The present study was aimed to assess the antihyperlipidemic, antihypertensive and antioxidant effect of D-carvone, a monoterpene against Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME) induced hypertension. Hypertension was prompted in adult male albino rats of the Wistar strain by oral administration of the L-NAME (40 mg/kg body weight) in drinking water for 4 weeks. Rats were treated with D-carvone (5, 10 and 20 mg/kg body weight) for four weeks. L-NAME treated rats exhibited significant increase in water intake, heart rate, aortic lipids level such as triglycerides (TG), total cholesterol (TC), free fatty acids (FFA) and significant decrease in the level of phospholipids (PL), plasma nitric oxide (NO). The activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were decreased in erythrocytes of L-NAME induced hypertensive rats. Treatment with D-carvone restored all the above parameters to near normal level. These results suggest that D-carvone acts as an antihyperlipidemic, antihypertensive and antioxidant agent against L-NAME induced hypertensive rats.
Exercise induces extensive generation of reactive oxygen species, which are responsible for tissue damage: enzymes inactivation, lipid peroxidation and single strand breaks in DNA. Defense system against free radicals is consisting of enzymes such as superoxide dismutase, catalase, glutathione peroxidase, and numerous non-enzymatic antioxidants. The study was performed to evaluate the effect of a single bout of submaximal running exercise, on the lymphocyte DNA strand breaks and also to test how supplementation with tempol – a membrane-permeable SOD-mimetic (0.2 mmol/kg/day) influences the eventually evoked damage. Male, Wistar rats were challenged with graded 50 min. running on treadmill at intensity up to 75-85% of predicted O2 max. The DNA strand breaks in individual lymphocytes were determined by using a gel electrophoretic technique – “comet” assay. We found substantial lymphocyte DNA damage 60 min. after the exercise. Tempol failed to prevent from oxidative damage in rats challenged with exercise. Moreover tempol by itself induced higher DNA damage than the exercise bout.
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