Fipronil (FPN), a commonly used phenylpyrazole pesticide can induce oxidative tissue damage following hazard usage. Due to the extensive household and commercial usage of FPN, its toxic effects on mammals received considerable attention. Finding the proper antioxidant that can overcome FPN-induced damage is essential. Therefore, the present study aimed to assess the hepatorenal ameliorative outcomes of N-acetyl cysteine (NAC) and taurine (TAU) against hepatorenal damage induced by FPN in male Wistar rats. Compared to control rats, oral FPN (at a dose of 19.4 mg kg-1 BW for five successive days) significantly increased serum activities (p ≤ 0.05) of alkaline phosphatase, lactate dehydrogenase and transaminases, in addition to total cholesterol, urea and creatinine levels. Moreover, FPN provoked oxidative damage indicated by increased malondialdehyde and nitric oxide formation and decreased glutathione concentration and activities of enzymatic antioxidants (superoxide dismutase, glutathione peroxidase and catalase) in the hepatic and renal tissues. Furthermore, FPN administration induced overexpression of the proapoptotic (Bax), while it downregulated the expression of the anti-apoptotic (Bcl-2) protein. Interestingly, oral administration of TAU (50 mg Kg-1 BW) and NAC (50 mg Kg-1 BW), alone or in combination, five days prior to and five days along with FPN administration, significantly ameliorated (p ≤ 0.05) and normalized the harmful effects of FPN on serum biomarkers of hepatorenal injury, lipid peroxidation and tissue antioxidants. In conclusion, TAU and NAC, alone or in combination, provided significant hepatorenal protection against oxidative stress and apoptosis induced by FPN.
Keywords: Fipronil; Kidney; Liver; N-acetylcysteine; Oxidative stress; Taurine.
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