Gallic acid modulates oxido-inflammatory response in acrylamide-induced hepato-renal toxicity

Dietary and environmental exposure to acrylamide (ACR) has been linked with liver and kidney illnesses, cardiopulmonary diseases, and neurological problems. Nevertheless, gallic acid (GA) is a potent polyphenolic compound with many therapeutic attributes. This present research explored the protective effect of GA against ACR hepato-renal toxicity. GA treatment was initially for 7 days followed by subsequent co-administration with ACR for a further 21 days. Twenty-four male Wistar rats were randomly distributed into six groups: Group I (control) was orally administered normal saline (2 ml/kg b.wt/day), Groups II and III were orally administered GA only (20 and 40 mg/kg b.wt/day respectively), Group IV received 20 mg/kg b.wt/day ACR only, Groups V, and VI were both given 20 mg/kg b.wt/day ACR co-administered with GA (20 and 40 mg/kg b.wt/day)The level of malondialdehyde (MDA), glutathione (GSH), and the activity of glutathione peroxidase (GPx) were evaluated in kidney and liver tissues while alanine amino transaminase (ALT), aspartate amino transaminase (AST), alkaline phosphatase (ALP), TNF-α and IL-6 were assayed in the serum. Treatment of GA remarkably improved ACR-induced perturbation of the biochemical and inflammatory indicators. The levels of MDA, urea, creatinine, TNF-α, and IL-6 as well as the activities of ALT, and AST were significantly increased while GSH levels and GPx activity were significantly decreased in ACR-exposed rats.Taken together, GA treatment exhibited antiinflammatory and antioxidant protective properties in ACR-induced hepato-renal toxicity