I405V and TaqIB polymorphisms of the cholesteryl ester transfer protein and their relation to serum lipid and lipoprotein levels in a Turkish population.

Cholesteryl ester transfer protein (CETP) plays a central role in high-density lipoprotein (HDL) metabolism. Genetic polymorphisms of the CETP gene can influence levels of serum lipoproteins. It has been reported that mean HDL-cholesterol (HDL-C) concentrations are low in Turkish population. Thus, we investigated the frequencies of the common I405V and TaqIB polymorphisms of the CETP gene and their relation to serum lipid and lipoprotein levels in a Turkish population. The variant allele frequencies of I405V and TaqIB polymorphisms of the CETP gene were found to be 0.38 and 0.46, respectively and similar to some of the European populations. Subjects for the VV genotype of I405V polymorphism had higher HDL-C levels than did II subjects. The covariance analysis showed that gender and triglyceride (TG) levels have an effect on the association of HDL-C and I405V polymorphism. In conclusion, our results indicate that I405V polymorphism may affect the HDL-C levels in Turkish population. The association of this polymorphism and HDL-C levels could be modified by other factors, such as gender and TG levels.

The role of heat shock protein 70 (Hsp 70) in male infertility: is it a line of defense against sperm DNA fragmentation?

OBJECTIVE: To clarify the role of heat shock protein 70 (Hsp 70) and its relation with DNA damage in male infertility. DESIGN: Prospective study. SETTING: Andrology laboratory of Istanbul Medical Faculty. PATIENT(S): Semen samples from 37 infertile men and 13 fertile men (as controls). INTERVENTION(S): The percentage of DNA fragmentation was assayed with the use of terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL). Sperm Hsp 70 expression was determined by using Western blot analysis. MAIN OUTCOME MEASURE(S): Both the percentages of sperm DNA fragmentation and Hsp 70 expression were correlated with semen analysis parameters. RESULTS: TUNEL-positive spermatozoa in the infertile group (18.7% for asthenospermics and 13.0% for oligoasthenospermics) were higher than the fertile group (4.9%). Significant inverse correlations were detected between percentage of TUNEL-positive cells and both concentration (r = -0.487) and motility (r = -0.377) of spermatozoa. No expression of Hsp 70 was observed in azospermic group, whereas Hsp 70 levels were found increased significantly in infertile group (U = 62 for asthenospermics and U = 38 for oligoasthenospermics) compared to fertile group as analyzed by using Mann-Whitney U Wilcoxon rank sum test. Furthermore, significant positive correlation was found between percentage of TUNEL-positive cells and Hsp 70 expression (r = 0.357). CONCLUSION(S): Hsp 70 expression may have been increased as a protective mechanism against apoptosis in spermatozoa of infertile men.

Nitrotyrosine formation and heme oxygenase-1 expression in endotoxemic cirrhotic rats.

BACKGROUND: Endotoxemia increases hepatic toxicity and mortality in cirrhosis. Because the mechanism of augmented hepatotoxicity in endotoxemic cirrhotic rats is still unclear, we wanted to investigate whether oxidative and nitrosative stress play a causative role in lipopolysaccharide (LPS)-treated cirrhotic rats. METHODS: Liver cirrhosis was produced by the administration of thioacetamide (0.3 g/L of tap water) for a period of 3 months in rats. At the end of this period, cirrhotic rats were sacrificed 6 h after LPS injection (5 mg/kg, intraperitoneally). Serum transaminase activities, plasma total nitrite and nitrotyrosine (NT) levels as well as hepatic lipid peroxides, NT formation and heme oxygenase 1 (HO-1) expression were determined. RESULTS: LPS administration to cirrhotic rats caused further increases in serum transaminase activities, and plasma total nitrite and NT levels as well as hepatic lipid peroxide levels as compared to cirrhotic rats. Hepatic NT formation and HO-1 expression were also found to be increased in LPS-injected cirrhotic rats. CONCLUSIONS: Our results indicate that increased oxidative and nitrosative stress may have a synergistic effect in LPS-augmented hepatotoxicity in cirrhotic rats.

Polymorphisms in the DNA repair genes XPD (ERCC2) and XPF (ERCC4) are not associated with sporadic late-onset Alzheimer's disease.

Nucleotide excision repair (NER) is the most versatile mechanism of DNA repair, recognizing and dealing a variety of helix-distorting lesions. Xeroderma pigmentosum group D (XPD) and group F (XPF) are essential participants in NER pathway. There is evidence that two common polymorphisms of XPD gene (g.22541C>A; exon 6 and g.35931A>C; Lys>Gln; exon 23) may be associated with differential DNA repair activities. Alzheimer's disease (AD) is characterized by progressive neuronal loss correlated in time with the symptoms of disease considered. Although deficient DNA repair was proposed in the etiology of AD by several researchers, polymorphisms of DNA repair genes have not been studied in AD yet. We conducted a case-control study including 97 patients with AD and age- and sex-matched 101 control subjects to examine the role of genetic polymorphisms of XPD and XPF (g.30028T>C; exon 11) as a risk factor for AD. The frequencies of the XPD/exon 6, XPD/exon 23, and XPF/exon 11 variant alleles in our control group were 0.41, 0.35, and 0.35, respectively. No significant association was observed between the variant alleles of XPD/exon 6 (OR=0.94, 95% CI=0.63-1.41), XPD/exon 23 (OR=1.24, 95% CI=0.82-1.86) and XPF/exon 11 (OR=1.08, 95% CI=0.72-1.64) and AD. Our results suggest that the polymorphic variants of these NER genes do not contribute to the risk of developing AD.

The effect of taurine or betaine pretreatment on hepatotoxicity and prooxidant status induced by lipopolysaccharide treatment in the liver of rats.

BACKGROUND: Taurine or betaine have been reported to have antioxidative potential and inhibit Kupffer cell activation. These effects may play an important role in their hepatoprotective effects. Therefore, they may also have protective effects in lipopolysaccharide hepatotoxicity by both inhibiting Kupffer cell activation and behaving as antioxidants. DESIGN: The prophylactic efficiency of taurine or betaine pretreatment for the prevention of peroxidative changes induced by lipopolysaccharide treatment in the rat liver was investigated. METHODS: Lipopolysaccharide (10 mg/kg intraperitoneally) was given to rats pretreated with taurine (1.5%, w/v) or betaine (1.5%, w/v) in drinking water for 4 weeks and plasma transaminase activities as well as hepatic malondialdehyde, diene conjugate (DC), glutathione, alpha-tocopherol and ascorbic acid levels, and superoxide dismutase (SOD) and glutathione peroxidase activities were determined. RESULTS: Significant increases in plasma transaminase activities and hepatic malondialdehyde and DC levels and decreases in hepatic glutathione and alpha-tocopherol levels and SOD and glutathione peroxidase activities were observed 6 h after lipopolysaccharide treatment. This treatment did not alter ascorbic acid levels in the liver compared with controls. Taurine or betaine pretreatment in lipopolysaccharide-injected rats caused significant decreases in plasma transaminase activities and hepatic malondialdehyde and DC levels, and significant increases in glutathione and alpha-tocopherol (not betaine) levels without changing ascorbic acid levels and SOD and glutathione peroxidase activities in the liver. CONCLUSIONS: Our findings clearly indicate that taurine or betaine pretreatment was effective in the prevention of lipopolysaccharide-induced hepatotoxicity and prooxidant status.

Resistance of erythrocytes to lipid peroxidation in cirrhotic rats.

BACKGROUND: The aim of the present study was to investigate erythrocyte prooxidant-antioxidant balance in relation to liver and plasma lipid peroxidation in thioacetamide (TAA)-induced liver cirrhosis in rats. METHODS: Liver cirrhosis was produced by the administration of TAA (0.3 g/L of tap water) for a period of 3 months in rats. Serum, liver and erythrocyte lipid peroxide levels as well as liver glutathione (GSH) levels and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were determined in cirrhotic rats. RESULTS: Hepatic cirrhosis was assessed by biochemical and histopathological findings. Serum alanine transaminase (ALT) and aspartate transaminase (AST) activities and malondialdehyde (MDA) levels increased in cirrhotic rats. This treatment caused increased MDA and diene conjugate (DC) levels as well as decreased GSH levels and GSH-Px activities in the liver of cirrhotic rats. In these conditions, no significant changes in erythrocyte cholesterol, phospholipid levels as well as endogenous DC, and GSH levels and spontaneous hemolysis values were observed in erythrocytes of rats with TAA-induced liver cirrhosis. However, H(2)O(2)-induced MDA levels were detected to decrease significantly in erythrocytes of cirrhotic rats. CONCLUSIONS: Our results indicate that erythrocytes of TAA-induced cirrhotic rats have a resistance against peroxidative stress in contrast to the findings in plasma and liver.

Increased LDL+VLDL oxidizability and plasma homocysteine levels in chronic alcoholic patients.

The purpose of this study was to investigate the effect of heavy alcohol consumption on peroxidation status in apolipoprotein B-containing lipoproteins (LDL+VLDL) and plasma as well as plasma homocysteine (HC) levels in patients with chronic alcoholism who drank raki, a national Turkish beverage. For this reason, endogenous diene conjugate (DC) and lipid hydroperoxide (LOOH) levels and lag phase, maximum DC formation and propagation rate following copper induction were measured in apolipoprotein B-containing lipoproteins (LDL+VLDL) isolated by precipitation with dextrane sulfate and MgCl2 from plasma. In addition, serum malondialdehyde (MDA), DC, HC, folate and vitamin B12 levels as well as paraoxonase activity were determined. Serum MDA and DC levels were higher in heavy raki drinkers compared to control subjects. Significant increases in endogenous DC and LOOH levels in LDL+VLDL together with shortened lag phase were also observed in patients. In addition, HDL-cholesterol, HC and vitamin B12 levels and HDL-associated paraoxonase activity were found to be higher, but folate levels to be lower in serum of heavy raki consumers. In conclusion, our results indicate that increases in LDL+VLDL oxidizability and plasma HC levels may enhance the susceptibility to vascular diseases in heavy raki drinkers.

Peroxynitrite induced decrease in Na+, K+-ATPase activity is restored by taurine.

AIM: Peroxynitrite (ONOO-) is a powerful oxidant shown to damage membranes. In the present study, the effect of taurine on changes of liver plasma membrane Na+, K+-ATPase induced by ONOO- was investigated. METHODS: Liver plasma membrane was exposed to ONOO- with or without taurine. Na+, K+-ATPase activity and lipid peroxidation as thiobarbituric acid reactive substances (TBARS) levels were measured. RESULTS: Different concentrations of ONOO- (100, 200, 500, and 1000 micromol/L) were found to decrease liver plasma membrane Na+, K+-ATPase activity significantly. The depletion of enzyme activity was not concentration dependent. Effects of different concentrations of taurine on liver plasma membrane Na+, K+-ATPase activity were also measured. Taurine did not cause any increase in enzyme activity. When plasma membranes were treated with 200 micromol/L ONOO- with different concentrations of taurine, a restoring effect of taurine on enzyme activity was observed. TBARS levels were also measured and taurine was found to decrease the elevated values. CONCLUSION: Taurine is observed to act as an antioxidant of ONOO- to decrease lipid peroxidation and thus affect liver plasma membrane Na+, K+-ATPase by restoring its activity.

Methionine supplementation did not augment oxidative stress, atherosclerotic changes and hepatotoxicity induced by high cholesterol diet in C57BL/6J mice.

The purpose of this study was to investigate the effect of a high-methionine plus cholesterol diet (HM+HC) on plasma, erythrocyte, liver and aorta lipid, lipid peroxide levels, and the liver antioxidant system, as well as hepatic and aortic histopathology in CS 7BL/6J mice, and to compare these results to those observed following administration of a high-methionine (HM) or high-cholesterol diet (HC) alone. Mice were fed diets containing 1.5% methionine, 1.5%, cholesterol and 0.5% cholic acid, or a combination of the two diets, for 4 mo. The HM diet did not alter cholesterol or diene conjugate (DC) levels in the plasma or aorta, but this diet caused increases in cholesterol, triglyceride, malondialdehyde (MDA) and DC levels and a decrease in a-tocopherol levels without any change in the levels of glutathione and ascorbic acid or the activities of superoxide dismutase, glutathione peroxidase and glutathione transferase in the liver of mice. However, the HC diet alone was found to further increase cholesterol, triglyceride. MDA and DC levels in the plasma and liver together with changes in hepatic antioxidant system elements, but aortic cholesterol and DC levels remained unchanged as compared to the control group. There were no changes in blood hemoglobin and erythrocyte MDA levels or erythrocyte hemolysis values in both the HM and HC groups. However, the parameters related to lipid and lipid peroxide and antioxidant systems did not change in the plasma or tissues of the HM+HC and HC groups. Only plasma cholesterol was observed to increase in the HM+HC group as compared to the HC group. In addition, histopathological findings in the liver and aorta were similar in the HC and HM+HC groups. In conclusion, our results indicate that the addition of methionine to the HC diet did not augment oxidative stress, hepatotoxicity or atherosclerotic changes induced by the HC diet in mice.

Hazelnut oil administration reduces aortic cholesterol accumulation and lipid peroxides in the plasma, liver, and aorta of rabbits fed a high-cholesterol diet.

Hazelnut oil (HO) is rich in monounsaturated fatty acids and antioxidants. We wanted to investigate the effect of HO on lipid levels and prooxidant-antioxidant status in rabbits fed a high-cholesterol (HC) diet. An HC diet caused significant increases in lipids and lipid peroxide levels in the plasma, liver, and aorta together with histopathological atherosclerotic changes in the aorta. Glutathione levels, glutathione peroxidase, and glutathione transferase activities decreased significantly, but superoxide dismutase activity and vitamin E and C levels remained unchanged in the livers of rabbits following HC diet. HO supplementation reduced plasma, liver, and aorta lipid peroxide levels and aorta cholesterol levels together with amelioration in atherosclerotic lesions in the aortas of rabbits fed an HC diet, without any decreasing effect on cholesterol levels in the plasma or liver. HO did not alter the antioxidant system in the liver in the HC group. Our findings indicate that HO reduced oxidative stress and cholesterol accumulation in the aortas of rabbits fed an HC diet.

Effect of a taurine treatment on the regression of existing atherosclerotic lesions in rabbits fed on a high-cholesterol diet.

We studied whether taurine has any regressive effect on existing atherosclerotic lesions and lipid peroxidation in rabbits fed on a high-cholesterol (HC) diet. The cholesterol, triglyceride, malondialdehyde (MDA) and diene conjugate (DC) levels, as well as the aortic histopathological findings were examined in rabbits that had been fed on a cholesterol-containing diet for 8 months [0.5% cholesterol (w/w) for 3 months and subsequently 0.25% cholesterol (w/w) for 5 months], and then for a further 4 months on a normal diet with or without taurine treatment [1% (w/v) in the drinking water]. High levels of lipid and lipid peroxide induced by the HC diet were observed to decline in the plasma, liver and aorta of atherosclerotic rabbits, as well as a slight retardation in aortic atherosclerotic lesions during the regression period. Although no significant differences in the lipid and lipid peroxide levels in the plasma and aorta were found between the regressed groups with or without the taurine treatment, the extent of atherosclerotic lesions in the aorta was less in the taurine-treated regressed group than in the non-treated regressed group. However, the liver MDA and DC levels were lower in the regressed rabbits with the taurine treatment in the non-treated group. These results indicate that the taurine treatment may accelerate the regression of cholesterol-induced atherosclerotic lesions in rabbits without having any effect on the plasma and aorta lipid and lipid peroxide levels.

Heme oxygenase induction protects liver against oxidative stress in x-irradiated aged rats.

We studied the effect of total body X-ray irradiation on the heme oxygenase-1 (HO-1) induction in the livers of young and aged rats. For this purpose, male rats were irradiated with a dose of 17 Gy. The animals were killed 5 h after irradiation. HO-1 protein expression was found to be increased two fold in aged rat liver, but lipid peroxide levels had decreased significantly where no change was observed either in inducible nitric oxide synthase protein expression or in glutathione levels. Contradictory results with respect to HO-1 and lipid peroxidation levels were obtained in the livers of young animals. These results suggest that the additional oxidative stress produced in irradiated rats may be compensated by HO-1 induction as decreased lipid peroxide levels were shown in the livers of aged animals.

Dose-related effects of theophylline added to modified Euro-Collins solution used for hypothermic preservation of lung.

OBJECTIVE: To investigate the dose-related effects of theophylline in prevention of ischemia-reperfusion injury of the lung. DESIGN: Experimental study. SETTINGS: University hospital. PARTICIPANTS: Thirty Wistar rats. INTERVENTIONS: In experimental group 1 (G-I) (n = 5) 20 mg/L, in G-II (n = 5) 100 mg/L, in G-III (n = 5) 400 mg/L, and in G-IV (n = 5) 1000 mg/L of theophylline was added to modified Euro-Collins solution and perfused the lungs. Lungs were extracted without an ischemic period in control group 1 (C-I) and perfused with modified Euro-Collins solution in control group 2 (C-II). Lungs were kept in a hypothermic state for 6 hours and then ventilated for 30 minutes with 100% O(2). MEASUREMENTS AND MAIN RESULTS: Tissue levels of dien congugate (DC) and malonylaldehyde (MDA) were measured. Comparison of 6 groups revealed statistically significant differences for DC and MDA (p < 0.0001 for both comparisons). Both DC and MDA levels of C-II were found to be higher than G-III and G-IV (p = 0.008). DC and MDA levels of G-III and G-IV were significantly lower than G-I and G-II (p = 0.008 for all comparisons). CONCLUSION: The results of this study showed that 400 mg/L and 1000 mg/L of theophylline added to the modified Euro-Collins solution decreased the intermediate products of lipid peroxidation. Theophylline merits further investigation in ischemia-reperfusion studies as a potentially beneficial agent.

Age-related increases in plasma malondialdehyde and protein carbonyl levels and lymphocyte DNA damage in elderly subjects.

OBJECTIVES: Increased oxidative stress has been hypothesized to play an important role in the aging process. A role for oxidative damage in normal aging is supported by studies in experimental animals, but there is limited evidence in humans. To investigate the relationship between the oxidative stress and aging in humans, we determined lipid and protein oxidation in plasma as well as DNA damage in lymphocytes in young and elderly subjects. DESIGN AND METHODS: 55 healthy subjects were divided into young (21-40 years) and elderly (61-85 years) groups. Plasma malondialdehyde (MDA), protein carbonyl (PC) levels, and grade of DNA damage in lymphocytes using comet assay as well as total ferric reducing antioxidant power (FRAP) in plasma were determined in young and elderly subjects. RESULTS: Plasma MDA and PC levels were found to be increased in plasma of elderly subjects as compared to young subjects. Increases in endogenous and H2O2-induced DNA damage were also observed in lymphocytes of elderly subjects. In addition, we detected a significant decrease in FRAP values in elderly subjects. Plasma MDA, PC levels and endogenous and H2O2-induced DNA damage were positively correlated with aging, but negatively with FRAP values. CONCLUSION: We evaluated MDA, PC levels and lymphocyte DNA damage altogether in both young and elderly subjects for the first time. The results of this study strongly support the presence of increased oxidative stress in elderly subjects.

Influence on hazelnut oil administration on peroxidation status of erythrocytes and apolipoprotein B 100-containing lipoproteins in rabbits fed on a high cholesterol diet.

Hazelnut oil (HO) is rich in monounsaturated fatty acids (MUFA). The effect of a high cholesterol (HC) diet with and without HO on lipids and lipid peroxide levels in plasma, apolipoprotein B 100-containing lipoproteins (VLDL + LDL), and erythrocytes as well as hematological data was investigated in rabbits. A HC diet caused significant increases in lipid peroxide levels in plasma and apo B-containing lipoproteins together with histopathological atherosclerotic findings in aorta. In addition, this diet resulted in hemolytic anemia associated with increased endogenous diene conjugate (DC) levels, but H(2)O(2)-induced malondialdehyde (MDA) levels remained unchanged in erythrocytes. HO supplementation reduced lipid peroxide levels in plasma and apolipoprotein B 100-containing lipoproteins as well as aortic atherosclerotic lesions in rabbits fed an HC diet without any decreasing effect on lipid levels. In addition, HO was found to reduce hemolytic anemia together with significant decreases in DC and H(2)O(2)-induced MDA levels.

Increased lipid peroxidation in serum and low-density lipoproteins associated with aging in humans.

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.

Hepatic mitochondrial prooxidant and antioxidant status in ethanol-induced liver injury in rats.

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.

Bone healing regulated by nitric oxide: an experimental study in rats.

Nitric oxide has many functions in wound healing and metabolism of bone. In the current study the role of nitric oxide on bone healing was investigated. Thirty-six young adult male Sprague-Dawley rats were divided into three groups: control, nitroso-bovine serum albumin, and aminoguanidine. Five millimeter segmental defects were created in the middle of the right femora. A polyethylene plate and screw posts were used for rigid fixation. Demineralized bone matrix served as the graft material in all groups. Nitroso-bovine serum albumin (an active nitric oxide congener) carried by demineralized bone matrix was applied locally at the defect in the nitroso-bovine serum albumin group. Aminoguanidine (an inducible nitric oxide synthase inhibitor) group received oral aminoguanidine treatment. Formation and healing of bone were determined by radiographic and histologic analyses. In comparison to the control group the healing rate was faster in both experimental groups as indicated by radiographic and histologic data. If accompanied by bone graft with a suitable delivery system, nitric oxide may be useful as a therapeutic adjuvant in clinical situations when local formation of bone is needed. Moreover, when combined appropriately, treatment with orthotopic nitric oxide supplementation and systemic inducible nitric oxide synthase inhibition may enhance bone healing.

Improving effect of dietary taurine supplementation on the oxidative stress and lipid levels in the plasma, liver and aorta of rabbits fed on a high-cholesterol diet.

The effect of a high-cholesterol diet with or without taurine on lipids and oxidative stress in the plasma, liver and aorta of rabbits was investigated. The animals were maintained on a basal diet (control), a high-cholesterol diet (HC, 1% w/w), or a high- cholesterol diet supplemented with taurine (HCHT, 2.5% w/w) for two months. Taurine has an ameliorating effect on atherosclerosis together with a decreasing effect on the cholesterol and triglyceride levels in rabbits fed on an HC diet. The HCHT diet caused a significant decrease in the malondialdehyde (MDA) and diene conjugate (DC) levels in the plasma, liver and aorta of rabbits as compared to the HC group. This treatment did not alter the antioxidant system in the liver of rabbits in the HC group. Our findings indicate that taurine ameliorated oxidative stress and cholesterol accumulation in the aorta of rabbits fed on the HC diet and that this effect may be related to its antioxidative potential as well as its reducing effect on serum lipids.

Taurine treatment reduces hepatic lipids and oxidative stress in chronically ethanol-treated rats.

In this study, we evaluated whether taurine treatment has a protective effect on the prooxidant-antioxidant state following chronic ethanol treatment in rats. Rats were given water containing 20% ethanol (v/v) as drinking water for 3 months. Chronic ethanol treatment in drinking water resulted in increased oxidative stress in the liver of rats. Taurine treatment was performed by adding 1% taurine (w/v) to the drinking water plus injection (400 mg/kg body weight) intraperitoneally 3 times/week for 28 d after ethanol cessation in chronically ethanol-treatad rats. This treatment starting after ethanol cessation caused a significant decreases in serum transaminase activities and hepatic total lipid, triglyceride, malondialdehyde, and diene conjugate levels and significant increases in hepatic glutathione, vitamin E, and vitamin C levels, but did not alter the activities of superoxide dismutase, glutathione peroxidase, and glutathione transferase in the liver as compared with chronically ethanol-treated rats. Accordingly, we propose that taurine has a restorative effect on ethanol-induced hepatic damage by decreasing oxidative stress.