Prooxidant and antioxidant hepatic factors in rats chronically fed an ethanol regimen and treated with an acute dose of lindane

Azzalis, Ligia Ajaime; Junqueira, Virgínia; Simon, Karin Argenti; Giavarotti, Leandro; Silva, Márcia A.; Kogake, M; Simizu, K; Barros, S. B. M.; Fraga, César G.; Porta, Eduardo A.

doi:10.1016/0891-5849(94)00235-c

Cited by 19 publications

(7 citation statements)

References 80 publications

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“…Low intakes of alcohol have not been related to depletion of antioxidant vitamins in the human body (Clot et al, 1994), but plasma concentration of a-tocopherol is lower in alcoholics than in people with low intakes of alcohol (Lecomte et al, 1994). Epidemiological and experimental studies have shown that the oxidative stress by alcohol consumption depends on the amount and frequency of ethanol intake (Lecomte et al, 1994;Clot et al, 1994;Azzalis et al, 1995). In our study; alcohol intake was low compared to other regions in Spain (Aranceta et al, 1990).…”

Section: Discussionmentioning

confidence: 41%

Determinants of the nutritional status of vitamin E in a non-smoking Mediterranean population. Analysis of the effect of vitamin E intake, alcohol consumption and body mass index on the serum alpha-tocopherol concentration

et al. 1997

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Objectives: Study was conducted in order to investigate the association of vitamin E intake and other factors with plasma a-tocopherol concentration in a non-smoking Mediterranean population. Design: A cross-sectional study was conducted in a subsample of a representative sample of the Catalan population. Subjects: Sample size was 143 men and women, aged between 18 and 75 y, and ®nal response rate reached 61.9% of the initial sample. Interventions: Serum alpha-tocopherol concentration standardized by serum total lipids was used as a proxy of the nutritional status of vitamin E. Vitamin E intake and alcohol consumption were estimated by a replicated 24 h recall method. Dietary data were collected in two different periods, winter and summer, in order to account for seasonal variation in nutrient intake, and were corrected for random within-person variability in order to account for day-to-day variation in nutrient intake. Multivariate linear regression models were ®tted in order to estimate the determinants of serum a-tocopherol concentration. Results: In this population study, for each one mg increase in vitamin E intake, serum a-tocopherol concentration increased, on average, 0.66 micromol/L, after adjusting for age, gender, Body Mass Index (BMI), alcohol consumption and energy intake. BMI also in¯uenced signi®cantly serum a-tocopherol concentration, whereas alcohol intake, age and gender did not show signi®cant associations with serum a-tocopherol.

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Section: Discussionmentioning

confidence: 41%

Determinants of the nutritional status of vitamin E in a non-smoking Mediterranean population. Analysis of the effect of vitamin E intake, alcohol consumption and body mass index on the serum alpha-tocopherol concentration

et al. 1997

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“…However, conflicting results are reported in the literature concerning oxidative stress following chronic ethanol treatment in rats. [28][29][30] These discrepancies may be due to the techniques used for assessing oxidative stress as well as varying conditions of ethanol administration. Several types of rat models are used for alcoholic liver disease studies, such as the Lieber-DeCarli liquid diet or by adding ethanol to rats' drinking water.…”

Section: Resultsmentioning

confidence: 99%

Hepatic Mitochondrial Prooxidant and Antioxidant Status in Ethanol-Induced Liver Injury in Rats.

Kanbagli

Balkan

Aykaç‐Toker

et al. 2002

Biological & Pharmaceutical Bulletin

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In this study, prooxidant and antioxidant status in liver homogenates and their mitochondrial fractions were investigated in both chronic and chronic plus acute ethanol-treated rats. Increases in serum transaminase activities, as well as increases in total lipid, triglyceride, malondialdehyde (MDA) and diene conjugate (DC) levels and decreases in glutathione (GSH), vitamin E and vitamin C levels, have been observed in liver homogenates following chronic ethanol treatment (20% ethanol, v/v as drinking water for 3 months), but CuZn-superoxide dismutase (CuZnSOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities remained unchanged in postmitochondrial fractions. When an acute dose of ethanol (5 g/kg, i.p.) was given rats which had received ethanol chronically, serum transaminase activities and hepatic lipid and MDA and DC levels increased further, but GSH levels and antioxidant enzymes decreased more compared to the chronic ethanol-treated rats. There were no significant differences in the levels of MDA, DC and protein carbonyl and the activities of GSH-Px and GST in the hepatic mitochondrial fraction of rats following both chronic and chronic plus acute treatments. Mn-superoxide dismutase (MnSOD) activities increased in both groups, but mitochondrial GSH levels decreased only after chronic plus acute treatment. Therefore, we suggest that the increase in MnSOD activity may play an important role in the regulation of mitochondrial susceptibility against ethanol-induced oxidative stress.

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“…However, conflicting results are reported in the literature concerning oxidative stress following chronic ethanol treatment in rats. 5,10,12,13,27,28) These discripancies may be due to the techniques used for assessing oxidative stress as well as the conditions of ethanol administration. Several types of rat model are used for alcoholic liver disease studies such as the Lieber-DeCarli liquid diet or by adding ethanol to rats' drinking water.…”

Section: Resultsmentioning

confidence: 99%

Taurine Treatment Reduces Hepatic Lipids and Oxidative Stress in Chronically Ethanol-Treated Rats.

Balkan

Kanbagli

Aykaç‐Toker

et al. 2002

Biological & Pharmaceutical Bulletin

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Taurine (2-aminoethane sulfonic acid), a nonprotein amino acid, has hypolipidemic 1) and antiatherosclerotic effects. 2,3) In addition, taurine has been thought to be a hepatoprotective agent.4) Some investigators have demonstrated that taurine, when coadministered with ethanol, reduced ethanol-induced hepatic steatosis and lipid peroxidation. 5) Our recent studies have also shown that taurine treatment has a protective effect against thioacetamide-induced hepatic necrosis 6) and cirrhosis 7) by decreasing oxidative stress. Oxidative stress is known to play an important role in the pathogenesis of ethanol-induced liver injury. 8,9) Several experimental [10][11][12][13] and clinical 14) studies have shown that ethanol ingestion alters the prooxidant-antioxidant balance in the organism. Therefore the potential role of several substances such as antioxidants 15,16) and thiol compounds 5,12,13) has been investigated in ethanol-induced liver injury. The aim of the present study was to evaluate whether taurine treatment has a protective effect in postalcoholic liver injury in rats. For this reason, hepatic lipid levels as well as prooxidant and antioxidant status were determined in rats that received taurine 28 d after cessation of chronic ethanol ingestion. MATERIALS AND METHODS Rats and TreatmentMale Wistar rats (180-200 g) were used for all experiments. Animals were obtained from the Experimental Medical Research Institute of Istanbul University. Rats were fed a standard diet and had free access to water. Ethanol was added to drinking water 20% (v/v) for 3 months (approximately 8.5 g ethanol/kg body weight/d). Control rats (nϭ8) were given tap water as drinking fluid.At the end of this period, some rats were killed after overnight fasting. Other rats were divided into two groups. The first group did not receive any treatment, but the second group received taurine for 28 d after ethanol cessation. Taurine treatment was performed by adding taurine to the drinking water 1% (w/v) plus injection (400 mg/kg body weight) intraperitoneally 3 times per week. Experimental Procedure and DeterminationsBlood samples were collected from animals by cardiac puncture and serum transaminase (ALT and AST) activities were determined using kits from Sigma. The livers were rapidly removed, washed in 0.9% NaCl and kept in ice. Liver portions were homogenized in ice-cold 0.15 M KCI 10% (w/v). Lipids were extracted by chloroform : methanol (2 : 1) and hepatic total lipid levels were measured according to the methods of Chiang et al. 17) Hepatic triglyceride levels were determined in the lipid extracts with kits from Sigma. The degree of lipid peroxidation was assessed measuring malondialdehyde (MDA) levels using the thiobarbituric acid test 18) and diene conjugate levels.19) Liver glutathione (GSH) levels were measured with 5,5Ј-dithiobis-(2-nitrobenzoate) at 412 nm according to the method of Beutler et al. 20) Liver vitamin E and vitamin C levels were determined in homogenates by the method of Desai 21) and Omaye et al., 22) respectiv...

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Prooxidant and antioxidant hepatic factors in rats chronically fed an ethanol regimen and treated with an acute dose of lindane

Cited by 19 publications

References 80 publications

Determinants of the nutritional status of vitamin E in a non-smoking Mediterranean population. Analysis of the effect of vitamin E intake, alcohol consumption and body mass index on the serum alpha-tocopherol concentration

Determinants of the nutritional status of vitamin E in a non-smoking Mediterranean population. Analysis of the effect of vitamin E intake, alcohol consumption and body mass index on the serum alpha-tocopherol concentration

Hepatic Mitochondrial Prooxidant and Antioxidant Status in Ethanol-Induced Liver Injury in Rats.

Taurine Treatment Reduces Hepatic Lipids and Oxidative Stress in Chronically Ethanol-Treated Rats.

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