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Methanol-Induced Oxidative Stress in Rat Ly m p h o i d O r g a n s : N a r a y a n a p e r u m a l J . PARTHASARATHY, et al. Immunology Laboratory, Department of Physiology, Dr. ALM. PG. Institute of Basic Medical Sciences, University of Madras, Taramani Campus, India-Methanol is primarily metabolized by oxidation to formaldehyde and then to formate. These processes are accompanied by formation of superoxide anion and hydrogen peroxide. This paper reports data on the effect of methanol on antioxidant status and lipid peroxidation in lymphoid organs such as the spleen, thymus, lymph nodes and bone marrow of rats. Male Wistar albino rats were i n t o x i c a t e d w i t h m e t h a n o l ( 2 . 3 7 g / k g b . w intraperitoneally) for detecting toxicity levels for one day, 15 d and 30 d, respectively. Administration of methanol at 15 and 30 d significantly (p<0.05) increased lipid peroxidation and decreased the enzymatic (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymatic antioxidants (reduced glutathione and vitamin C) in lymphoid organs. However, lipid peroxidation and enzymatic and nonenzymatic antioxidants in the acute methanol exposed group animals were found to be significantly (p<0.05) increased. In one day methanol intoxication, the levels of free radicals initially increased, and to remove these free radicals, antioxidants levels were elevated, which generally prevented oxidative cell damage. But in longer periods of intoxication, when the generation of reactive free radicals overwhelmed the antioxidant defense, lipid peroxidation increased. Further, decreased antioxidants in 15 and 30 d methanol intoxication may have been due to overutilization of non-enzymatic and enzymatic antioxidants to scavenge the products of lipid peroxidation. In addition, the liver a n d k i d n e y m a r k e r s o f s e r u m a s p a r t a t e aminotransferase (AST), alanine aminotransferase (ALT), urea and creatinine significantly increased. This study concludes that exposure to methanol causes oxidative stress by altering the oxidant/antioxidant balance in lymphoid organs of the rat. (J Occup Health 2006; 48: 20-27)

Exposure to continuous loud noise is a serious health problem due to excess production of oxygen free radicals. In medical research, more attention is paid to the antioxidant properties of medicinal plants to minimize the harmful effects of radicals. The aim of this study was to evaluate the protective effect of both ethyl acetate and methanolic extract of Acorus calamus LINN against noise stress (30 d, 100 dBA/4h/d) induced changes in the rat brain. We measured the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and the levels of reduced glutathione (GSH), vitamin C, vitamin E, protein thiols and lipid peroxidation (LPO) for the evaluation of oxidative stress status in discrete regions of the rat brain like cerebral cortex, cerebellum, pons-medulla, midbrain, hippocampus and hypothalamus. The results indicated that during exposure of noisy environment ROS generation led to increase in corticosterone, LPO and SOD, but decrease in CAT, GPx, GSH, protein thiols, vitamins C and E levels. Both the ethyl acetate and methanolic extract of Acorus calamus protected most of the changes in the rat brain induced by noise-stress.

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Hypercholesteremia is one of the risk factors for coronary artery disease. The present study highlights the e‹cacy of Ayurvedic herbal formulation Triphala (Terminalia chebula, Terminalia belerica, and Emblica o‹cinalis) on total cholesterol, Low density lipoprotein (LDL), Very low density lipoprotein (VLDL), High density lipoprotein (HDL) and free fatty acid in experimentally induced hypercholesteremic rats. Four groups of rats were employed namely control, Triphala treated, hypercholesterolemia rats (4％ Cholesterol＋1％ cholic acid＋egg yolk) and Triphala pre-treatment in hypercholesteremic rats. Results showed signiˆcant increase in the total cholesterol, LDL, VLDL, and free fatty acid in hypercholesteremic rats were signiˆcantly reduced in Triphala treated hypercholesteremic rats. The data demonstrated that Triphala formulation was associated with hypolipidemic eŠects on the experimentally induced hypercholesteremic rats.