L-arginine supplement ameliorates dichlorvos-induced systemic inflammatory response and liver dysfunction in male wistar rats

Abstract

Dichlorvos (DDVP), a frequently used organophosphate insecticide, has been shown to cause systemic inflammation and liver damage via oxidative stress and inflammatory pathways. L-arginine, a semi-essential amino acid, has been shown to protect against oxidative damage and inflammation in a variety of animals. The study's main goal was to raise awareness of Dichlorvos's (DDVP) harmful effects on systemic inflammation and liver function, as well as L-arginine's possible mitigating impact. In order to assess the preventive benefits of L-arginine against induced liver dysfunction and systemic inflammation, liver tissue was selected for this investigation due to its vital role in detoxification and its high susceptibility to harm from toxic chemicals such as Dichlorvos. A total of 40 adult Wistar rats were separated into four groups: control, dichlorvos only, L-arginine only, and dichlorvos plus L-arginine. Dichlorvos was provided orally at a dose of 8 mg/kg body weight, whereas L-arginine was given orally at a dose of 100 mg/kg body weight for six weeks. The study investigated systemic inflammation markers (C-reactive protein, TNF-α, IL-6, and Caspase 3) as well as liver function markers (ALT, AST, ALP, albumin, total protein and gamma glutamyl). The findings revealed that dichlorvos significantly (p < 0.05) enhanced systemic inflammation and decreased (p < 0.05) liver function when compared to the control group. However, L-arginine supplementation greatly improved these effects by significantly (p < 0.05) lowering inflammatory indicators and restoring liver enzyme levels to normal. Histopathological findings validated L-arginine's protective function against dichlorvos-induced liver injury. These data indicate that L-arginine supplement may reduce the negative effects of dichlorvos on systemic inflammation and liver function, providing a possible therapeutic method for controlling organophosphate toxicity.