IJSRSET1841168 | Received : 12 Feb 2018 | Accepted : 25 Feb 2018 | January-February-2018 [(4) 1 : 1280-1287 ] © 2018 IJSRSET | Volume 4 | Issue 1 | Print ISSN: 2395-1990 | Online ISSN : 2394-4099 Themed Section : Engineering and Technology 1280 Metabolic Dyshomeostasis in Rats Administered a Single dose of Monocrotophos is not Associated with Oxidative Damage in Liver and Kidney Apurva Kumar Ramesh Joshi* 1,2 , Raju Nagaraju 1,2 , Padmanabhan Sharda Rajini 1 1 Food Protectants and Infestation Control Department, CSIR-Central Food Technological Research Institute, Mysore, Karnataka, India, Email: apurvakmr@gmail.com 2 Food Chemistry Division, National Institute of Nutrition, Jamai-Osmania, Hyderabad, Telangana, India ABSTRACT We have earlier demonstrated the potential of monocrotophos, an organophosphorus insecticide to cause transient hyperglycemia in rats after administration of a single dose. This study was conducted to understand whether hyperglycemia in rats administered a single dose of monocrotophos is associated with oxidative damage in liver and kidney. Oral administration of a single dose of monocrotophos promptly caused classical acute organophosphate toxicity as evidenced by severe inhibition of brain acetylcholinesterase activity. Further, metabolic alterations such as transient hyperglycemia, hypercorticosteronemia, hyperlacticidemia and increase in the activity of hepatic tyrosine aminotransferase were observed in rats treated with monocrotophos. These changes were associated with marginal decrease in glutathione levels in liver and kidney. However, extent of lipid peroxidation and activities of catalase and superoxide dismutase in liver and kidney of monocrotophos-treated rats were comparable to that of vehicle-treated rats. This suggests that single dose of monocrotophos fails to induce oxidative damage in rats in spite of occurrence significant neurotoxicity and metabolic alterations. Keywords : Acetylcholinesterase Inhibition, Hyperglycemia, Metabolic Dyshomeostasis, Monocrotophos, Oxidative Stress I. INTRODUCTION Organophosphorus insecticides (OPI) represent a major class of insecticides used worldwide today for mitigating pest populations in agriculture and other scenario. This group of insecticides includes a large number of compounds of varying toxicities. Mechanistically, OPI act on the target insects by inhibiting the enzyme acetylcholinesterase (AChE) and leading to toxicity underlined by cholinergic overstimulation [1–3]. However, ubiquitous nature and conserved role of AChE in regulation of neurotransmission has rendered human physiology equally vulnerable to the toxicity of OPI. Most often, clinical cases of OPI toxicity are attributable to exposure to OPI at doses sufficient to cause strong AChE inhibition and cholinergic stress [4,5]. However, longer exposure to OPI as a result of occupational hazard or through food chain is a realistic issue. Hence, OPI have come under intense scientific scrutiny for evaluating their effects in milieus other than nervous system.