Effect of methanol-induced oxidative stress on the neuroimmune system of experimental rats.
It is well known that the nervous system has increased susceptibility to methanol intoxication. The present study reveals the effect of methanol intoxication on antioxidant status, lipid peroxidation and DNA integrity in hypothalamic-pituitary-adrenal (HPA) axis organs and spleen. Non-specific and specific immune functions were analyzed. In addition, open field behavior, plasma corticosterone level and blood methanol level were estimated. Male Wistar albino rats were intoxicated with methanol (2.37 g/kg b.wt., i.p.) for 1 day, 15 and 30 days. Administration of methanol showed significant increase in enzymatic (superoxide dismutase, catalase, glutathione peroxidase), non-enzymatic (reduced glutathione and Vitamin C) antioxidants and lipid peroxidation (LPO) in hypothalamus and adrenal gland of day 1 group. However, decrease in enzymatic and non-enzymatic antioxidants with concomitant increase in LPO level were observed in 15 and 30 days groups. Plasma corticosterone level was significantly increased in day 1 and 15 days groups whereas, 30 days methanol intoxication group showed considerable decrease in corticosterone level compared with control animals. Cell-mediated immune response of footpad thickness was significantly decreased with an increased leukocyte migration inhibition. Humoral immune response of antibody titers was elevated in methanol-intoxicated groups. Neutrophil functions, adherence and phagocytic index (PI) were found to be significantly decreases. Furthermore, significant increase in the avidity index and nitro blue tetrozolium reduction was observed in the methanol exposed animals. Day 1 methanol exposed group showed increased PI compared to the control ones. Methanol exposure for 30 days showed an increased DNA fragmentation in the hypothalamus, adrenal glands, and spleen. In conclusion, exposure to methanol-induced oxidative stress disturbs the HPA-axis function altering the level of corticosterone, which lead to varied non-specific and specific immune response in experimental rats.
Parthasarathy
Narayanaperumal Jeya
NJ
Immunology Laboratory, Department of Physiology, Dr. ALM PG Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600113, India.
Kumar
Ramasundaram Sri
RS
Manikandan
Sundaramahalingam
S
Narayanan
Govindarajulu Sathya
GS
Kumar
Raman Vijaya
RV
Devi
Rathinasamy Sheela
RS
D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism; D001522:Behavior, Animal / Q000187:drug effects; D002374:Catalase / Q000378:metabolism; D002464:Cell Migration Inhibition; D003345:Corticosterone / Q000097:blood; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006614:Hindlimb / Q000276:immunology; D006968:Hypersensitivity, Delayed; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects* / Q000502:physiology; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D000432:Methanol / Q000097:blood / Q000493:pharmacokinetics / Q000633:toxicity*; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology; D018384:Oxidative Stress; D010913:Pituitary-Adrenal System / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism
D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D001205:Ascorbic Acid; D003345:Corticosterone; D000432:Methanol