The common use of insecticides in public health and agricultural schedules has caused severe acute and chronic cases of human and animal poisoning [1]. The acute toxicity of organphosphorus compounds (ops) are believed to be due to primarily to the inhibition of acetylchonesterase (AChE) resulting in an accumulation of acetylcholine (Ach) with a sustained overstimulation of Ach receptors in the clefts of central and peripheral neuronal synapses.[2].

Dimethoate is an insecticide referred to as organophosphates, which is cholinesterase inhibitor. Cholinesterase is an enzyme that is essential for the proper working of the nervous systems of both humans and insects. Administration of dimethoate to pregnant rats produced enzymatic changes associated with mild pathomorphological changes in liver and brain,[3]. Previous studies indicate that dimethoate intoxication causes cellular injury and oxidation stress which leads to lipid peroxidation and free radical production [4, 5, 6] Recent studies have shown that acute and sub chronic exposure to dimethoate alters the antioxidant status and histology of liver, brain and testes of rats [7, 8, 9] and human erythrocytes [10]. Also the effect of two organophosphorous pesticide were studied on the hepatic and intestinal metabolism in the rat and found that the metabolizing enzymes responsible for both the bioactivation and detoxification are present in the small intestine at lower level than the liver but still significant [11]. The pyrethroid insecticide, cypermethrin, significantly (P< 0.05) induced free radical production in plasma, liver, brain and testes [12].