The effects of caloric restriction against ethanol-induced oxidative and nitrosative cardiotoxicity and plasma lipids in rats

Abstract

Caloric restriction (CR) prevents or delays a wide range of aging-related diseases possibly through alleviation of oxidative stress. The aim of our study was to examine the effect of CR on oxidative and nitrosative cardiac damage in rats, induced by acute ethanol intoxication. Male Wistar rats were divided into following groups: control; calorie-restricted groups with intake of 60–70% (CR60–70) and 40–50% of daily energy needs (CR40–50); ethanol-treated group (E); calorie-restricted, ethanol-treated groups (CR60–70 + E, CR40–50 + E). Ethanol was administered in five doses of 2 g/kg every 12 h, while the duration of CR was five weeks before ethanol treatment. Malondialdehyde level was significantly lower in CR60–70 + E and significantly higher in CR40–50 + E vs. control. Nitrite and nitrate level was significantly higher in CR40–50 + E compared to control group. Activity of total superoxide dismutase (SOD) and its isoenzyme, copper/zinc-SOD (Cu/ZnSOD), was significantly higher in CR60–70 + E and lower in CR40–50 + E vs. control. Activity of manganese-SOD (MnSOD), that is also SOD isoenzyme, was significantly lower in  CR40–50 + E compared to control group. Plasma content of sulfhydryl (SH) groups was significantly higher in CR60–70 group vs. control. Plasma concentration of total cholesterol, triacylglycerol, low-density lipoproteins and high-density lipoproteins was significantly lower in CR60–70 group compared to control values. Food restriction to 60–70% of daily energy needs has a protective effect on acute ethanol-induced oxidative and nitrosative cardiac damage, at least partly due to alleviation of ethanol-induced decrease in SOD activity, while restriction to 40–50% of energy needs aggravates lipid peroxidation and nitrosative stress.