Curcumin modulates oxidative stress and genotoxicity induced by a type II fluorinated pyrethroid, beta-cyfluthrin.

Present study examines the possibility of β-cyfluthrin (β-CYF) induced oxidative stress, genotoxicity, histopathological alterations and the role of curcumin (CUR) in alleviating its toxic effects. CUR is a naturally occurring phenolic compound of turmeric (Curcuma longa) and is used as a spice, food-coloring agent and in cosmetics and medicines. CUR provides vital protection against many pathological conditions due to its antioxidant and anti-inflammatory properties. Male Swiss albino mice were distributed into six groups, I: control, II: CUR (0.2%), III: β-CYF low dose (1/20 of LD50), IV: β-CYF high dose (1/10 of LD50), V: β-CYF low dose + CUR and VI: β-CYF high dose + CUR. Mice were orally administered their respective doses daily for 21 days. β-CYF caused elevation in AST, ALT, LPO and decline in GPx, CAT and SOD activities. A significant decrease in MI and increase in chromosomal aberrations, TL, TI and TM was recorded in β-CYF exposed groups. CUR co-administration modulated AST, ALT, LPO, GPx, CAT and SOD activity. CUR supplementation improved the MI and reduced the chromosomal aberrations, TL, TI and TM. β-CYF caused serious pathological alterations in liver and these were alleviated by CUR. It is concluded that CUR scavenges ROS and renders a protection against β-CYF genotoxicity.