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At least 145 records · Page 8Linked to original sources
PubMed2003

Protective effect of lipoic acid on adriamycin induced lipid peroxidation in rat kidney.

Adriamycin, which is widely used in the treatment of various neoplastic conditions, exerts toxic effects in many organs. The present study was designed to investigate the effect of lipoic acid upon adriamycin induced peroxidative damages in rat kidney. The increase in peroxidated lipids on adriamycin administration was accompanied by alterations in the antioxidant defense systems. The extent of nephrotoxicity induced by adriamycin was evident from the decreased activities of the enzymes gamma-glutamyl transferase and beta-glucuronidase in the rat renal tissues. The study was carried out with adult male albino rats of Wistar strain, which comprised of one control and three experimental groups. Group I rats served as controls. Group II rats received adriamycin (1 mg kg(-1) body wt day(-1)) intravenously through the tail vein. Group III rats were given lipoic acid (35 mg kg(-1) body wt day(-1)) intraperitoneally. Group IV rats were given lipoic acid 24 h before the administration of adriamycin. Rats subjected to adriamycin administration showed a decline in the thiol capacity of the cell accompanied by high malondialdehyde levels along with lowered activities of catalase, superoxide dismutase, glutathione peroxidase and glutathione metabolizing enzymes (glutathione reductase, glucose-6-phosphate dehydrogenase, glutathione-S-transferase). Lipoic acid pretreatment also restored the activities of gamma-glutamyl transferase and beta-glucuronidase nearly to control levels thereby suggesting nephroprotection. The study has highlighted the beneficial effects of lipoic acid pretreatment in reversing the damages caused by adriamycin and thereby bringing about an improvement in the oxidative stress parameters.

Animals↗
PubMed2002

[The dependence of lipid peroxidation and blood hemostasis from antioxidant activity of different tissues].

The experiments with rabbits show that animal maintenance on the antioxidant-free diet leads to the peroxidative lipid oxidation (PLO), hemostasis activation and to the superoxidedismutase (SOD) level reducing in a blood and tissues (of cerebrum, heart, kidney, stomach). The greatest SOD activity decreasing is observed in the cerebrum and heart tissues. Probably, these organs make the most considerable contribution in PLO and hemostasis course in the antioxidative reducing conditions.

Animals↗
PubMedDate not supplied

[The characteristics of the behavior and brain lipid peroxidation function of rats in acute inhalation exposure to a hydrogen sulfide-containing gas condensate].

As a result of the effect of the gas condensate containing hydrogen sulfide a depression takes place of orienting-investigatory activity of Wistar male rats in conditions of open field, disturbance of elaboration and reproduction of conditioned reflex of two-way avoidance, surplus accumulation in the cerebral cortex tissue of products of peroxide lipids oxidation and depression of catalase. The changes were of cyclic character and returned to the level of the control animals in 48 h after the finishing of the effect.

Administration, Inhalation↗
PubMed1994

[A comparative genetic analysis of interlinear differences in intensity of lipid peroxidation and life span in Drosophila melanogaster. Inbred lines and hybrids].

The interrelationship between the level of peroxidation lipid and longevity was studied as based on highly inbred lines of Drosophila melanogaster, bred for adaptively important characters. The concepts of the free-radical theory proved valid for the lines and failed to be supported for the crosses. The dominant role of heterosis in the protecting against the "aging action" of free radicals is postulated.

Animals↗
PubMed1996

[The characteristics of tissue lipid peroxidation of the internal organs in anaphylaxis under the action of a hypo- or hypermagnetic field].

An effective form of physiotherapy of anaphylactic shock of guinea-pigs by the hypo-hypermagnetic field was discovered introducing the alternating magnetic field in accordant "depressing" regime after 1-hour exposition of the animals under the conditions of hypogeomagnetic environment. This form of influence by the physical factor increases the antioxidation activity of the peroxide lipid oxidation in the lungs, heart at the caused of the exhaustion of the protective mechanisms of the organism.

Anaphylaxis↗
PubMed1987

Human placental lipid peroxidation--II. NADPH and iron dependent stimulation of microsomal lipid peroxidation by paraquat.

Paraquat, a widely used herbicide, was found to cause a marked stimulation of lipid peroxidation in the human placental microsomes in vitro. Both NADPH and chelated iron were necessary to observe paraquat-stimulated lipid peroxidation. The malondialdehyde accumulation in the incubation medium increased with increase in time, protein and paraquat concentration. The reaction did not exhibit the initial lag phase suggesting that endogenous membrane-bound antioxidants in human placental microsomes are either absent or present in extremely small quantities.

Humans↗
PubMed1990

The 8-hydroxyguanine content of isolated mitochondria increases with lipid peroxidation.

When lipid peroxidation was induced in isolated mitochondria there was a marked increase in the 8-hydroxyguanine content of the nucleic acids extracted from these mitochondria. The elevation of 8-hydroxyguanine levels was associated with an extensive alteration of normal electrophoretic mobility of mitochondrial DNA. However, suppression of lipid peroxidation with alpha-tocopherol proportionally attenuated 8-hydroxyguanine production and limited the electrophoretic mobility change of mitochondrial DNA.

Animals↗
PubMed1980

Promethazine administration to rats and CCl4 induced lipid peroxidation of liver microsomal lipids.

Promethazine inhibited CCl4 stimulated microsomal lipid peroxidation in vitro at concentrations ranging from 10(-3) to 10(-8)M. CCl4 administered to rats at a dose of 1 ml/kg decreased the arachidonic acid content of microsomal lipids after 6 hours of intoxication. Prior promethazine treatment, at dosage regimes that preclude CCl4 induced liver necrosis at 24 hours, did not significantly prevent the CCl4 induced decrease in arachidonic acid content. Moreover, promethazine itself produced a similar decrease but in complete absence of liver damage. Results suggest that either lipid peroxidation is not relevant to liver injury or that the arachidonic acid decrease in microsomal lipids is not evidence for lipid peroxidation occurrence or that promethazine effects are not related to inhibition of lipid peroxidation.

Animals↗
PubMed1989

tert-butyl hydroperoxide-dependent microsomal release of iron and lipid peroxidation. II. Evidence for the involvement of nonheme, nonferritin iron in lipid peroxidation.

In a previous study tert-butyl hydroperoxide (t-BOOH) was found to promote reductive release of nonheme, nonferritin iron from rat liver microsomes. The reaction was catalyzed by cytochrome P450 and was strictly contingent on the availability of ADP. In this study, t-BOOH was also found to promote microsomal lipid peroxidation, as evidenced by formation of malondialdehyde. t-BOOH-dependent lipid peroxidation was stimulated by ADP, and four lines of evidence suggested that such stimulation was mediated by reductive release and subsequent redox cycling of nonheme, nonferritin iron. First, lipid peroxidation was stimulated by the same concentration of ADP that promoted iron release. Second, depletion of nonheme, nonferritin iron by pretreatment of rats with phenobarbital decreased the stimulation of lipid peroxidation by ADP. Third, the effect of ADP was maximal when the concentration of t-BOOH was adjusted to values that yielded maximum iron release. Fourth, the effect of ADP was abolished by bathophenanthroline, which is known to chelate ferrous iron in a redox inactive form. These results suggest that the reductive release of nonheme, nonferritin iron exacerbates the deleterious effects of t-BOOH on microsomal lipids.

Adenosine Diphosphate↗
PubMed1979

Inhibition of lipid peroxidation by calcium ions and their protection of steroid hydroxylase activity from peroxidative damage.

Lipid peroxidation of adrenocortical mitochondria and microsomes was greatly stimulated by addition of 1.0 mM or less ferric ions. In the presence of NADPH-yielding system, the formation of corticosterone from endogeneous cholesterol and exogeneous deoxycorticosterone was inhibited as the concentrations of iron increased. Of interest is the fact that 0.5 mM ferric ion-mediated lipid peroxidation was completely abroagated upon addition of 2 mM calcium ions. Accordingly, protected from the peroxidative damage.

Adrenal Cortex↗
PubMed1978

Ethanol-induced hepatotoxicity; experimental observations on the role of lipid peroxidation.

Hepatic lipid peroxidation in vivo or in vitro as measured by UV absorption spectra of microsomal lipids or by production of TBA-reacting substances by whole liver homogenates, was studied after acute or during prolonged administration of ethanol. No evidence of peroxidative derangement of liver microsomal lipids in vivo was detected in either experimental situation, while the production of TBA-reacting substances by pooled liver homogenates incubated in vitro appeared slightly increased. Treatment with reduced glutathione (GSH and 2-mercaptopropionylglycine (2-MPG) was able to reduce fatty liver in acute and prolonged ethanol dosing, as well as the production of TBA-reacting compounds. Similar effects were obtained with 3-amino-1,2,4-triazole which was assayed only in acute experiments. By contrast, hepatic triglyceride accumulation induced by a single intoxicating dose of ethanol was not affected by preventive treatment with pyrazole which seemed to act as a pro-oxidant agent as far as the production of TBA-reacting substances is concerned. The role of lipid peroxidation as a pathogenic mechanism for acute and chronic ethanol-induced hepatotoxicity is discussed in relation to the action of anti-oxidant compounds which are active in preventing liver injury. It is concluded that lipid peroxidation is unlikely to be an important mechanism in alcohol hepatotoxicity.

Animals↗
PubMed1994

Effects of dietary oils and methyl ethyl ketone peroxide on in vivo lipid peroxidation and antioxidants in rat heart and liver.

Weanling male Sprague-Dawley rats were fed diets for four weeks which differed in their content of n-6 (corn oil; CO) and n-3 fatty acids (fish oil; FO), but were similar in their content of saturated and monounsaturated fatty acids and vitamin E. At the end of the four-week feeding period, each dietary group was subdivided into two groups. One group received a single placebo injection of alpha-tocopherol-stripped corn oil (TSCO); the other group received a single injection of the free radical generator; methyl ethyl ketone peroxide (MEKP), in TSCO. Twenty-four hours after injection, the effect of dietary oil and MEKP treatment on endogenous lipid peroxide (LPO) production (measured as methylene blue formed by the "Determiner LPO" assay), glutathione (GSH) and vitamin E content, and fatty acid composition of phosphatidylcholine and phosphatidylethanolamine in heart and liver from unfasted animals were measured. FO-fed rats had significantly heavier hearts and livers, increased levels of n-3 fatty acids in membrane phospholipids, and higher liver LPO levels than CO-fed rats. MEKP treatment resulted in significantly lower body weights and liver GSH levels. The data indicate that dietary n-3 fatty acids increase lipid peroxidation in liver somewhat more than in heart. The study also demonstrates that the effect of induced oxidative stress due to a single dose of MEKP on lipid peroxide formation and antioxidant status in tissues from unfasted animals was independent of the dietary oils.

Animals↗
PubMed1990

Depressive effects of lipid peroxides mediated via a purine receptor. Effect of lipid peroxide on the cortical synaptosomal GTPase activity.

A circadian rhythm of lipid peroxides (LPO) in mouse whole brain was observed with a negative correlation between LPO levels in cerebral cortex and the locomotor activity of mice. Intraperitoneal administration of t-butyl hydroperoxide (BPO) to mice decreased spontaneous locomotor activity in a dose-dependent manner, and the effect was competitively antagonized by caffeine, suggesting a similar receptor. Cumene peroxide (CPO), BPO and known depressants such as phenobarbital and NaBr all stimulated GTPase activity in rat cerebral cortex synaptosomes. In contrast, stimulants, such as caffeine and amphetamine, inhibited GTPase activity. Using fresh and aged synaptosomes which differed markedly in endogenous LPO levels, it appeared as if the LPO competitively inhibited inosine-induced GTPase activity, suggesting that the receptor of LPO is the same as that of inosine. From these results, it is concluded that LPO in brain act as depressants whose activity can be competitively antagonized by caffeine, and that the effects of LPO are mediated through a purine receptor.

Adenosine↗
PubMed1996

Normolipidemic xanthelasma palpebrarum: lipid composition, cholesterol metabolism in monocyte-derived macrophages, and plasma lipid peroxidation.

The lipid compositions of 8 normolipidemic xanthelasma palpebrarum (XP) lesions were analyzed using thin-layer chromatography, with the adjacent uninvolved skin used as control. The lesions were found to be composed predominantly of cholesterol, mostly cholesteryl ester, whereas in the control specimens phospholipids predominated. The degradation rates of 125I-low-density lipoprotein (LDL), oxidized LDL, and acetyl LDL, and the rates of intracellular cholesterol synthesis from 1,2-(14)C-acetate, in blood monocyte-derived macrophages (MDM) from 3 normolipidemic patients, were similar to those of MDM from 3 normal control subjects. The mean levels of lipid peroxides and conjugated dienes under basal conditions, as well as following the addition of a free radical-generating compound (2,2-azobis-2-amidinopropane hydrochloride) to the plasma of 14 normolipidemic XP patients were significantly higher than those of 14 age- and sex-matched normal controls. We conclude that the predominant lipid accumulated in normolipidemic XP lesions is cholesteryl ester, but there is no evidence for intrinsic cellular cholesterol metabolism derangement in blood MDM from patients which could account for this. Since macrophage cholesterol accumulation can also result from enhanced uptake of increased levels of oxidized LDL, the increased plasma lipid peroxidation (derived from oxidized LDL) might lead to accumulation of cholesterol in macrophages and formation of foam cells via this mechanism.

Adult↗
PubMed1982

Potentiation of lipid peroxides by ischemia in rat brain.

Post-ischemic changes in energy metabolites and natural antioxidant compounds have been measured in rat brain in vitro concurrent with two different assays for peroxidized lipids. No exogenous free radical initiators were employed. In vitro oxygenation of minced brain preparations for periods of 10 minutes to 4 hours, following 5 minutes of preparatory ischemia, yielded increased levels of lipid conjugated dienes and TBA-reactive material, in contrast to anaerobically incubated preparations. However, either aerobic or anaerobic incubation of brain minces facilitated increased ratios of lactate:pyruvate and glutathione (oxidized):glutathione (reduced), as well as increased total ubiquinone content and loss of alpha-tocopherol. Observation of lipid radical formation in vivo was then attempted using rats given embolic stroke in one hemisphere and left in the post-ischemic condition for times up to 24 hours. Conjugated dienes were found in lipids extracted from the ipsilateral hemisphere but not from the contralateral hemisphere. These observations of conjugated dienes in vivo (formed presumably during post-ischemic reperfusion) and in vitro (facilitated by oxygenation of brain minces), indicate that lipid radical intermediates and associated chain peroxidation processes are potentiated by ischemia and occur during tissue reoxygenation.

Aerobiosis↗