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=30) were used. the rats were randomly grouped into six of five rats each. groups a (control), b, and c were treated with normal saline (0.2 ml), gm (80 mg/kg), and bpa (50 mg/kg), respectively for 60 days. groups d-f were treated with gm (20 mg/kg)+bpa (50 mg/kg), gm (40 mg/kg)+bpa (50 mg/kg), and gm (80 mg/ kg)+bpa (50 mg/kg), respectively for 60 days. after treatment, blood and liver samples were obtained for biochemical and histological assessments, respectively. results: significantly (p<0.01) decreased body weight and significantly (p<0.01) increased liver weight occurred in the bpa-administered group when compared to the control group. the bpa-administered group showed significantly (p<0.001) 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<0.001) 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; 20 mg/kg (p<0.05), 40 mg/kg (p<0.01), and 80 mg/kg (p<0.001) in a dose-related fashion when compared to bpa. conclusion: gm may be effective against bpa-associated hepatotoxicity