Olive leaf extract decreases age-induced oxidative stress in major organs of aged rats.

AIM: Olive leaf (Olea europaea L.) extract (OLE) is a powerful anti-oxidant rich in polyphenols. As oxidative stress plays an important role in aging, we investigated the effect of OLE on oxidative stress in the liver, heart and brain of aged rats. METHODS: Young (age 3 months) and aged (age 20 months) Wistar rats were used. Aged rats received OLE (500 and 1000 mg/kg/day) in drinking water for 2 months. Malondialdehyde (MDA), diene conjugate (DC), protein carbonyl (PC), glutathione (GSH), vitamin E and vitamin C levels, and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities were determined. RESULTS: MDA, DC and PC levels increased in tissues of aged rats. GSH levels decreased in the liver, but not in the heart and brain. There was no change of other anti-oxidant parameters in tissues. Hepatic SOD and GSH-Px protein expressions also remained unchanged. OLE treatment caused decreased tissue MDA, DC and PC levels, and increased hepatic GSH levels in aged rats. Other anti-oxidant parameters, hepatic SOD and GSH-Px protein expressions did not alter in aged rats by OLE treatment. CONCLUSION: The present results suggest that OLE seems to be useful for decreasing oxidative stress in examined tissues by acting as an anti-oxidant itself without affecting the anti-oxidant system.

Carnosine and taurine treatments decreased oxidative stress and tissue damage induced by D-galactose in rat liver

D-galactose (GAL) causes aging-related changes and oxidative stress in the organism. We investigated the effect of carnosine (CAR) or taurine (TAU), having antioxidant effects, on hepatic injury and oxidative stress in GAL-treated rats. Rats received GAL (300 mg/kg; s.c.; 5 days/week) alone or together with CAR (250 mg/kg/daily; i.p.; 5 days/week) or TAU (2.5 % w/w; in rat chow) for 2 months. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and hepatic malondialdehyde (MDA), protein carbonyl (PC) and glutathione (GSH) levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-0050x), and glutathione transferase (GST) activities were determined. Hepatic expressions of B cell lymphoma-2 (Bcl-2), Bax and Ki-67 were evaluated. Serum ALT, AST, hepatic MDA, and PC levels were observed to increase in GAL-treated rats. Hepatic Bax expression, but not Bcl-2, increased, Ki-67 expression decreased. GAL treatment caused decreases in GSH levels, SOD and GSH-Px activities in the liver. Hepatic mRNA expressions of SOD, but not GSH-Px, also diminished. CAR or TAU treatments caused significant decreases in serum ALT and AST activities. These treatments decreased apoptosis and increased proliferation and ameliorated histopathological findings in the livers of GAL-treated rats. Both CAR and TAU reduced MDA and PC levels and elevated GSH levels, SOD and GSH-Px (non significant in TAU + GAL group) activities. These treatments did not alter hepatic mRNA expressions of SOD and GSH-Px enzymes. Our results indicate that CAR and TAU restored liver prooxidant status together with histopathological amelioration in GAL-induced liver damage

Carnosine and taurine treatments decreased oxidative stress and tissue damage induced by D-galactose in rat liver.

D-galactose (GAL) causes aging-related changes and oxidative stress in the organism. We investigated the effect of carnosine (CAR) or taurine (TAU), having antioxidant effects, on hepatic injury and oxidative stress in GAL-treated rats. Rats received GAL (300 mg/kg; s.c.; 5 days/week) alone or together with CAR (250 mg/kg/daily; i.p.; 5 days/week) or TAU (2.5 % w/w; in rat chow) for 2 months. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and hepatic malondialdehyde (MDA), protein carbonyl (PC) and glutathione (GSH) levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-0050x), and glutathione transferase (GST) activities were determined. Hepatic expressions of B cell lymphoma-2 (Bcl-2), Bax and Ki-67 were evaluated. Serum ALT, AST, hepatic MDA, and PC levels were observed to increase in GAL-treated rats. Hepatic Bax expression, but not Bcl-2, increased, Ki-67 expression decreased. GAL treatment caused decreases in GSH levels, SOD and GSH-Px activities in the liver. Hepatic mRNA expressions of SOD, but not GSH-Px, also diminished. CAR or TAU treatments caused significant decreases in serum ALT and AST activities. These treatments decreased apoptosis and increased proliferation and ameliorated histopathological findings in the livers of GAL-treated rats. Both CAR and TAU reduced MDA and PC levels and elevated GSH levels, SOD and GSH-Px (non significant in TAU + GAL group) activities. These treatments did not alter hepatic mRNA expressions of SOD and GSH-Px enzymes. Our results indicate that CAR and TAU restored liver prooxidant status together with histopathological amelioration in GAL-induced liver damage.

Effects of carnosine plus vitamin E and betaine treatments on oxidative stress in some tissues of aged rats.

Oxidative stress plays an important role in aging. Effects of several antioxidants on age-related oxidative stress have been investigated. Carnosine (CAR) and betaine have antioxidant actions. The combination of CAR with vitamin E(CAR+E) increases its antioxidant efficiency. We investigated the effects of CAR+E and betaine treatments on oxidative and antioxidative status in liver, heart and brain tissues of aged rats. Experiments were carried out on young (5 months)and aged (22 months) male Wistar rats. Aged rats were given CAR (250 mg/kg; i.p.; 5 days per week) and vitamin E (200mg/kg; i.m.; twice per week) or betaine (1% w/v) for two months. Malondialdehyde (MDA) and diene conjugate (DC)levels and antioxidants were measured. MDA and DC levels were higher in tissues of aged rats than young rats. Glutathione(GSH) levels decreased in liver, but not heart and brain. There were no changes in vitamin E and vitamin C levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities in tissues of aged rats. CAR+E treatment was observed to decrease MDA and DC levels in tissues of aged rats. However, betaine decreased only hepatic MDA and DC levels. Both CAR+E and betaine increased hepatic GSH and vitamin E levels, but these treatments did not affect antioxidant enzyme activities. These results suggest that CAR+E treatment seems to be useful to decrease oxidative stress in liver, heart and brain tissues, but betaine is only effective in liver tissue of aged rats.

Peroxisome proliferator-activated receptor-gamma-mediated positive energy balance in the rat is associated with reduced sympathetic drive to adipose tissues and thyroid status.

Peroxisome proliferator-activated receptor-gamma (PPARgamma) activation up-regulates thermogenesis-related genes in rodent white and brown adipose tissues (WAT and BAT) without increasing whole-body energy expenditure. We tested here whether such dissociation is the result of a negative modulation of sympathetic activity to WAT and BAT and thyroid axis components by PPARgamma activation. Administration of the PPARgamma agonist rosiglitazone (15 mg/kg.d) for 7 d to male Sprague Dawley rats increased food intake (10%), feed efficiency (31%), weight gain (45%), spontaneous motor activity (60%), and BAT and WAT mass and reduced whole-body oxygen consumption. Consistent with an anabolic setting, rosiglitazone markedly reduced sympathetic activity to BAT and WAT (>50%) and thyroid status as evidenced by reduced levels of plasma thyroid hormones (T(4) and T(3)) and mRNA levels of BAT and liver T(3)-generating enzymes iodothyronine type 2 (-40%) and type 1 (-32%) deiodinases, respectively. Rosiglitazone also decreased mRNA levels of the thyroid hormone receptor (THR) isoforms alpha1 (-34%) and beta (-66%) in BAT and isoforms alpha1 (-20%) and alpha2 (-47%) in retroperitoneal WAT. These metabolic effects were associated with a reduction in mRNA levels of the pro-energy expenditure peptides CRH and CART in specific hypothalamic nuclei. A direct central action of rosiglitazone is, however, unlikely based on its low brain uptake and lack of metabolic effects of intracerebroventricular administration. In conclusion, a reduction in BAT sympathetic activity and thyroid status appears to, at least partly, explain the PPARgamma-induced reduction in energy expenditure and the fact that up-regulation of thermogenic gene expression does not translate into functional stimulation of whole-body thermogenesis in vivo.

Early prediction of anastomotic leakage after colorectal surgery by measuring peritoneal cytokines: prospective study.

BACKGROUND: Anastomotic leakage (AL) is a major cause of postoperative mortality and morbidity in colorectal surgery. We investigated the early prediction of peritoneal cytokine levels in developing AL after colorectal surgery. METHODS: Thirty-four patients with colorectal carcinoma, who underwent elective surgery, were included prospectively. Peritoneal samples were collected on the fifth postoperative day and interleukin (IL)-6, IL-10 and tumor necrosis factor-alpha were measured. Patients were divided into two groups: those with clinical evidence of AL (group 1) and those without any evidence of AL (group 2). RESULTS: Of the 34 patients undergoing anastomoses, clinically evident AL occurred in 4 patients (11.7%). There was a positive correlation between AL and peritoneal cytokine levels and blood loss and operation time and hospital stay. Peritoneal cytokine levels were significantly higher in group 1 as compared to group 2. The significant increase in patients with AL was observed between peritoneal cytokine levels and the postoperative days. However, a significant decrease in patients without AL was observed. CONCLUSION: The peritoneal cytokine levels can be an additional diagnostic tool that can support the early prediction of AL in colorectal surgery.

The effect of glutamine on pancreatic damage in TNBS-induced colitis.

Ulcerative colitis is a multifactorial inflammatory disease of the colon and rectum with an unknown etiology. The present study was undertaken to investigate the effect of glutamine administration on oxidative damage and apoptosis in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Rats received 1 g/kg/day glutamine for intragastric gavage for 7 days before TNBS solution administration and 3 days following TNBS solution administration until sacrifice. Then colonic and pancreatic malondialdehyde (MDA) and glutathione (GSH) levels, and colonic caspase-3 activities of the sacrified rats were measured. TNBS-induced colitis caused significantly increased in the caspase-3 activity and colonic and pancreatic MDA levels and decreased colonic and pancreatic GSH levels compared to those in the sham group. Glutamine treatment was associated with decreased MDA levels and caspase-3 activity and increased GSH levels in the colinic and pancreatic tissue. Histopathological examination revealed that the colonic mucosal structure was preserved and pancreatic inflammation decreased in the glutamine-treated group. In conclusion, glutamine appears to have protective effects against TNBS-induced colonic and pancreatic damage. These results imply a reduction in mucosal damage due to anti-inflammatory and antiapoptotic effects of glutamine.

The effect of heme oxygenase-1 induction by glutamine on radiation-induced intestinal damage: the effect of heme oxygenase-1 on radiation enteritis.

BACKGROUND: Radiation enteritis is a significant clinical problem in patients receiving ionizing radiation directed at the abdomen or pelvis. The small intestine is the most radiosensitive gastrointestinal organ. Myeloperoxidase (MPO) activity and malondialdehyde (MDA) levels of the small intestine were measured to determine the oxidative damage caused by radiation. In addition, caspase-3 activity of the small intestine was measured to define the degree of apoptosis. The present study was undertaken to investigate the effect of glutamine administration on heme oxygenase-1 (HO-1) expression of the radiation enteritis model. METHODS: Rats received 1 g/kg/d glutamine (HO-1-inducer) for 7 days before irradiation and continued for 3 days after irradiation. Zn-prothoporphyin (Zn-PP) 40 micromol/kg was delivered subcutaneously for 1 day before irradiation. Intestinal MPO activities and MDA levels are indicators of oxidative damage, whereas caspase-3 activities show the degree of apoptosis of the small intestine. At histopathologic examination, terminal ileum tissue was analyzed for morphologic changes. Also, the nuclear factor-kappa (NF-kappa) expression level of the terminal ileum was determined with immunohistochemistry methods to show the mucosal inflammatory process. RESULTS: Irradiation significantly increased the intestinal MPO and caspase-3 activities, MDA levels, and HO-1 expression in comparison with the sham group. Glutamine treatment was associated with increased HO-1 expression, decreased MPO activity, caspase-3 activity, and MDA levels. Inhibition of HO-1 activity by Zn-PP completely eliminated the protective effects of glutamine. Histopathologic examination showed that the intestinal mucosal structure was preserved in the glutamine-treated group. In the irradiation group, NF-kappaB overexpression was detected. NF-kappaB positivity was strongest in the intestine of animals in the radiation alone group and the Zn-PP-treated irradiation group. CONCLUSIONS: Glutamine appears to have protective effects against radiation-induced intestinal damage. This protective effect is mediated in part by the induction of HO-1 activity because inhibition of Zn-PP resulted in the complete abolishment of the protective effect of glutamine.

The efficacy of octreotide in pancreatic and intestinal changes: radiation-induced enteritis in animals.

Radiation enteritis occurs during the radiotherapy of many intraabdominal malignancies. Radiation induces cellular injury directly and through the generation of free radicals. In the present study we aimed to investigate the effect of octreotide (OCT) pretreatment in irradiation-induced enteritis. For this aim, rats were injected with 50 microg/kg OCT 4 days before irradiation and continued for 3 more days, until sacrifice. Then intestinal and pancreatic myeloperoxidase (MPO) activities and intestinal malondialdehyde (MDA) levels of the rats were measured. Irradiation significantly increased intestinal and pancreatic MPO activities and MDA levels of intestinal tissues in comparison to those of the sham group. OCT treatment improved this elevation. The histopathologic evaluation of the mucosal structure was also preserved in the OCT-treated group. Inflammation of pancreatic tissue was also confirmed with histopathological examinations. In the irradiation group, NFkappa-B overexpression was detected. OCT treatment decreased the end organ damage and inflammation of the small intestine. In conclusion, OCT appears to have beneficial effects on intestinal and pancreatic damage in abdominal irradiation through the inflammatory process.

The effect of glutamine on radiation-induced organ damage.

Radiation enteritis is a significant clinical problem in patients receiving ionizing radiation directed to the abdomen or pelvis. Although radiation is aimed to be directed against the malignant tissue, adjacent healthy tissues are also affected. The small intestine is the most sensitive organ to radiation. The present study was undertaken to investigate the possible protective effect of glutamine against radiation-induced intestinal, hepatic and pancreatic toxicity. Rats received 1 g/kg/day glutamine for seven days before irradiation and continued for three days after irradiation until sacrifice. Then intestinal, pancreatic and hepatic myeloperoxidase (MPO) activities, malondialdehyde (MDA) levels and caspase-3 activities of the sacrificed rats were measured. Irradiation significantly increased the intestinal and pancreatic MPO and caspase-3 activities and MDA levels in comparison to sham group. Glutamine treatment significantly decreased this elevation. Histopathological examination revealed that the intestinal mucosal structure was preserved and pancreatic inflammation decreased in the glutamine treated group. In irradiation group, NF-kappaB over expression was detected. There was no significant difference in histopathological and biochemical examinations of the liver between the groups. In conclusion, glutamine has beneficial effects on intestinal and pancreatic damage in abdominal irradiation through the inflammatory process and apoptosis.

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.

The effect of betaine treatment on triglyceride levels and oxidative stress in the liver of ethanol-treated guinea pigs.

We investigated the effect of betaine supplementation on ethanol induced steatosis and alterations in prooxidant and antioxidant status in the liver of guinea pigs. Animals were fed with normal chow or betaine containing chow (2% w/w) for 30 days. Ethanol (3 g/kg, i.p.) was given for the last 10 days. We found that ethanol treatment caused significant increases in plasma transaminase activities, hepatic triglyceride and lipid peroxide levels. Significant decreases in glutathione (GSH), alpha-tocopherol and total ascorbic acid (AA) levels were also observed, but hepatic superoxide dismutase, glutathione peroxidase and glutathione transferase activities remained unchanged as compared with those in controls. Betaine treatment together with ethanol in guinea pigs is found to decrease hepatic triglyceride, lipid peroxide levels and serum transaminase activities and to increase GSH levels. No changes in alpha-tocopherol and total AA levels and antioxidant enzyme activities were observed with betaine treatment in alcohol treated guinea pigs. In addition, histopathological assessment of guinea pigs showed that betaine reduced the alcoholic fat accumulation in the liver. Based on these data, betaine treatment has a restoring effect on the alterations in triglyceride, lipid peroxide and GSH levels following ethanol ingestion.

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.

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.

Cholesterol plus methionine feeding do not induce lipid peroxidation and atherosclerotic changes in the rat aorta.

The purpose of this study was to investigate whether cholesterol plus methionine feeding may be a convenient model to produce atherosclerosis in rats, and also to examine the contribution of oxidative stress to this development. For this reason, lipid peroxide levels and antioxidant enzyme activities in the liver and aorta as well as histopathological findings were determined in male Wistar-albino rats fed a diet supplemented with cholesterol plus cholic acid and methionine for six months. This diet was found to increase lipid peroxide levels in the liver of rats. Hepatic glutathione peroxidase (GSH-Px) and catalase (CAT) activities increased, but superoxide dismutase (SOD) activity remained unchanged. In conclusion, cholesterol and methionine feeding in rats did not cause oxidative stress and atherosclerotic changes in the aorta, although hepatic prooxidant-antioxidant balance was affected by this diet.

The investigation of prooxidant-antioxidant balance in serum of children with family histories of essential hypertension.

It has been accepted that essential hypertension is associated with a loss of the balance between prooxidation and antioxidation. Thus, excessive oxygen free radical production may be an early event in the pathogenesis of hypertension. To compare lipid peroxidation and antioxidant system in serum of children of essential hypertensive and normotensive parents. Serum malondialdehyde (MDA) levels were measured spectrofluorometrically. Antioxidant activity, glutathione peroxidase, selenium levels in serum were measured as indices of antioxidant power. The peroxidation of apo B containing lipoproteins (VLDL+LDL) was measured as the susceptibility to oxidation in vitro. Serum MDA levels increased, but no marked differences in total antioxidant activity, glutathione peroxidase activity, selenium levels and VLDL+LDL oxidation were found in serum of children with family histories of essential hypertension as compared to children of normotensive parents.

Effects of added dietary taurine on erythrocyte lipids and oxidative stress in rabbits fed a high cholesterol diet.

Lipid peroxidation leads to damage of polyunsaturated fatty acids of membrane phospholipids. The contribution of oxidative stress to hypercholesterolemia-induced hemolytic anemia and the effects of addition of taurine on erythrocyte lipid composition, oxidative stress, and hematological data were studied in rabbits fed on a high cholesterol (HC) diet (1%, w/w) for 2 months. The effects of taurine on erythrocyte hemolysis and H2O2-induced lipid peroxidation were investigated in normal rabbit erythrocytes in vitro. The HC diet resulted in increases in plasma lipids and lipid peroxide levels as well as increases in cholesterol levels and the cholesterol:phospholipid ratio in the erythrocytes. This diet caused a hemolytic anemia, but lipid peroxide levels remained unchanged in the erythrocytes of the rabbits. Taurine (2.5%, w/w) added to the food has an ameliorating effect on plasma lipids and lipid peroxide levels in rabbits fed on a HC diet. This treatment also caused decreases in elevated erythrocyte cholesterol levels and cholesterol:phospholipid ratio due to the HC diet, but it did not prevent the hemolytic anemia and did not change erythrocyte lipid peroxide levels. In addition, in an in vitro study, taurine did not protect erythrocytes against H2O2-induced hemolysis or lipid peroxidation. These results show that the HC diet causes hemolytic anemia without any changes in erythrocyte lipid peroxidation, and taurine treatment was not effective against hemolytic anemia caused by the HC diet.