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PubMed1995

Oxidative stress and erythrocyte membrane fluidity in patients undergoing regular dialysis.

Oxidative damage due to free radical production is increased in uraemic patients and has been suggested as a possible factor contributing to the anaemia of chronic renal failure (CRF) and the pathogenesis of atherosclerosis. Oxidative stress was assessed in 40 patients with CRF maintained by either haemodialysis (HD) or continuous ambulatory peritoneal dialysis (CAPD) and in 18 healthy controls. Lipid peroxidation (assessed as malondialdehyde, MDA), total glutathione (TG), antioxidant enzyme (glutathione reductase (GSHRx), glutathione peroxidase (GSHPx) and superoxide dismutase (SOD)) activity and antioxidant associated trace metal (selenium, copper, zinc) levels were studied. Erythrocyte membrane fluidity was examined using the fluorescent probe 1,6 diphenyl-1,3,5-hexatriene (DPH). The results indicate increased levels of oxidative stress and altered erythrocyte membrane fluidity in patients treated with CAPD compared with controls and patients treated with HD. Only minor changes were observed in patients treated with HD. Altered free radical activity, oxidative stress and altered erythrocyte membrane fluidity observed in patients with CRF may contribute to the increase in vascular disease in such patients and to the anaemia of CRF.

Adult↗

PubMed1992

Biochemical changes and cataract formation in lenses from rats receiving multiple, low doses of sodium selenite.

Nuclear cataract formed in rat lens in response to a protocol of multiple, low doses of sodium selenite. Nuclear cataract occurred, in both Wistar and Sprague-Dawley rats, following five subcutaneous injections of selenite over an 8-day period with an accumulated dose of 40-50 nmol selenite g-1 body weight. Glutathione content decreased within the first 24 hr of treatment and remained at 60% of controls. Lipid peroxidation occurred in Wistar rats prior to nuclear cataract formation. A two to three-fold increase in calcium concentration and decreased protein content accompanied nuclear cataract development. Enzyme activities were measured for glutathione peroxidase, glutathione reductase, and glutathione S-transferase, and only the peroxidase activity remained constant through the period of cataract formation. This protocol resulted in nuclear cataracts similar in appearance to those observed with a single, acute dose of selenite. The opportunity to control the rate of selenite-dependent cataract formation allows further definition of precataractous events.

Animals↗

PubMed1988

Effect of chronic ethanol treatment under partial catalase inhibition on the activity of enzymes related to peroxide metabolism in rat liver and heart.

1. In order to test the hypothesis that the alcoholic cardiomyopathy under partial catalase inhibition is associated with the activation of lipid peroxidation in cardiomyocytes (Panchenko et al., Experientia 43, 580-581, 1987), the effects of ethanol and catalase inhibitor 3-amino-1,2,4-triazole (aminotriazole) on rat heart and liver content of reduced glutathione and on the activity of enzymes related to peroxide metabolism: catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase were investigated. 2. In accordance with the data obtained by Kino (J. molec, cell. Cardiol. 13, 5-12, 1981), when ethanol (36% of dietary calories) and aminotriazole were simultaneously administered an alcoholic cardiomyopathy developed while in the liver moderate fatty degeneration was revealed. 3. Chronic combined or separate administration of ethanol and aminotriazole was shown to increase glutathione concentration and glutathione-S-transferase activity in rat liver. In the groups of animals which received isocaloric carbohydrates in the diet instead of ethanol the liver glucose-6-phosphate dehydrogenase was increased. 4. Acute and chronic aminotriazole injections led to catalase inactivation and in the latter case also to inhibition of the liver superoxide dismutase and glutathione peroxidase activities. 5. Ethanol and aminotriazole treatment did not alter the glutathione level and the activity of all enzymes tested (except catalase) in rat myocardium.

Amitrole↗

PubMed1986

The effect of high glucose and oxidative stress on lens metabolism, aldose reductase, and senile cataractogenesis.

Diabetic cataractogenesis, a multifactorial process, was examined with nuclear magnetic resonance (NMR). P-31 NMR spectroscopic studies showed substantial alteration of both energy and membrane metabolism in the diabetic lens. Findings from a C-13 NMR spectroscopic determination of the sorbitol pathway flux in lenses incubated in 35.5 mmol/L glucose revealed that (1) one-third of total glucose consumed was channeled through this pathway, and (2) the turnover rate of NADPH to NADP was 3,000%/hr. Furthermore, a competition for NADPH between aldose reductase and glutathione reductase was demonstrated. It is important to note that all metabolic changes in hyperglycemic/diabetic lenses can be prevented by aldose reductase inhibitors, eg, sorbinil.

Adenosine Triphosphate↗

PubMed1991

Differential inhibition of rat hepatic glutathione S-transferase isoenzymes in the course of fascioliasis.

The effects of a subclinical fascioliasis at various stages of its development (at week 3, 6 and 9 after infection by oral administration of 20 metacercariae of Fasciola hepatica) in rats were determined on the activity of enzymes involved in liver metabolism of glutathione and on the subunit pattern of cytosolic glutathione S-transferase. The parasitic pathology was ascertained by clinical observation of the rats and at autopsy. Hepatic microsomal cytochrome P-450 content was significantly decreased in infected rats by week 3 and 6 post-infection. Not correlatively, the catalytic activities of glutathione S-transferase towards 1-chloro-2,4-dinitrobenzene and 1,2-dichloro-4-nitrobenzene were significantly lowered in last stages of the experimental fascioliasis (by week 6 and 9 post-infection). These decreases were correlated to that of subunit 1 as determined by means of high-performance liquid chromatography of cytosolic proteins whereas subunit 6 could also be decreased. Fascioliasis did not alter cytosolic glutathione, glutathione reductase and glutathione peroxidase activities or plasma glutathione S-transferase activity accepting 1-chloro-2,4-dinitrobenzene as the substrate.

Animals↗

PubMed1986

Comparative acute toxicity of four nickel compounds to F344 rat lung.

Nickel subsulfide (Ni3S2), nickel chloride (NiCl2), nickel sulfate (NiSO4), and nickel oxide (NiO) are compounds of widely differing solubility encountered in the nickel-refining and electroplating industries. Inhalation is a common route of exposure and toxicity to the respiratory tract is possible. The purpose of this study was to evaluate the biochemical, cytological, and morphological changes in lung following administration of these compounds by intratracheal instillation. F344/Crl rats were administered a single dose of nickel compound containing 0.0, 0.01, 0.10, or 1.0 mumol Ni by intratracheal instillation. Rats were sacrificed at 1 or 7 days after compound administration, with half the animals in each exposure group taken for determination of nickel lung burden and the remaining half used for evaluation of biochemical, cytological, and histological changes. In the latter group, the right lung was lavaged and the fluid obtained was analyzed for indicators of pulmonary inflammation: lactate dehydrogenase (LDH), beta-glucuronidase (BG), total protein (TP), glutathione reductase (GR), glutathione peroxidase (GP), and sialic acid (SA). Total and differential cell counts on cells recovered in lavage fluid were also determined. The left lobe was examined for morphological changes. Clearance of nickel from the lung was most rapid for NiCl2 and NiSO4, followed by Ni3S2 and NiO. Minimal changes in all parameters were observed at 1 day after exposure. No significant changes in any parameter occurred in rats exposed to NiO, while Ni3S2, NiSO4, and NiCl2 caused increased in LDH, BG, TP, GR, SA, and total nucleated cells at 7 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1982

Glutathione and non-protein sulfhydryl in cerebral cortex and lung in mice exposed to high oxygen pressure.

Mice were exposed to 6 atm of 100% O2, and killed at the onset of hyperactivity, convulsions, and 10(s) post convulsions. Examination of brain cortex from mice killed at these stages of O2 toxicity revealed no change in oxidized glutathione (GSSG), non-protein sulfhydryls (NPSH), total glutathione (GSH + GSSG), the GSH/GSSG ratio, glutathione reductase and glutathione peroxidase. Mice exposed to 4 atm for 1 h or 6 atm for 16 min exhibited a 36% and 33% decrease in lung NPSH respectively, but no change in cortical NPSH was observed. Although intraventricular diethylmaleate (DEM) decreased cerebral NPSH 72%, no change in the susceptibility of mice to O2 convulsions was found. Disulfiram, an effective O2 convulsive protectant had no effect on either cortical NPSH or total glutathione.

Animals↗

PubMed1986

Dose-dependent study of the effects of acute lindane administration on rat liver superoxide anion production, antioxidant enzyme activities and lipid peroxidation.

The administration of single i.p. doses of lindane (20, 40, 60 and 80 mg/kg) to rats produced a progressive increase in the liver microsomal content of cytochrome P-450 and in the rate of superoxide anion generation, as measured by adrenochrome formation. A dose-dependent increase in lipid peroxidation of liver homogenates, assessed by measuring thiobarbituric acid reactants, was also found. Lindane treatment did not alter the activity of liver glucose-6-phosphate dehydrogenase, glutathione reductase or glutathione peroxidase, while that of superoxide dismutase and catalase was significantly reduced. These changes were accompanied by a progressive liver steatosis. The collected metabolic data were interpreted in terms of a causal relationship between an increase in superoxide radical generation, secondary to cytochrome P-450 induction and a resulting increase in lipid peroxidation. The decrease in superoxide dismutase and catalase activities is likely to contribute to the increased levels of lipid peroxidation in view of their antioxidant properties.

Animals↗

PubMed1991

Biochemical effects of combined gases of nitrogen dioxide and ozone. IV. Changes of lipid peroxidation and antioxidative protective systems in rat lungs upon life span exposure.

Lipid peroxide production, antioxidant contents and activities of antioxidative protective enzymes were examined in lungs of rats exposed to clean air (control group), 0.05 ppm O3, 0.05 ppm O3 + 0.04 ppm NO2 and 0.05 ppm O3 + 0.4 ppm NO2 for 22 months. The results were compared with our previous data in rats exposed to 0.04 ppm NO2, 0.4 ppm NO2 and 4 ppm NO2 for their life span (Sagai et al., Toxicol. Appl. Pharmacol., 73, (1984) 444-456). TBA values used as an index of lipid peroxidation in the lungs were increased maximally at 9 months, but were decreased below control values in animals exposed for 18 and 22 months. Nonprotein sulfhydryl (NPSH) contents were increased maximally at 9 months, and after 18 and 22 months were decreased significantly below control values. Vitamin E (VE) contents showed a similar trend. On the other hand, enzyme activities of glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), glutathione reductase (GR), glutathione peroxidase measured by using cumene hydroperoxide (cum.OOH) substrate (GPx-cum.OOH), glutathione peroxidase measured by using H2O2 as a substrate (GPx-H2O2), glutathione S-transferase (GSH-Tase) and superoxide dismutase (SOD) did not show any significant changes during this experiment. The results show that lipid peroxidation in lungs was increased synergistically by a combination of NO2 and O3 at ambient levels, and that the time of maximum lipid peroxide production was shorter than with NO2 alone. The protective ability against lipid peroxides was higher with increased lipid peroxide levels, but the inducibility was not maintained through a life span exposure to the combined gases. Additionally, two small adenomas were observed in 2 out of 18 rats in the 0.05 ppm O3 + 0.04 ppm NO2 group and a large adenoma was observed in 1 out of 18 animals in the 0.05 ppm + 0.4 ppm NO2 group exposed for 22 months.

Adenoma↗

PubMed1983

Selenium-dependent and non-selenium-dependent glutathione peroxidases in human tissue extracts.

A method for the assessment of both selenium-dependent and non-selenium-dependent glutathione peroxidases on crude tissue extracts in human is described. The enzyme activity is measured by the coupled assay system in which oxidation of reduced glutathione (GSH) is coupled to NADPH oxidation catalyzed by glutathione reductase. Total glutathione peroxidase activity is measured with cumene hydroperoxide as substrate. Selenium-dependent glutathione peroxidase is measured with tert-butyl hydroperoxide. This substrate is preferable to H2O2 which gives too high blank values compared to the assay values. The difference between total glutathione peroxidase and selenium-dependent glutathione peroxidase activities represents the non-selenium-dependent glutathione peroxidase activity. Studies of substrate specificity of the two glutathione peroxidases separated by gel filtration as well as linearity and recovery studies are presented. For a given tissue, the relative amounts of the two glutathione peroxidases given by our assay are identical to those estimated by quantifying the elution peaks after gel filtration. Based on the percentages of the two glutathione peroxidases, human tissues can be classified in four groups: (1) the non-selenium-dependent glutathione peroxidase is predominant in liver, in renal cortex and skeletal muscle; (2) non-selenium-dependent and selenium-dependent glutathione peroxidases are in equal amounts in renal medulla; (3) the selenium-dependent glutathione peroxidase is predominant in adrenal glands and platelets; (4) the selenium-dependent glutathione peroxidase represents 100% of the glutathione peroxidase activity in the other organs. The heart and the brain are of special interest in this group because of the physiological role and the regulation of the selenoenzyme.

Chromatography, Gel↗

PubMed1983

Effect of anaemia on red cell metabolism in cattle.

Six enzymes: glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), glutathione reductase (GR), glutathione peroxidase (GSHPx), catalase and superoxide dismutase (SOD), and three metabolites: 2,3-diphosphoglycerate (DPG), adenosine triphosphate (ATP) and reduced glutathione (GSH), were measured in the red blood cells of cattle during experimental anaemia. There was a significant rise in the mean levels of DPG (from 0.85 to 1.69 mumol/gHb) and ATP (from 2.16 to 3.25 mumol/gHb) in the early phase of recovery. Enzyme activities also increased during the early recovery period.

2,3-Diphosphoglycerate↗

PubMed1990

Endrin-induced depletion of glutathione and inhibition of glutathione peroxidase activity in rats.

1. Recent studies have shown that endrin induces lipid peroxidation and may produce toxicity through an oxidative stress. We have therefore examined the effect of endrin administration to rats on glutathione content and the activities of glutathione metabolizing enzymes. 2. The oral administration of endrin resulted in dose- and time-dependent decreases in hepatic and renal glutathione content with maximum depletion (90%) occurring in liver at approximately 24 hr post-treatment. 3. Decreases in glutathione content were also observed in lung, brain, spleen and heart. 4. Endrin (4 mg/kg) decreased selenium dependent glutathione peroxidase activity in liver and kidney by 64 and 50%, respectively, while small increases were observed in the activities of glutathione reductase and glutathione S-transferase. 5. The toxicity of endrin may be at least in part related to oxidative tissue damage associated with depletion of glutathione and inhibition of glutathione peroxidase activity.

Animals↗

PubMed1993

Turnover of hepatic glutathione after acute lindane intoxication.

The administration of lindane (60 mg/kg) to fed rats diminished the content of hepatic glutathione (GSH) 4 h after treatment, which was recovered at 24 h. At these experimental times, the activities of glutathione peroxidase, glutathione reductase, glutathione-S-transferases and gamma-glutamyltransferase in the liver of lindane-treated rats and control animals were comparable. Liver GSH turnover, measured after a pulse of [35S]cysteine, was enhanced by 69% (P < 0.05) in lindane-treated rats 24 h after intoxication compared to controls, with a 63% (P < 0.05) increase in the estimated rate of GSH synthesis. It is concluded that lindane enhances GSH synthesis in rat liver 24 h after treatment as a consequence of the decrement in its content observed at early times of intoxication (4 h), thus allowing the recovery of the normal level of hepatic GSH.

Animals↗

PubMed1992

Lead-induced lipid peroxidation and antioxidant defense components of developing chick embryos.

Administration of lead (1.25 and 2.5 mumol/kg egg weight) to 14-day-old chick embryos enhanced the level of lipid peroxides (LPO) in tissues of liver, brain, and heart. Accumulation of LPO was maximum at 9 h after treatment with lead and returned to normal level by 72 h. Further, we have studied the levels of glutathione-S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase. At 9 h posttreatment, the hepatic GR was reduced significantly with the induction of GST and considerable depletion of GSH. However, in brain and heart, both GR and GST activities were unaltered with significant reduction of GSH. Further, an increase of non-Se-dependent GPx and SOD activities were observed in liver, brain, and heart. Similarly, at 72 h, although the GPx activity was found decreased in liver and brain, the GST, catalase, and SOD activities were significantly increased in all the three tissues alike, suggesting tissue-specific changes of antioxidant defense components in response to lead treatment. Our results suggests that the elevated levels of GST, SOD, and catalase at 72 h were successful in bringing LPO levels back to normal.

Animals↗

PubMed2005

Neuroprotective effect of N-acetyl cysteine on hypoxia-induced oxidative stress in primary hippocampal culture.

Hippocampus has received a considerable attention in the recent past due to its role in a number of important functions such as learning and memory. The effect of hypoxia on neuronal cell injury especially on hippocampal cells is not well known. The aim of the present study was to characterize the biochemical changes in primary cultured hippocampal neurons during hypoxic exposure and the protective effect of N-acetyl cysteine on hypoxia-induced cytotoxicity. The hippocampal culture grown in 24-well plates was exposed to hypoxia for 3 h in a dessicator in 95% N(2), 5% CO(2) atmosphere at 37 degrees C. Later, the cells were allowed to recover for 1 h under normoxia. It was observed that there is an appreciable increase in cytotoxicity in cells exposed to hypoxia. Further, there was a significant decrease in mitochondrial membrane potential and appreciable increase in reactive oxygen species and single-strand DNA breaks in cells exposed to hypoxia compared to control. There is a significant fall in glutathione peroxidase, glutathione reductase, reduced glutathione levels, and nitric oxide in the cells exposed to hypoxia. Significant elevation in the intracellular calcium level in the cells on exposure to hypoxia was observed. Supplementation with NAC (50 microM) resulted in a significant cytoprotection, fall in ROS generation, and higher antioxidant levels similar to that of control cells. NAC also inhibited DNA strand breaks induced by hypoxia. The study indicates that NAC has significant neuroprotective activity during hypoxia in primary hippocampal culture.

Acetylcysteine↗

PubMed2006

Chemopreventive activity of glycyrrhizin on lead acetate mediated hepatic oxidative stress and its hyperproliferative activity in Wistar rats.

Lead is a pervasive environmental pollutant with no beneficial biological role and its toxicity continues to be a major health problem due to its interference with natural environment. In the present study we have evaluated the chemopreventive effect of glycyrrhizin on lead acetate mediated hepatic oxidative stress, toxicity and tumor promotion related alterations in rats. Lead acetate (100mg/kg bwt., i.p.) enhanced lipid peroxidation with concomitant reduction in glutathione, glutathione reductase, glutathione-S-transferase and glutathione peroxidase activities. There was an increase in the levels of transaminase enzymes and LDH. Lead acetate treatment also enhanced ornithine decarboxylase (ODC) activity and [(3)H] thymidine incorporation into hepatic DNA. Pretreatment of rats orally with glycyrrhizin (150 and 300 mg/kg bwt., orally) resulted in a significant decrease in hepatic microsomal lipid peroxidation (P<0.001) and increase in the level of GSH content (P<0.001) and its dependent enzyme. There was significant reduction in the levels of SGPT, SGOT and LDH (P<0.001). A significant inhibition in ODC activity and DNA synthesis (P<0.001) was also observed. On the basis of the above results it can be hypothesized that glycyrrhizin is a potent chemopreventive compound against lead acetate mediated hepatic oxidative stress, toxicity and tumor promotion related responses in rats.

Animals↗

PubMed2006

Attenuation of tamoxifen-induced hepatotoxicity by taurine in mice.

BACKGROUND: One of the most attractive approaches to disease prevention involves the use of natural antioxidants to protect tissue against toxic injury. We investigated the modulatory effects of exogenously administered taurine on the toxicity of the anticancer drug tamoxifen with special reference to protection against disruption of drug metabolizing and antioxidant enzymes in Swiss albino mice. METHODS: Male Swiss albino mice were divided into 4 groups. The extent of lipid peroxidation was evaluated in terms of thiobarbituric acid reactive substances formed. The following assays were performed in the hepatic tissue (a) antioxidant enzymes such as superoxide dismutase and catalase, (b) cytochrome P450 content, (c) glutathione-metabolizing enzymes such as glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glucose 6-phosphate dehydrogenase, and (d) low molecular weight antioxidants (reduced glutathione, ascorbic acid) and protein carbonyl content. RESULTS: Tamoxifen induced lipid peroxidation, protein carbonyl content and inhibited the enzymes of antioxidant defense system. It was also observed that the activities of antioxidant enzymes and glutathione-metabolizing enzymes were considerably stabilized in mice pretreated with taurine. CONCLUSION: Taurine protects the integrity of the hepatic tissue by stabilizing the reactive oxygen species mediated lipid peroxidation and protein carbonyl formation. Additionally taurine may prove to be efficacious as an antioxidant in tamoxifen-induced hepatotoxicity.

Animals↗

PubMed2006

Role of lipoic acid in reducing the oxidative stress induced by cyclosporine A.

BACKGROUND: Cyclosporine A (CsA) is the first choice immunosuppressant universally used for the prevention of allograft rejection in solid organ transplantation and immune-mediated diseases. However, with increasing use, evidence has accumulated that CsA therapy is associated with a variety of side effects, the most important being nephrotoxicity. We investigated the potential role of DL-alpha lipoic acid (LA), a universal antioxidant in combating the oxidative stress induced by CsA. METHODS: Adult male albino Wistar rats were divided into 4 treatment groups. Two groups received CsA (25 mg/kg body weight, orally for 21 days) to induce nephrotoxicity. One of these groups received LA treatment (20 mg/kg body weight, orally) for 21 days concurrently during CsA administration. A vehicle treated control group and a LA drug control were also included. RESULTS: CsA-induced nephrotoxicity was assessed in terms of increased activities of serum marker enzymes; alkaline phosphatase, acid phosphatase and lactate dehydrogenase. An apparent rise in the activities of N-acetyl-beta-D-glucosaminidase, beta-glucuronidase and cathepsin D were seen in the renal tissue of CsA given rats, which were reversed upon treatment with LA. CsA administration induced significant elevation in lipid peroxidation along with abnormal levels of enzymic (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase) and non-enzymic antioxidants (glutathione, vitamins C and E) in the rat kidney. LA administration improved renal function, by bringing about a significant decrease in peroxidative levels and increase in antioxidant status. CONCLUSION: These results indicate that LA has a protective action against CsA nephrotoxicity and suggest that the LA may find clinical application against a variety of toxins where cellular damage is a consequence of reactive oxygen species.

Animals↗