Background: Bisphenol-A (BPA) is the building block of polycarbonate plastics, a hard plastic used to make numerous consumer products, including most baby  bottles and water bottles. Objective: Assessing the adverse effect of oral administration of   BPA on liver and kidney of adult male albino rats and evaluation of  the  role  of  vitamin C and thymoquinone (TQ) in alleviating the possible detrimental effects of  BPA. Material and Methods: Fifty six adult  male  albino  rats of  local strain were housed in 14 suitable metal cages(20 ×32× 20 cm for every 4 rats).They were divided into seven equal groups : The 1st group was served as a control group, the 2nd group was treated with bisphenol-A, the 3 ^rd group was normal and treated with vitamin C alone ,the 4 ^th group was  normal and treated with thymoquinone  alone, the 5 ^th group  was  administered by bisphenol-A and treated with vitamin C, the  6 ^th group was administered by  bisphenol-A and treated with  thymoquinone and the 7 ^th group was administered by bisphenol-A and treated with  both vitamin C and thymoquinone. All animals were treated for four weeks. Results: Administration of  bisphenol-A (50mg/Kg body weight orally) to rats resulted in an increase in alanine transaminase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), urea , creatine, and hepatic and renal MDA level, and decreased reduced glutathione (GSH) and superoxide dismutase (SOD) contents of  the liver and  kidney as compared to control group. In contrast, the administration of vitamin C (500 mg/ kg body weight) and/ or thymoquinone(10 mg /kg body weight) to bisphenol-A treated rats attenuated the toxicity of  bisphenol. This alleviation was more pronounced in the   bisphenol-A group treated with both vitamin C and  thymoquinone. Conclusion: BPA has detrimental effect on liver and kidney of  adult male albino rats. It supported the possibility that the synergistic effect of thymoquinone and vitamin C played a notable role in protecting the liver and kidney against BPA-induced toxicity and oxidative stress in male rats.