Effects of betaine supplementation on nitric oxide metabolism, atherosclerotic parameters, and fatty liver in guinea pigs fed a high cholesterol plus methionine diet.

OBJECTIVE: The aim of this study was to investigate the effect of high cholesterol (CHOL) and CHOL + methionine (MET) diets on atherogenic and oxidative index parameters and on the factors that influence nitric oxide (NO) bioavailability. Also, attempts were made to determine whether dietary betaine (BET) resulted in any improvement in the changes that occurred after CHOL + MET administration. METHODS: Guinea pigs were fed chow containing 1.5% CHOL with or without 2% MET for 10 wk. A third group received the CHOL + MET + BET diet. Control groups were given standard chow or standard chow + BET. Arginine, NO, nitrotyrosine (NT), and asymmetric dimethylarginine (ADMA) levels; lipid profile; and dimethylarginine dimethylaminohydrolase (DDAH) activity were measured. The liver and aorta were subjected to histopathologic analysis. RESULTS: The CHOL + MET diet caused higher serum CHOL and homocysteine levels, but no further increases were seen in aortic CHOL and diene conjugate (DC) levels and histopathologic lesions as compared with the CHOL group. Hepatic lipids and DC levels were also higher, and histopathologic lesions were more severe. CHOL + MET feeding increased ADMA and NT levels as compared with those of the CHOL-fed group. When BET (1 g/kg body weight/d) was added to the CHOL + MET diet, homocysteine and lipid levels decreased and histopathologic changes were reversed. BET diet decreased serum ADMA and hepatic and aortic DC levels and partly restored DDAH activity. CONCLUSIONS: BET supplementation may be effective in preventing hyperlipidemia, disturbed NO availability, oxidative stress, and the development of fatty liver and atherosclerotic lesions that might result from excess amounts of cholesterol and methionine in the diet.

Effects of high methionine diet on oxidative stress in serum, apo-B containing lipoproteins, heart, and aorta in rabbits.

This study investigated in rabbits whether a high methionine (HM) diet influences oxidative stress parameters in serum, apo-B containing lipoproteins (LDL+VLDL), heart, and aorta. Rabbits received a normal commercial chow supplemented with 2% L-methionine (w/w) for 6 mo (approximately 1 g/kg body wt/day). Serum homocysteine (HCys), malondialdehyde (MDA), diene conjugate (DC), and cholesterol levels were found to be increased, but protein carbonyl (PC) and triglyceride levels remained unchanged in the HM group as compared to controls. Cholesterol, endogenous DC, and copper-induced MDA levels were significantly higher in the LDL+VLDL fraction of plasma lipoproteins in the HM group. MDA and DC levels were found to be increased in homogenates of heart and aorta in the HM group. The HM diet caused significant increases in cardiac glutathione peroxidase activity, but glutathione, vitamin E, and vitamin C levels and superoxide dismutase and glutathione transferase activities remained unchanged. There were no significant differences in the cholesterol levels and histopathological findings in the aortas of the control vs the HM group. This study demonstrates that a HM diet induces oxidative stress in serum, apo-B containing lipoproteins, heart, and aorta in rabbits.

Methionine-supplemented diet augments hepatotoxicity and prooxidant status in chronically ethanol-treated rats.

The purpose of this study was to investigate whether high methionine (HM) diet may influence the development of ethanol-induced hepatotoxicity and prooxidant-antioxidant balance in the liver. Rats received drinking water containing ethanol (20% v/v) and/or methionine supplemented diet (2% w/w) for 75 days. Although prooxidant-antioxidant balance did not change in the liver of rats in HM group, ethanol treatment was observed to increase plasma transaminase activities, and malondialdehyde (MDA) and protein carbonyl (PC) levels, but not glutathione (GSH), vitamin E and vitamin C levels, and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities in the liver of rats as compared to controls. However, ethanol plus HM diet caused further increases in plasma transaminase activities and hepatic MDA and PC levels. In addition, SOD, GSH-Px and GST activities were observed to decrease, but GSH, vitamin E and vitamin C levels remained unchanged in the liver as compared to ethanol, HM and control groups. Our results show that HM diet may augment hepatotoxicity and oxidative stress in the liver of chronically ethanol-treated rats.

[The role of supplementation or inhibition of nitric oxide production in burn injury to reduce ischemic damage]. / Yanikta nitrik oksit üremtiminin desteklenmesi veya azaltilmasinin iskemik hasari azaltmadaki rolü.

BACKGROUND: To determine the role of nitric oxide (NO) which is vasodilator agent and inflammatory cytokine, in burn injury. METHODS: Rats were divided into 5 groups, and a 30 % burn was inflicted. In addition to sham control and burn control groups, other 3 groups were given L-Arginine, and L-nitro-L-Arginine methylester (L-NAME), and both. Neutrophil and hematocrit percentage in blood, NO, TNF-alpha and malondialdehyde (MDA) levels in plasma and neutrophil infiltration in the lung were evaluated at 24 hours after thermal injury. RESULTS: The inhibition of NO production with L-NAME treatment significantly decreased these parameters when compared to burned control group. MDA was decreased significantly in all groups which were given drugs. CONCLUSION: The induction and inhibition of NO production both reduced lipid peroxidation but induction increased the mortality, plasma TNF-alpha and neutrophil in the blood. Inhibition of NO production is found more useful after thermal injury in rats.