Genistein Mitigates the Gastro-Toxic Effects of Bisphenol A in Male Wistar Rats

Abstract

Exposure to Bisphenol A (BPA) worldwide is on the increase. Its toxicities in various tissues expressing estrogen receptors have been reported. However, limited information exists on its effects on the gastric tissue. This study therefore investigated the gastric effects of BPA exposure and the likely ameliorative potential of genistein, a phytoestrogen antioxidant, known to interact with estrogen receptors. Eighty-four male Wistar rats were randomly divided into 6 groups (n = 14) and orally treated for 28 days. Group I-IV received distilled water (0.2 ml), corn oil (3 ml/kg), BPA (50 mg/kg) and genistein (50 mg/kg) respectively. Group V was pre-treated daily with BPA one hour prior to genistein administration while Group VI was pre-treated daily with genistein one hour prior to BPA treatment. Thereafter, blood was collected into heparinized bottles for hematological analysis. Gastric juice was collected for pH and electrolytes determination. Gastric tissue was excised and analyzed for superoxide dismutase (SOD), reduced glutathione (GSH), malondialdehyde, nitric oxide (NO), mucin, parietal and mucous cell counts, and histology. The BPA only treatment group exhibited significant increases (p < 0.05) in white blood cell count, neutrophil-lymphocyte ratio, mucin concentration, NO, and malondialdehyde while gastric juice pH, bicarbonate, SOD, and GSH levels were reduced compared to control. The gastric mucosa also showed pathologies consistent with inflammation. Genistein pre-and post-treatment in BPA exposed rats significantly (p < 0.05) ameliorated these effects of BPA. However, some signs of gastric inflammation were still evident in the mucosal samples. Bisphenol A induces gastro-toxicity by increasing gastric acidity, reducing gastric juice bicarbonate level and disrupting prooxidant/antioxidant balance. Genistein pre- and post-treatment ameliorated these gastro-toxic effects of Bisphenol A via gastroprotective, antioxidant and anti-inflammatory mechanisms.