Taurine Mitigates Metaflumizone-Induced Hepatonephrotoxicity in Rats by Inhibiting Oxidative Stress, Inflammation, and Apoptosis

Abstract

Metaflumizone (MTF) is a pyrazoline sodium channel blocker (SBI) insecticide, and data on its toxicity are limited. Taurine (2-aminoethanesulfonic acid) is a sulfur-containing beta-amino acid that is naturally found in high concentrations in cells. In this study, we thoroughly evaluated the impact of taurine on MTF-induced hepatonephrotoxicity in a rat model, focusing on oxidative stress, inflammatory responses, and programmed cell death. In the present study, MTF (500 mg/kg, orally) to induce hepatonephrotoxicity was delivered to male rats for 30 days, and taurine at different concentrations (50, 100, and 200 mg/kg, orally) was used for protective effect for the same period. Taurine treatment alleviated the elevated levels of AST, ALT, ALP, BUN, and creatinine caused by MTF. It further suppressed malate dehydrogenase levels and enhanced antioxidant defense by elevating SOD, GSH, and CAT levels. Additionally, taurine increased the mRNA expression levels of Bcl-2, which had been reduced due to oxidative stress, inflammatory, and apoptotic pathways, while suppressing the elevated gene expression levels of NF kappa B, TNF-alpha, Bax, and Cas-3. Furthermore, taurine regulated the altered protein expression levels of Bcl-2, Bax, and TNF-alpha induced by MTF. Microscopically, taurine also mitigated liver and kidney tissue damage caused by MTF. In conclusion, taurine significantly reduced MTF-induced hepatonephrotoxicity by suppressing oxidative stress, inflammatory responses, and programmed cell death. These findings indicate that taurine has the potential to be a treatment option in the case of the prevention of liver and kidney damage caused by SBI.