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Objective The present study was aimed to investigate the effects of betaine (BET) on streptozotocin (STZ)-induced diabetes mellitus (DM) in rats. Additionally, the efficiency of BET was compared with metformin (MET), a standard oral antidiabetic drug. Methods STZ (55 mg/kg body weight; i.p.) was injected to male Wistar rats. Rats with DM were treated with BET (1 g/kg body weight/day;) or MET (500 mg/kg body weight/day;) for 4 weeks. Blood glycated hemoglobin (HbA1c), serum glucose, lipids, hepatic and renal function tests and urinary protein levels were examined. Reactive oxygen species (ROS) formation, malondialdehyde (MDA), glutathione (GSH) levels, and ferric reducing antioxidant power (FRAP) were also determined in liver and kidney. Results Glucose, HbA1c, and serum lipids increased and liver and kidney function tests were impaired in diabetic rats. Hepatic and renal ROS formation and MDA levels were elevated, hepatic, but not renal GSH and FRAP levels were decreased. BET decreased blood HbA1c, serum glucose and lipid levels and urine protein levels. BET diminished hepatic and renal prooxidant status. Conclusion Our results indicate that BET may be effective in decreasing STZ-induced high levels of blood HbA1c, and serum glucose and lipid levels and prooxidant status in liver and kidney tissues.

Rats were injected with isoproterenol (ISO; 110 mg/kg, ip, 2 doses, 24 h interval) to induce acute myocardial infarction (AMI) and were sacrificed 6 and 24 h after the last ISO injection. The heart tissue, plasma and erythrocytes of these rats were evaluated for cardiac markers and oxidative stress parameters. Levels of cardiac troponin T (cTnT) and the activities of creatine kinase (CK), lactate dehydrogenase (LDH), and aspartate aminotransferase (AST) in plasma were increased 6 and 24 h after ISO treatment. The levels of malondialdehyde (MDA), diene conjugate (DC), and protein carbonyl (PC) were increased in heart tissue and plasma, while levels of erythrocyte MDA and glutathione (GSH) and plasma ferric reducing antioxidant power (FRAP) were also increased. However, GSH levels and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) decreased in heart tissue of rats with AMI. We also investigated the effects of carnosine (CAR) treatment on these parameters 24 h after the last ISO injection. CAR (250 mg/kg/day; ip) treatments were carried out either 10 days before ISO injection or 2 days concomitant with ISO. Pretreatment with CAR decreased plasma LDH and AST activities and ameliorated cardiac histopathological changes in ISO-treated rats. Cardiac MDA, DC and PC levels decreased, but GSH levels and SOD and GSH-Px activities increased. However, the increases in plasma MDA and PC levels as well as erythrocyte H(2)O(2)-induced MDA and GSH levels did not change due to CAR pretreatment. In conclusion, our findings indicate that CAR pretreatment may have protective effects on ISO-induced cardiac toxicity by decreasing oxidative stress.

This study was designed to investigate the role of HO-1 induction in prevention of thioacetamide (TAA)-induced oxidative stress, inflammation and liver damage. The changes in hepatic dimethylarginine dimethylaminohydrolase (DDAH) activity as well as plasma arginine and asymmetric dimethylarginine (ADMA) levels were also measured to evaluate nitric oxide (NO) bioavailability. Rats were divided into four groups as control, hemin, TAA and hemin + TAA groups. Hemin (50 mg kg−1, i.p.) was injected to rats 18 h before TAA treatment to induce HO-1 enzyme expression. Rats were given TAA (300 mg kg−1, i.p.) and killed 24 h after treatment. Although TAA treatment produced severe hepatic injury, upregulation of HO-1 ameliorated TAA-induced liver damage up to some extent as evidence by decreased serum alanine transaminase, aspartate transaminase and arginase activities and histopathological findings. Induction of HO-1 stimulated antioxidant system and decreased lipid peroxidation in TAA-treated rats. Myeloperoxidase activity and inducible NO synthase protein expression were decreased, whereas DDAH activity was increased by hemin injection in TAA-treated rats. Induction of HO-1 was associated with increased arginine levels and decreased ADMA levels, being the main determinants of NO production, in plasma of TAA-treated rats. In conclusion, our results indicate that HO-1 induction alleviated increased oxidative stress and inflammatory reactions together with deterioration in NO production in TAA-induced liver damage in rats. Copyright © 2012 John Wiley & Sons, Ltd.

Binge drinking of alcohol is known to cause cardiac dysfunction in some drinkers. This study was designed to examine the effect of ethanol on rat heart tissue with an experimental model mimicking human binge drinking. Female Sprague-Dawley rats were given ethanol diluted with normal saline (40%, v:v) by gavage at the dose of 5.0g/kg every 12h for 3 doses as total. Serum activities of lactate dehydrogenase (LDH), creatine phosphokinase (CK) and aspartate transaminase (AST) were determined. Endogenous lipid peroxidation was assessed by measuring the levels of malondialdehyde (MDA) in heart homogenates. In vitro susceptibility of tissues to oxidative stress was assessed by using two different media. Tissue glutathione (GSH) and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities were determined. All serum enzymatic activities were found markedly elevated in ethanol group. Binge ethanol administration significantly enhanced endogenous lipid peroxidation and caused an enhanced in vitro susceptibility to lipid peroxidation. Levels of reduced GSH and GSH-Px and GST activities were found unchanged as compared to controls. SOD activity was found significantly increased. As a conclusion, binge ethanol consumption which was applied to rats to investigate acute tissue injury, appeared to confirm the generation of oxidative stress in rat hearts.

In this study, we investigated the effect of l-carnosine (CAR) on prooxidant–antioxidant balance in several tissues of rats exposed to chronic stress. Both cold and immobilization stresses were applied to rats at the same time. In the stress group, rats were placed in restraint cages and kept in a cold room (+4°C) for 1 h for 21 days (5 days a week). Rats were injected with CAR (250 mg/kg, i.p.) at 30 min before stress application. Malondialdehyde, diene conjugate, protein carbonyl and nitrotyrosine levels, nonenzymatic (glutathione, vitamin E, and vitamin C), and enzymatic (catalase, superoxide dismutase and glutathione peroxidase) antioxidants were determined in the liver, heart, and brain tissues. Chronic cold plus immobilization stress was observed to affect especially the prooxidant–antioxidant status in the brain tissue of rats. This is the first report showing the beneficial effects of CAR on oxidative stress in the brain in rats exposed to stress. Keywords:: cold plus immobilization stress, l-carnosine, prooxidant–antioxidant balance, liver, brain

Aim Nigella sativa L. (Ranunculaceae) is considered as a therapeutic plant-based medicine for liver damage. In this study, the aim was to study the effect of Nigella sativa oil (NSO) pretreatment on ethanol-induced hepatotoxicity in rats. Method Rats were given Nigella sativa oil at doses of 2.5 and 5.0 mL·kg −1 , orally for 3 weeks, followed by oral ethanol (EtOH) administration (5 g·kg −1 ) every 12 h three times (binge model). Results Binge ethanol application caused significant increases in plasma transaminase activities and hepatic triglyceride and malondialdehyde (MDA) levels. It decreased hepatic glutathione (GSH) levels, but did not change vitamins E and vitamin C levels and antioxidant enzyme activities. NSO (5.0 mL·kg −1 ) pretreatment significantly decreased plasma transaminase activities, hepatic MDA, and triglyceride levels together with amelioration in hepatic histopathological findings. Conclusion NSO pretreatment may be effective in protecting oxidative stress-induced hepatotoxicity after ethanol administration

We investigated the effect of blueberries (BB) on lipids and oxidative stress parameters in hypercholesterolemic guinea pigs. The animals were fed for 75 d on a high-cholesterol (HC) diet supplemented with fresh BB. BB reduced oxidative stress and cholesterol accumulation in the aorta and liver of the guinea pigs. This effect may be related to its antioxidative potential and lipid-reducing effect. Istanbul Üniversitesi: 19285 This study was supported by the Research Fund of Istanbul University (Project no. 19285).