Correlation of Oxidative Stress and Antioxidant Status with Cholinesterases in Different Grades of Organophosphorus Toxicity

Organophosphorus poisoning occurs as a result of accidental exposure, suicidal and homicidal attempts. The mechanism of toxicity of organophosphorus compounds is the inhibition of cholinesterases (ChE), resulting in an accumulation of acetylcholine and the continued stimulation of acetylcholine receptors. Decrease in cholinesterases activity co-relates well with severity of organophosphorus toxicity; however it cannot indicate the oxidation damage occurring inside body. The current study also indicate that there is a significant decrease in the level of total thiol (p < 0.01) while malondialdehyde (MDA) level was significantly increased (p < 0.01) in all stages of acute organophosphorus poisoning over controls. There was a significant linear negative correlation between MDA and cholinesterases (AChE and BuChE), while there was a significant positive correlation between cholinesterases and total thiol. We have also observed increase in the activity of catalase and su-peroxide dismutase in erythrocytes after organophosphate poisoning. Thus, the measurement of cholinesterases activities along with oxidative stress markers including MDA, ferric reducing ability of plasma and total thiol groups can be a good monitoring factor for oxidative stress caused by organophosphorus toxicity.