The Preclinical Benefit of Glutamine in bisphenol A-induced Hepatotoxicity in Wistar Rats

Background: Oxidative stress may be a causative factor for bisphenol A (BPA) -induced hepatotoxicity. Glutamine (GM) is an amino acid with the ability to inhibit oxidative stress.  Objective: This study evaluated the ability of GM to prevent BPA-induced hepatotoxicity in rats.  Methods: Adult Wistar rats of both sexes (n=۳۰) were used. The rats were randomly grouped into six of five rats each. Groups A (Control), B, and C were treated with normal saline (۰.۲ mL), GM (۸۰ mg/kg), and BPA (۵۰ mg/kg), respectively for ۶۰ days. Groups D-F were treated with GM (۲۰ mg/kg)+BPA (۵۰ mg/kg), GM (۴۰ mg/kg)+BPA (۵۰ mg/kg), and GM (۸۰ mg/kg)+BPA (۵۰ mg/kg), respectively for ۶۰ days. After treatment, blood and liver samples were obtained for biochemical and histological assessments, respectively.  Results: Significantly (P<۰.۰۱) decreased body weight and significantly (P<۰.۰۱) increased liver weight occurred in the BPA-administered group when compared to the control group. The BPA-administered group showed significantly (P<۰.۰۰۱) elevated serum total bilirubin, lactate dehydrogenase, aminotransferases, conjugated bilirubin, gamma-glutamyl transferase, alkaline phosphatase, and liver malondialdehyde concentrations when compared to the control group. Significantly (P<۰.۰۰۱) decreased liver superoxide dismutase, glutathione peroxidase, catalase, and glutathione levels occurred in the PBA-administered group when compared to the control group. BPA caused hepatocyte necrosis, sinusoids, and central vein congestion. BPA-induced hepatotoxicity was reversed by GM; ۲۰ mg/kg (P<۰.۰۵), ۴۰ mg/kg (P<۰.۰۱), and ۸۰ mg/kg (P<۰.۰۰۱) in a dose-related fashion when compared to BPA.  Conclusion: GM may be effective against BPA-associated hepatotoxicity.

کلیدواژه ها:

Bisphenol A ، Liver ، Toxicity ، Glutamine ، Attenuation ، Rat