Stress induced by beta-cyfluthrin, a type-2 pyrethroid, on brain biochemistry of Albino rat (Rattus norvegicus)

Beta-Cyfluthrin is one of the most widely used type-II pyrethroid in agriculture. Toxic effects of beta-cyfluthrin are due to the presence of cyano moiety in its chemical structure. This study was designed the effect of betacyfluthrin at different doses on brain tissue, the most important vital organ in animal body and in which dose level beta-cyfluthrin shows its effects. Animal were initially divided into control and beta-cyfluthrin given groups. There were five animals in the control group and twenty five animals in beta-cyfluthrin administered group. The latter was divided into five equal subgroups: 35.48, and 5.06, 2.53, 1.68, 1.27mg/kg body weight of beta-cyfluthrin administered groups, acute (1 day) and sub-acute (7, 14, 21 and 28 days) by gavage respectively. Control group was given only water. The effect of these treatments were studied on activities of four potential biomarkers were assayed in the brain of albino rat along with neurosomatic index viz. Body weight, brain weight and brain weight body weight ratio and neurobehavioural changes. Beta-cyfluthrin treatment resulted in a significant decrease in brain acetyl-cholinesterase. Acetylcholinesterase which found to be decreased (inhibition range 53 to 18%) in albino rats after acute and sub-acute treatment (vide-supra). Further glutathione-s-transferase (GST) was also found to be decreased in brain of albino rats (inhibition range 47 to29%) after beta-cyfluthrin administration. Again brain adenosine triphosphtase (total ATPase) activity was seen to decrease in albino rats (inhibition range 36 to19%) along with succinic dehydrogenase (SDH) was also seen decreased in brain of albino rats (inhibition range 31 to 9%)) after acute and sub-acute beta-cyfluthrin intoxication. Further hypnoatremia (inhibition range 31 to 20%) along with hypokalemia (inhibition range 19 to 14%) has also been observed after acute and sub-acute intoxication of beta-cyfluthrin. Apart from AChE, which is a specific marker of pyrethroid neurotoxicity, the levels of brain GST, ATPase, SDH along with Na and K may serve as important determinants of beta-cyfluthrin induced neuronal dysfunctioning along with neurobehavioural alterations; outcomes of fluctuated brain biochemistry because clinical signs of toxicity were observed in animals which received different doses of beta-cyfluthrin after 7 th , and 14 th days of sub-acute treatment. Animals showed overt cholinergic signs which included salivation, excitability, ataxia, muscle twisting, followed by general tremors and lethargyness. The treated groups did not reveal any mortality. Exposure of animals to beta-cyfluthrin caused extensive changes in neurosomatic, neurochemical and neurobehavioural parameters. So, oral administration of beta-cyfluthrin leads to negative response on animal health.