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Protective Effect of Quercetin against Oxidative Stress and Mitochondrial Bioenergetic Deficiency Caused by Lambda- Cyhalothrin

Nadia A. Hamed

Mitochondria are a convenient model to understand the oxidative damage induced by various xenobioticprooxidants. This study was designed to investigate (1) the possibility of lambda-cyhalothrin (LCT), a type II pyrethroid, to induce oxidative stress response in rabbit liver mitochondria in vitro and its effect on selected parameters and (2) the role of quercetin in alleviating the cytotoxic effects of LCT. Mitochondria were divided into two groups. The first group, mitochondria were incubated for 30 min at 37oC with different concentrations (0, 5, 10, 15 and 20uM) of LCT. In the second group, mitochondria were pre-incubated with (10µM) quercetin for 30 min and followed by LCT incubation for 30 min at 37oC. Following in vitro exposure, LCT caused a significant induction of oxidative damage in mitochondria at all tested concentrations as evidenced by increased superoxide dismutase (SOD) activity and reduced glutathione (GSH) level. However, a significant decrease in the activities of NADH dehydrogenase and ATP synthase (ATPase) was obtained.  While the quercetin treated mitochondria showed significant enhancement in all tested parameters except GSH content, there was no significant change. Quercetin showed a significant protection against the cytotoxic effects induced by LCT on the studied parameters. In conclusion, antioxidant quercetin could be able to ameliorate LCT-induced oxidative stress by altering antioxidant defense system and recovered the bioenergetic activity of mitochondria.

Keywords: Mitochondria, Lambda cyhalothrin, Qurcetin,  Bioenergetic deficincey and oxidative stress.