Methanol‐Induced Oxidative Stress in Rat Lymphoid Organs

Abstract

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)

Imbalance of the oxidant - antioxidant status by aspartame in the organs of immune system of Wistar albino rats

“…Then ACTH acts on adrenal gland to release corticosterone secretion. Parthasarathy et al (2006) reported a similar increase in plasma corticosterone level in rats after methanol administration for day 1 and 15 days. However after 30 days of methanol intoxication it showed considerable decrease in corticosterone level.…”

“…This alteration after aspartame administration may be attributed to its metabolite methanol. Methanol is primarily metabolized by oxidation to formaldehyde and then to formate, these processes are accompanied by the formation of superoxide anion and hydrogen peroxide (Parthasarathy et al, 2006). Oxidative damage in a cell or tissue occurs when the concentration of reactive oxygen species (O 2 -, H 2 O 2 , and OH -) generated exceeds the antioxidant capability of the cell (Sies, 1991).…”

“…Methanol is being increasingly recognized as a substance that damages the liver cells where it is oxidized to formaldehyde and later to formate (Oppermann et al, 1984). These processes are accompanied by elevation of nicotinamide adenine dinucleotide (NADH) level and the formation of superoxide anion, which may be involved in lipid peroxidation (Parthasarathy et al, 2006). However, accumulating evidence has implied that the production of free radicals plays a critical role in oxidative stress (Liu and Mori, 1999).…”

Impact of Aspartame Consumption on Neurotransmitters in Rat Brain

“…The reduction in glutathione level observed in our study may be attributed to methanol release from aspartame, this is due to methanol metabolism depends upon glutathione (Parthasarathy et al, 2006). The reduction of reduced glutathione, elevation of oxidized GSSG and decrease of the reduced/oxidized ratio increase cell sensitivity to oxidative stress (Shelly et al, 2009).…”

“…It was reported that methanol is primarily oxidized to formaldehyde and then into formate, that is involved in methanol toxicity in human. This is accompanied by production of superoxide anion and hydrogen peroxide (Lee et al, 1994, Eells et al, 2000, Parthasarathy et al, 2006.There are a few data showed the effect of aspartame consumption on specific neurological conditions such as headache, insomnia and seizures (Johns, 1986), alterations in regional concentrations of catecholamine which is accompanied with behavioral disturbances (Coulombe andSharma, 1986, Humphries et al, 2008). The rational of this study was to investigate whether long-term uses of aspartame can affect oxidative stress and brain neurotransmitters in albino rats…”