Protective effect of folic acid against imidacloprid-induced toxicity in liver and kidney of adult female rats

Abstract

The widespread use of pesticides in agriculture has raised concerns about their potential impact on human health and the environment. Imidacloprid, a widely used neonicotinoid insecticide, has been associated with oxidative stress and cellular damage. This study investigated the potential protective role of folic acid (FA) against imidacloprid-induced toxicity. Previous studies have shown that imidacloprid can cause oxidative stress and toxicity in rat kidney and liver. However, the potential protective role of FA against imidacloprid-induced toxicity has not been fully investigated. This study aimed to fill this research gap by investigating the effects of FA on oxidative stress markers, serum ALT and AST levels, and histopathological damage in rats exposed to imidacloprid. Adult female Sprague Dawley rats were divided into four groups: control(G1), imidacloprid (IMI) treatment (G2), FA supplementation(G3), and combined IMI and FA treatment (G4). IMI treatment resulted in a significant increase in oxidative stress markers in the liver and kidney, including ROS (**p<0.01), TBARS (***p<0.001), and decreased SOD (**p<0.01), POD (*p<0.05), CAT (**p<0.01), and GSH (****p<0.0001) levels. FA treatment significantly reversed the effects of IMI on oxidative stress markers in the liver and kidney. This was evident by the significant decrease in ROS (**p<0.01), TBARS (**p<0.001), and increased SOD (**p<0.01), POD (*p<0.05), CAT (**p<0.01), and GSH (****p<0.0001) levels in the FA-treated groups compared to the IMI-treated groups. Folic acid treatment also significantly reduced serum ALT (****p<0.0001) and AST (****p<0.0001) levels. Histopathological analysis of the liver and kidney tissues showed that IMI treatment caused significant damage, including the presence of lipofuscin, dilation and congestion of hepatic sinusoids, leucocytic infiltration, Kupffer cells hyperplasia, granuloma formation, and eosinophilic infiltration. FA treatment partially protected against this damage, as evidenced by the decreased severity of these histopathological findings in the FA-treated groups compared to the IMI-treated groups. The findings of this study suggest that folic acid has a protective effect against imidacloprid-induced oxidative stress and toxicity in rat kidney and liver. This is supported by the significant decrease in oxidative stress markers and histopathological damage in the FA-treated groups. These findings highlight the potential benefits of FA in reducing imidacloprid-induced toxicity and contribute to the broader conversation about safeguarding human health and the environment from pesticide-related challenges. The study has few limitations, including the small sample size and the short duration of the study. Further studies are needed to confirm the findings of this study and to investigate the mechanisms by which FA VIII exerts its protective effects against imidacloprid-induced toxicity. Overall, the findings of this study suggest that FA is a promising candidate for the prevention and treatment of imidacloprid induced toxicity.