid environment confers on it great antioxidant potential.

Antioxidants↗
PubMed2001

The dose-dependent effect of copper-chelating agents on the kinetics of peroxidation of low-density lipoprotein (LDL).

Copper-induced peroxidation of lipoproteins involves continuous production of free radicals via a redox cycle of copper. Formation of Cu(I) during Cu(II)-induced peroxidation of LDL was previously demonstrated by accumulation of the colored complexes of Cu(I) in the presence of one of the Cu(I)-specific chelators bathocuproine (BC) or neocuproine (NC). All the studies conducted thus far employed high concentrations of these chelators (chelator/Cu(II) > 10). Under these conditions, at low copper concentrations the chelators prolonged the lag preceding oxidation, whereas at high copper concentrations the chelators shortened the lag. In an attempt to gain understanding of these non-monotonic effects, we have studied systematically the peroxidation of LDL (0.1 microM, 50 microg protein/mL) at varying concentrations of NC or BC over a wide range of concentrations of the chelators and copper. These studies revealed that: (i) At copper concentrations of 5 microM and below, NC prolonged the lag in a monotonic, dose-dependent fashion typical for other complexing agents. However, unlike with other chelators, the maximal rate of oxidation was only slightly reduced (if at all). (ii) At copper concentrations of 15 microM and above, the addition of about 20 microM NC or BC resulted in prolongation of the lag, but this effect became smaller at higher concentrations of the chelators, and at yet higher concentrations the lag became much shorter than that observed in the absence of chelators. Throughout the whole range of NC concentrations, the maximal rate of peroxidation increased monotonically upon increasing the NC concentration. (iii) Unlike in the absence of chelators, the prooxidative effect of copper did not exhibit saturation with respect to copper, up to copper concentrations of 30 microM. Based on these results we conclude that the copper-chelates can partition into the hydrophobic core of LDL particles and induce peroxidation by forming free radicals within the core. This may be significant with respect to the understanding of the possible mechanisms of peroxidation by chelated transition metals in vivo.

Chelating Agents↗
PubMed2001

Supplementation with vitamin E but not with vitamin C lowers lipid peroxidation in vivo in mildly hypercholesterolemic men.

Although the use of vitamin E supplements has been associated with a reduction in coronary events, assumed to be due to lowered lipid peroxidation, there are no previous long-term clinical trials into the effects of vitamin C or E supplementation on lipid peroxidation in vivo. Here, we have studied the long-term effects of vitamins C and E on plasma F2-isoprostanes, a widely used marker of lipid peroxidation in vivo. As a study cohort, a subset of the "Antioxidant Supplementation in Atherosclerosis Prevention" (ASAP) study was used. ASAP is a double-masked placebo-controlled randomized clinical trial to study the long-term effect of vitamin C (500 mg of slow release ascorbate daily), vitamin E (200 mg of D-alpha-tocopheryl acetate daily), both vitamins (CellaVie), or placebo on lipid peroxidation, atherosclerotic progression, blood pressure and myocardial infarction (n = 520 at baseline). Lipid peroxidation measurements were carried out in 100 consecutive men at entry and repeated at 12 months. The plasma F2-isoprostane concentration was lowered by 17.3% (95% CI 3.9-30.8%) in the vitamin E group (p = 0.006 for the change, as compared with the placebo group). On the contrary, vitamin C had no significant effect on plasma F2-isoprostanes as compared with the placebo group. There was also no interaction in the effect between these vitamins. In conclusion, long-term oral supplementation of clinically healthy, but hypercholesterolemic men, who have normal vitamin C and E levels with a reasonable dose of vitamin E lowers lipid peroxidation in vivo, but a relatively high dose of vitamin C does not. This observation may provide a mechanism for the observed ability of vitamin E supplements to prevent atherosclerosis.

Aged↗
PubMed2005

Effect of auranofin on the mitochondrial generation of hydrogen peroxide. Role of thioredoxin reductase.

The mitochondrial production of hydrogen peroxide, in the presence of different respiratory substrates (succinate, glutamate, malate and isocitrate), is stimulated by submicromolar concentrations of auranofin, a highly specific inhibitor of thioredoxin reductase. This effect is particularly evident in the presence of antimycin. Auranofin was also able to unmask the production of hydrogen peroxide occurring in the presence of rotenone. However, at variance with whole mitochondria, auranofin does not stimulate hydrogen peroxide production in submitochondrial particles indicating that it does not alter the formation of hydrogen peroxide by the respiratory chain but prevents its removal. As the mitochondrial metabolism of hydrogen peroxide proceeds through the peroxidases linked to glutathione or thioredoxin, the relative efficiency of the two systems and the effects of auranofin were tested. In conclusion, the inhibition of thioredoxin reductase determines an increase of the basal flow of hydrogen peroxide leading to a more oxidized condition that alters the mitochondrial functions.

Animals↗
PubMed1982

Comparison of methods of assessment of metal-induced lipid peroxidation in isolated rat hepatocytes.

There is some controversy about which method of assessment of lipid peroxidation in isolated hepatocytes is most appropriate. The present study was undertaken primarily to compare measurement of concentrations of thiobarbituric acid (TBA) reacting substances with measurement of ethane concentrations in the gas phase of the incubation flask as indicators of lipid peroxidation. Four metal salts, FeCl2, NaVO3, CdCl2, and MnCl2, were selected as agents that interact with the lipid peroxidation process. Furthermore, reduced glutathione (GSH) concentrations and enzyme leakage were assayed to determine whether there was a consistent pattern of interaction between lipid peroxidation and change in GSH concentrations and enzyme leakage. The effects of the metal ions on the concentration of TBA reactants estimated in the whole cell suspension and on the gaseous ethane concentration were similar. However, the assessment of TBA reactants was a little more sensitive, and ethane concentrations continued to climb with incubation time rather than leveling off as observed for TBA reactants. In general, the results of both assays were in good agreement. No consistent pattern of interaction between lipid peroxidation, GSH, and enzyme leakage was discernible in the results of the present study. It is suggested that perhaps the best approach to an experimental situation where lipid peroxidation is thought to be of central importance is measurement of both parameters, TBA reactants and ethane concentrations.

Animals↗
PubMed2001

Evaluation of lipids peroxidation products vs. proinflammatory cytokines in hemodialized patients.

BACKGROUND: Patients with end-stage renal failure on chronic hemodialysis often demonstrate accelerated development of atherosclerotic changes and cardiovascular complications. In those patients oxidative stress facilitates the intensity of lipid peroxidation process, expressed as increased products of lipid peroxidation (malonaldehyde and 4-hydroxyalkenals). Simultaneously, structures modified by peroxidation and glycation of autoantigenic character are formed. Additionally, increase in proinflammatory cytokines is found in their patients on hemodialysis. The aim of the study was to find out the relations between the products of lipid peroxidation and proinflammatory cytokines in patients on hemodialysis. METHODS: Plasma concentrations of malonaldehyde and 4-hydroxyalkenals were estimated by spectrophotometric method, glutathione peroxidase as well as concentration of IL-6, its soluble receptor and TNFalpha were measured using ELISA kits. RESULTS: Aldehyde concentrations (malonaldehyde and 4-hydroxyalkenals) were found to be five fold higher in comparison with the controls. Concentrations of proinflammatory cytokines: IL-6, TNFalpha and soluble IL-6 receptor were also higher than in the control group. Patients on hemodialysis showed positive correlation between concentrations of MDA+4HNE and IL-6 and TNFalpha. CONCLUSION: The correlations found between the products of lipid peroxidation and proinflammatory cytokines suggest causative relation between the intensity of peroxidative processes and stimulation of immunological response in hemodialysed patients, which may increase the risk of atherosclerotic changes in those patients.

Humans↗
PubMed1980

Enhanced lipid peroxidation in liver microsomes of zinc-deficient rats.

The clinical association of decreased serum and hepatic zinc in patients with cirrhosis of the liver presumably arising from excess ethanol ingestion prompted a study of the activities of zinc and alcohol in experimental animals. The purpose of this study was to determine the effect of zinc deficiency upon lipid peroxidation in the liver. The effect of ethanol and zinc deficiency on lipid peroxidation was also evaluated. Rats were used in the experimental design, one group received a control diet, and one was maintained on a zinc-deficient diet. One-half of each group also received 3.85 g ethanol per kilogram body weight daily. Lipid peroxidation in vivo was determined by estimation of diene conjugation of microsomal lipids. The in vitro lipid peroxidation potential was measured by the generation of malonic dialdehyde by enzymatic as well as nonenzymatic reactions. Analysis of this data indicated that increased hepatic microsomal lipid peroxidation was associated with zinc deficiency whether using in vivo or in vitro indices of measurement. Review of the data from individual animals indicated that the lowest levels of serum zinc were associated with increased hepatic content of phospholipids. The degree of lipid peroxidation in the zinc deficient animals was not increased by ingestion of alcohol.

Animals↗
PubMed1991

Effect of dietary fat on growth of MCF-7 and MDA-MB231 human breast carcinomas in athymic nude mice: relationship between carcinoma growth and lipid peroxidation product levels.

Human breast carcinoma cell lines MCF-7 and MDA-MB231 were transplanted s.c. to female athymic nude mice at 3-4 weeks of age. At 7-10 days after transplantation, the mice were divided into groups and fed for 6-8 weeks one of the following semi-purified diets containing different amounts and types of fat, i.e. 5% corn oil, 20% corn oil, 20% butter, 19% beef tallow/1% corn oil and 19% fish (Menhaden) oil/1% corn oil. In addition experiments, the fish oil diets were supplemented with antioxidants (vitamin E, 8 g or 2000 IU/kg diet plus tertiary butyl hydroquinone, TBHQ, 4 g/kg diet) or ferric citrate (3 g/kg diet). Tumor peroxidation product levels were assessed by measuring 2-thiobarbituric acid reactants (TBA assay). At the termination of the studies (6-8 weeks of diet feeding) mean human breast carcinoma volume (MCF-7 and MDA-MB231) was the largest in mice fed the 20% corn oil diet, intermediate in mice fed the butter or beef tallow diets and the least in mice fed the fish oil diet. The difference in mean tumor volumes among mice fed the 20% corn oil diet and those fed the fish oil diet was significant (P less than 0.01). When comparing low (5% corn oil) and high (20% corn oil) fat diets, numerical increases in human breast carcinoma volume (MCF-7 and MDA-MB231) were consistently observed in the high-fat diet groups but these differences were not always significant. Tumor lipid peroxidation product levels were determined on the MDA-MB231 tumors; tumor lipid peroxidation levels were significantly (P less than 0.01) increased only in mice fed the fish oil diets. Supplementation of the fish oil diets with antioxidants (vitamin E + TBHQ) significantly reduced the level of tumor peroxidation products and significantly increased tumor volume (P less than 0.05). When tumor lipid peroxidation product levels in the fish oil plus antioxidant fed mice were reduced to the level of that observed in the tumors of the corn oil fed mice, no significant differences in tumor volumes were observed in these two groups. In contrast, supplementation of the fish oil diets with ferric citrate, significantly (P less than 0.05) increased tumor lipid peroxidation product levels and decreased tumor volume. Thus, the type of dietary fat can clearly affect the growth of human breast carcinomas (MCF-7 and MDA-MB231) maintained in athymic nude mice.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Increased endogenous catalase activity caused by heat stress does not protect the isolated rat heart against exogenous hydrogen peroxide.

OBJECTIVE: The aim was to investigate the potential for the enhancement of endogenous catalase activity after heat stress to protect the isolated rat myocardium from the injurious effects of exogenous hydrogen peroxide. METHODS: Male Sprague-Dawley rats were randomised to either heat stress or sham treatment. At 24 and 48 h after treatment hearts were retrogradely perfused at a constant flow rate of 10 ml.min-1. After a 15 min stabilisation period hearts were perfused with 75 microM hydrogen peroxide for 85 min. Mechanical function was measured by an intraventricular isovolumic latex balloon while coronary perfusate was collected for measurement of lactate dehydrogenase activity. At the end of the perfusion period the glutathione status of the hearts was determined. In separate experiments baseline cardiac catalase activity and glutathione state were measured 24 and 48 h after heat stress or sham treatment. RESULTS: Cardiac catalase activity was increased by 49% at both 24 and 48 h after heat stress in comparison with sham controls. Glutathione concentrations were reduced by 12% 24 h after heat stress but had recovered by 48 h. Perfusion of sham hearts with 75 microM hydrogen peroxide resulted in a progressive decline in mechanical function as evident by a fall in developed pressure and rise in diastolic pressure. Coronary resistance also rose during the perfusion period as shown by a progressive increase of coronary perfusion pressure. Coronary effluent lactate dehydrogenase release was only increased above basal concentrations at the end of the perfusion period, whereas cardiac glutathione concentrations were severely depleted. Hearts taken 24 h after heat stress showed a reduced resistance to the effect of 75 microM hydrogen peroxide on mechanical activity, although there was no difference in the pattern of lactate dehydrogenase release or depletion of glutathione. Perfusion of hearts taken 48 h after heat stress with 75 microM hydrogen peroxide resulted in the same effect on mechanical dysfunction, coronary resistance, lactate dehydrogenase release, and cardiac glutathione depletion as sham controls. CONCLUSIONS: The increase in endogenous cardiac catalase activity caused by prior heat stress is insufficient to protect the isolated rat heart from injury induced by exogenous hydrogen peroxide.

Animals↗
PubMed1992

Hydrogen peroxide production by Lactobacillus species: correlation with susceptibility to the spermicidal compound nonoxynol-9.

Facultative anaerobic lactobacilli were recovered from the vaginas of 96.8% of 63 nonpregnant, healthy, premenopausal women. The predominant species were Lactobacillus jensenii, Lactobacillus acidophilus, and Lactobacillus casei. Of the women, 74.6% had hydrogen peroxide-producing lactobacilli, 22.2% had non-hydrogen peroxide-producing lactobacilli, and 3.2% had no lactobacilli. None of the 68 isolates had catalase activity. Some 68.2% of the isolates were inhibited by concentrations of less than or equal to 1% (wt/vol) of nonoxynol-9 (bactericidal for 73.3% of isolates, bacteriostatic for 26.7%). The remaining 31.8% could grow in all concentrations to 25% (wt/vol) of nonoxynol-9. All of the lactobacilli that were sensitive to nonoxynol-9 produced hydrogen peroxide whereas only 3 of 21 resistant strains were hydrogen peroxide producers. A significant correlation (P less than .001, chi 2 test) was found between hydrogen peroxide production and sensitivity to nonoxynol-9. It is suggested that the vaginal flora of spermicide users could be depleted of hydrogen peroxide-producing lactobacilli, possibly increasing susceptibility to urogenital infection.

Adult↗
PubMed1990

Use of exogenous glutathione for metabolism of peroxidized methyl linoleate in rat small intestine.

The potential effects of dietary glutathione on the metabolism of peroxidized lipid ingested in the diet were studied using everted sacs of rat small intestine and peroxidized methyl linoleate. Peroxidized methyl linoleate was added to the luminal side, and the appearance of thiobarbituric acid-reactive (TBA-reactive) material on the contraluminal side was measured. Incubation with N,N,bis(2-chloroethyl)-N-nitrosourea (BCNU) under conditions in which it inhibits the glutathione disulfide reductase/glutathione peroxidase system increased the appearance of TBA-reactive material, indicating that at least a portion of the TBA-reactive material passing through the epithelium is peroxide in nature. Adding glutathione (GSH) to the luminal side substantially decreased the appearance of TBA-reactive material on the contraluminal side, either without or with BCNU treatment. Inhibition of GSH transport and control experiments with GSH, peroxidized methyl linoleate and purified brush border membranes showed that this decrease was due primarily to uptake of luminal GSH and its use to support intracellular GSH-dependent reactions. Thus, the results indicate that exogenous GSH, which can exist in certain diets, can be taken up by the small intestine and used to protect against absorption of lipid peroxidation products.

Animals↗
PubMed2003

Effect of vitamin E on lipid peroxidation and fertility after artificial insemination with liquid-stored turkey semen.

Turkey sperm plasma membranes contain high levels of polyunsaturated fatty acids that are susceptible to lipid peroxidation during in vitro storage at 4 degrees C. Herein we assessed the degree of lipid peroxidation and fertility potential of semen liquid-stored for 24 h with the antioxidant vitamin E. Semen was collected weekly from 44 males and pooled as pairs (total = 22); the individuals in paired samples exhibited similar semen quality parameters. After initial semen evaluation, pooled samples were extended with Beltsville Poultry Semen Extender containing no supplement (control) or 10 or 40 microg/mL vitamin E and then stored at 4 degrees C with constant aeration for 24 h. Lipid peroxidation was determined by measuring malonaldehyde (MDA) in aliquots (50 x 10(6) sperm) of fresh (0 h) and stored (24 h) semen. Sperm mobility was also evaluated. A total of 176 hens (8 hens/tom pair; 4 hens/0 h, 4 hens/24 h) were inseminated (150 x 10(6) sperm) weekly for 6 wk, and fertility was determined after 7 d of incubation. Initial MDA values of the 22 tom pairs ranged from 0.928 to 1.36 uM. Males varied in production of MDA during in vitro storage, with most pairs exhibiting a threefold increase. Results indicated that supplemental vitamin E did not reduce lipid peroxidation during liquid storage. Not surprisingly, artificial insemination with stored semen (with much higher MDA values) yielded lower fertility rates than control regardless of the presence of vitamin E. These results demonstrate that lipid peroxidation is a significant factor affecting the fertility of stored turkey sperm and that methods to prevent or reduce lipid peroxidation remain to be elucidated.

Animals↗
PubMed2000

Contractile response of skeletal muscle to low peroxide concentrations: myofibrillar calcium sensitivity as a likely target for redox-modulation.

Endogenous peroxides and related reactive oxygen species may influence various steps in the contractile process. Single mouse skeletal muscle fibers were used to study the effects of hydrogen peroxide (H2O2) and t-butyl hydroperoxide (t-BOOH) on force and myoplasmic Ca2+ concentration ([Ca2+]i). Both peroxides (1010 to 105 M) decreased tetanic [Ca2+]i and increased force during submaximal tetani. Catalase (1 kU/ml) blocked the effect of H2O2, but not of t-BOOH. The decrease in tetanic [Ca2+]i was constant, while the effect on force was biphasic: A transitory increase was followed by a steady decline to the initial level. Myofibrillar Ca2+ sensitivity remained increased during incubation with either peroxide. Only the highest peroxide concentration (10 mM) increased resting [Ca2+]i and slowed the return of [Ca2+]i to its resting level after a contraction, evidence of impaired sarcoplasmic reticulum Ca2+ re-uptake. The peroxides increased maximal force production and the rate of force redevelopment, and decreased maximum shortening velocity. N-ethylmaleimide (25 mM, thiol-alkylating agent) prevented the response to 1 mM H2O2. These results show that myofibrillar Ca2+ sensitivity and cross-bridge kinetics are influenced by H2O2 and t-BOOH concentrations that approach those found physiologically, and these findings indicate a role for endogenous oxidants in the regulation of skeletal muscle function.

Animals↗
PubMed1996

Demonstration of halothane-induced hepatic lipid peroxidation in rats by quantification of F2-isoprostanes.

BACKGROUND: Halothane can be reductively metabolized to free radical intermediates that may initiate lipid peroxidation. Hypoxia and phenobarbital pretreatment in Sprague-Dawley rats increases reductive metabolism of halothane. F(2)-isoprostanes, a novel measure of lipid peroxidation in vivo, were used to quantify halothane-induced lipid peroxidation in rats. METHODS: Rats were exposed to 1% halothane or 14% O(2) for 2 h. Pretreatments included phenobarbital, isoniazid, or vehicle. Rats also were exposed to halothane, enflurane, and desflurane at 21% O(2). Lipid peroxidation was assessed by mass spectrometric quantification of F(2)-isoprostanes. RESULTS: Exposure of phenobarbital-pretreated rats to 1% halothane at 21% O(2) for 2 h caused liver and plasma F(2)-isoprostane concentrations to increase fivefold compared to nonhalothane control rats. This halothane-induced increase was enhanced by 14% O(2), but hypoxia alone had no significant effect. Alanine aminotransferase activity at 24 h was significantly increased only in the 1% halothane/14% O(2) group. The effect of cytochrome P450 enzyme induction on halothane-induced F(2)-isoprostane production and liver injury was determined by comparing the effects of isoniazid and phenobarbital pretreatment with no pretreatment under hypoxic conditions. Halothane caused 4- and 11-fold increases in plasma and liver F(2)-isoprostanes, respectively, in non-pretreated rats, whereas isoniazid pretreatment had no effect. Phenobarbital pretreatment potentiated halothane-induced lipid peroxidation with 9- and 20-fold increases in plasma and liver F(2)-isoprostanes, respectively. Alanine aminotransferase activity was increased only in this group. At ambient oxygen concentrations, halothane but not enflurane or desflurane, caused F(2)-isoprostanes to increase. CONCLUSIONS: Specific halothane-induced lipid peroxidation was demonstrated in Sprague-Dawley rats using quantification of F(2)-isoprostanes and was increased by hypoxia and phenobarbital pretreatment, but not isoniazid pretreatment.

Anesthetics, Inhalation↗
PubMed1986

Lipid peroxidation in experimental septic rats.

We previously reported increased lipid peroxide and decreased alpha-tocopherol levels in the blood of critically ill septic patients. To clarify these results, we investigated lipid peroxidation in experimental septic rats and severely traumatized rats. In septic rats, both platelet count and plasma alpha-tocopherol decreased significantly, while lipid peroxide in plasma and major organs significantly increased. Serum transaminases also increased significantly. Traumatized rats had a significant but transient decrease in platelet count and a continuous decrease in plasma alpha-tocopherol; lipid peroxide did not change significantly in the plasma but increased significantly in the lung and kidney. Serum transaminases of traumatized rats showed transient increases. Thus, although traumatic stress caused lipid peroxidation similar to sepsis in the major organs, plasma lipid peroxide did not change.

Animals↗