Thioacetamide (TAA) administration (0.3 g/l of tap water for a period of 3 months) to rats resulted in hepatic cirrhosis as assessed by biochemical and histopathological findings. This treatment caused an increase in the levels of malondialdehyde (MDA) and diene conjugates (DCs) and a decrease in the levels of glutathione (GSH), vitamin E, vitamin C and the activities of glutathione peroxidase (GSH-Px) in the liver of rats. Superoxide dismutase (SOD) activities were unchanged. Taurine (2% w/w, added to the chow diet) was administered together with TAA (0.3 g/l of drinking water) for 3 months. Taurine was found to decrease TAA-induced hepatic lipid peroxidation and to increase TAA-depleted vitamin E levels and GSH-Px activities. Histopathological findings also suggested that taurine has an inhibitive effect on TAA-induced hepatic cirrhosis. These results indicate that taurine treatment has a protective effect against TAAinduced liver cirrhosis by decreasing oxidative stress.

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Thioacetamide (TAA) administration (three consecutive intraperitoneal injections of 400 mg/kg at 24-h interval) to rats resulted in hepatic injury as assessed by the measurement of serum transaminase activities and histopathological findings. This treatment caused an increase in the levels of malondialdehyde (MDA), diene conjugates (DCs) and glutathione (GSH) and the activity ofsuperoxide dismutase (SOD), and a decrease in the levels of vitamins E and C and the activity of glutathione peroxidase (GSH-Px) in the liver of rats. Taurine administration (400 mg/kg, i.p., every 12 h and started 24 h prior to the first TAA injection) was found to decrease serum transaminase activities and hepatic lipid peroxidation without any significant change in hepatic antioxidant system. Histopathological findings also suggested that taurine has ameliorated effect on TAA-induced hepatic necrosis. These results indicate that taurine treatment, together with TAA administration, diminished the severity of the liver injury by decreasing oxidative stress due to its possible scavenger effect.

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...

This study was carried out in 140 healthy subjects who were divided into three subgroups of age: young (21-40 years), mature (41-60 years), and elderly (61-85 years) to investigate lipid peroxides and the antioxidant system in serum and low-density lipoproteins (LDL). Serum levels of cholesterol and LDL-cholesterol increased with age. The elderly group was found to have higher polyunsaturated fatty acid (PUFA) levels, thiobarbituric acid reactive substances (TBARS), diene conjugates, and lower cholesterol-adjusted vitamin E levels and antioxidant activity (AOA) as compared to the young group. No age-related difference was detected in serum vitamin C levels. Age correlated positively with serum cholesterol, LDL-cholesterol, PUFA, TBARS, diene conjugates, and negatively with cholesterol-adjusted vitamin E levels and AOA. In addition, endogenous LDL diene conjugate levels and the susceptibility of LDL to copper-induced lipid peroxidation increased in elderly subjects as compared with young subjects. In addition, positive correlations were detected between age and LDL endogenous diene conjugate levels and TBARS formation after copper incubation. However, the susceptibility of whole serum to copper-induced lipid peroxidation did not change in young and elderly subjects. Our results show that endogenous lipid peroxide levels in serum and LDL, and the susceptibility of LDL to copper-induced oxidation, increased with aging in humans.