Background:The organic composite of two phenolic neighbors [BPA] is Bisphenol A [BPA]. It is also commonly called propane 2,2 bis [4-hydroxyphenyl]. BPA is a voluminous industrial chemical used to manufacture epoxy resins and plastics. Aim of the work:Evaluation of the effect of oral Bisphenol A on the liver and kidney of adult male albino rats.Materials and Methods: Forty adult male albino rats [local strain] were divided into four groups [each 10 rats]. First is the control group, second is the low does BPA, third is moderate does BPA, and four is the high does BPA. The duration of exposure extended to 30 days. Then, blood samples have been collected for the measurement of serum aspartate aminotransferase [AST], serum alanine aminotransferase [ALT], blood urea, serum creatinine, superoxide dismutase [SOD], catalase, and glutathione. Also, hepatic and renal tissue samples were prepared for histopathological study.Results: Oral administration of BPA in a dose of 50, 100, and 150 Mg/kg/day for 30 days led to a significant increase in the blood levels of ALT, AST, urea, and creatinine associated with a significant reduction in the blood levels of superoxide dismutase, Glutathione peroxidase, and catalase. There were few vacuolations of hepatocytes and congested blood vessels of the liver that were associated with changes in the kidney [narrow cortex, dilated tubules, and hypercellular glomeruli]. Conclusion:Bisphenol A oral exposure for 30 consecutive days is associated with several changes in biochemical parameters that indicate liver and kidney injury.

Objective: Cigarette smoking harms all body systems, and its effects are primarily related to nicotine. However, the heavy metal content (mainly lead and cadmium) could add to nicotine's hazardous effects. Thus, the current study aimed to investigate the effect of cigarette smoking content of cadmium and lead on bone mineral density. Subjects and Methods: A retrospective analysis of data from active, passive, and non-smokers (every 70 subjects) was analyzed for patient demographics, laboratory investigation, serum cotinine (as a confirmatory marker of smoking, bone mineral density (BMD), blood and urinary levels of cadmium and lead). Results: Hemoglobin concentrations and red blood cell count were significantly reduced, while erythrocyte sedimentation rate and liver enzymes were significantly increased in active and passive smokers than non-smokers. Serum cadmium, lead, and cotinine were raised considerably in passive and active than non-smokers (0.47±0.05, 21.94±3.99, 5.35±0.90 in active, 0.32±0.09, 18.91±3.30, and 4.35±0.89 in passive, versus 0.09±0.06, 9.84±2.63, and 1.28±0.21 in the control group, successively). Bone mineral density was reduced in active and passive than non-smokers at the radial shaft, femoral neck, and spine. Cotinine was significantly and proportionately correlated with serum cadmium and lead and inversely correlated with bone mineral density. Furthermore, cadmium and lead were inversely correlated with BMD. Conclusion: Cigarettesmoke was associated with higher concentrations of cadmium, and lead may directly and indirectly share in the harmful effects of smoking on BMD.  Keywords: Bone Mineral Density, Cotinine, Toxic Heavy Metals, Smoking

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