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J Occup Health year 2006 volume 48 number 1 page 20 - 27
Classification Original
Title Methanol-Induced Oxidative Stress in Rat Lymphoid Organs
Author Narayanaperumal J. PARTHASARATHY, Ramasundaram S. KUMAR, Sundaramahalingam MANIKANDAN and Rathinasamy S. DEVI
Organization Immunology Laboratory, Department of Physiology, Dr. ALM. PG. Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, Tamilnadu, India
Keywords Methanol, Antioxidants, Lipid peroxidation, Lymphoid organs
Correspondence R.S. Devi, Immunology Laboratory, Department of Physiology, Dr. ALM. PG. Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai, Tamilnadu 600 113, India (e-mail: drsheeladevi@yahoo.com)
Abstract Methanol-Induced Oxidative Stress in Rat Lymphoid Organs: Narayanaperumal 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 intoxicated with methanol (2.37 g/kg 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 non-enzymatic 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 and kidney markers of serum aspartate 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.