Toxicological assessment of sublethal dose of acetamiprid in male mice and the efficacy of quercetin.

Acetamiprid (ACP) is a neonicotinoid insecticide that is the most effective pesticide for crop protection as well as flea control in agricultural animals and pets in the world. The goal of this study was to look at the in vivo effects of a sublethal dose of ACP on hematotoxicity, oxidative stress, hepatotoxicity, nephrotoxicity, immunotoxicity, and histological alterations, as well as the role of quercetin (QE) in alleviating these effects. Twenty adult male mice were divided into four equal groups orally administered corn oil (control), QE (50 mg kg-1 b.wt.), ACP (1/10 LD50) or ACP plus QE for two weeks. The results showed that ACP significantly lowered the body weight gain, hematological indices, glutathione (GSH), and both cellular and humoral immunity, On the other hand, levels of lipid peroxidation (LPO), glutathione peroxidase (GPx), and liver and kidney marker values were considerably increased in male mice exposed to ACP. In addition, examination under light microscopic showed that ACP induces histological alterations in liver and kidney tissues. The results also revealed that treating intoxicated mice with QE significantly reduced the deleterious effects of ACP. In conclusion, current results show that ACP at the sub lethal dose poses toxic risks to the liver and kidneys, and QE as a natural material enhances antioxidant defenses, which can be used as a potential interventional therapy against negative effects of pesticides like ACP.

The role of vitamin C as antioxidant in protection of oxidative stress induced by imidacloprid.

Pesticides may induce oxidative stress leading to generate free radicals and alternate antioxidant or oxygen free radical scavenging enzyme system. This study was conducted to investigate the acute toxicity of imidacloprid toward male mice and the oxidative stress of the sublethal dose (1/10 LD(50)) on the lipid peroxidation level (LPO), reduced glutathione content (GSH) and activities of the antioxidant enzymes; catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glucose-6-phosphate dehydrogenase (G6PD), and glutathione-s-transferase (GST). Also, the protective effect of vitamin C (200mg/kg bw) 30 min before or after administration of imidacloprid were investigated. The results demonstrated that the median lethal dose (LD(50)) of imidacloprid after 24h was 149.76 mg/kg bw. The oral administration of 14.976 mg/kg imidacloprid significantly caused elevation in LPO level and the activities of antioxidant enzymes including CAT, SOD, GPx and GST. However, G6PD activity remained unchanged, while the level of GSH content was decreased. In addition, the results showed that vitamin C might ameliorate imidacloprid-induced oxidative damage by decreasing LPO and altering antioxidant defense system in liver. The protective effect of the pre-treatment with vitamin C against imidacloprid-induced oxidative stress in liver mice is better than the post-treatment.