Serum pro-oxidant-antioxidant balance and low-density lipoprotein oxidation in healthy subjects with different cholesterol levels.

In this study, we investigated serum pro-oxidantantioxidant balance in 210 healthy subjects divided into groups with low and high atherogenic risk according to the levels of serum total cholesterol (TC) and low-density lipoprotein-cholesterol (LDL-C) and high-density lipoprotein- cholesterol (HDL-C). Diene conjugate (DC), malondialdehyde (MDA), polyunsaturated fatty acid (PUFA), vitamin E, and vitamin C levels and antioxidant activity (AOA) were determined in the serum. Endogenous DC and copper-induced MDA levels were also measured in the LDL fraction isolated by precipitation with buffered heparin from plasma in 80 healthy subjects with different serum LDL-C levels. Subjects with a high atherogenic risk had significantly higher plasma DC, MDA, and PUFA levels, but lower vitamin E/TC values and AOA than subjects with low atherogenic risk. Endogenous DC and copper-induced MDA levels in the LDL fraction were increased in subjects with serum LDL-C levels higher than 4.14 mM compared with those with normal LDL-C levels. In conclusion, this study clearly indicates that a disturbance in serum pro-oxidant-antioxidant balance and an increase in LDL oxidation are concomitant with higher TC and LDL-C and lower HDL-C levels in the serum.

Taurine has a protective effect against thioacetamide-induced liver cirrhosis by decreasing oxidative stress.

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 TAA-induced liver cirrhosis by decreasing oxidative stress.

The protective effect of taurine against thioacetamide hepatotoxicity of rats.

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 of superoxide 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.

Aminoguanidine, an inducible nitric oxide synthase inhibitor, plus N-acetylcysteine treatment reduce the lipopolysaccharide-augmented hepatotoxicity in rats with cirrhosis.

Hepatic cirrhosis is produced in rats by administration of thioacetamide (TAA) (0.3 g/L tap water for a period of three months). This treatment caused an increase in oxidative stress in the liver. Lipopolysaccharide (LPS) administration (5 mg/kg) to rats with cirrhosis was observed to increase hepatotoxicity as well as oxidative stress according to biochemical and histopathological findings. However, aminoguanidine (AG), an inducible nitric oxide synthase (iNOS) inhibitor, plus N-acetylcysteine (NAC) treatment reduced the LPS-augmented hepatotoxicity in rats with cirrhosis without making any changes in oxidative stress in the liver.

Decreases in taurine levels induced by beta-alanine treatment did not affect the susceptibility of tissues to lipid peroxidation.

We aimed to investigate the effect of decreased taurine levels on endogenous and induced lipid peroxide levels in liver, brain, heart and erythrocytes as well as prooxidant and antioxidant balance in the liver of rats administered beta-alanine (3%, w/v) in drinking water for 1 month to decrease taurine levels of tissues. This treatment caused significant decreases in taurine levels of liver (86%), brain (36%) and heart (15%). We found that endogenous and ascorbic acid-, NADPH- and cumene hydroperoxide-induced malondialdehyde (MDA) levels did not change in the liver, brain and heart homogenates following beta-alanine treatment. Also, H(2)O(2)-induced MDA levels remained unchanged in erythrocytes. In addition, we did not observe any changes in levels of MDA, diene conjugates, glutathione, alpha-tocopherol, ascorbic acid and the activities of superoxide dismutase, glutathione peroxidase and glutathione transferase in the liver. According to this, buffering or sequestering capacity of tissues to exogenous stimuli was not influenced by reduced taurine levels in tissues of rats.

Betaine or taurine administration prevents fibrosis and lipid peroxidation induced by rat liver by ethanol plus carbon tetrachloride intoxication.

The aim of this study was to investigate the effect of betaine or taurine on liver fibrogenesis and lipid peroxidation in rats. Fibrosis was induced by treatment of rats with drinking water containing 5% ethanol and CCl(4) (2 x weekly, 0.2 ml/kg, i.p.) for 4 weeks. Ethanol plus CCl(4) treatment caused increased lipid peroxidation and disturbed antioxidant system in the liver. Histopathological findings suggested that the development of liver fibrosis was prevented in rats treated with betaine or taurine (1% v/v in drinking water) together with ethanol plus CCl(4) for 4 weeks. When hepatic taurine content was depleted with beta-alanine (3% v/v in drinking water), portal-central fibrosis induced by ethanol + CCl(4) treatment was observed to proceed cirrhotic structure. Betaine or taurine was also found to decrease serum transaminase activities and hepatic lipid peroxidation without any change in hepatic antioxidant system in rats with hepatic fibrosis. In conclusion, the administration of betaine or taurine prevented the development of liver fibrosis probably associated with decreased oxidative stress.