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Cardiovasc Toxicol. 2014 Jun;14(2):120-8.

Chronic exposure to bisphenol A can accelerate atherosclerosis in high-fat-fed apolipoprotein E knockout mice.


In epidemiological studies, there is growing concern regarding the association between human exposure to bisphenol A (BPA) and an increased risk for cardiovascular disease. Therefore, we investigated whether BPA accelerates atherosclerosis in mouse model. Apolipoprotein E knockout (ApoE(-/-)) mice were fed a high-fat and high-cholesterol diet with or without 50 μg/kg body weight/day BPA for 12 weeks. Atherosclerotic lesions of the aorta and aortic sinus were evaluated by Oil red O staining. After the 12-week BPA treatment, BPA significantly increased atherosclerotic lesions in the aortas of ApoE(-/-) mice by 1.7-fold (p = 0.03). Non-high-density lipoprotein (HDL) cholesterol levels in the BPA group were significantly higher compared to those in the control group (1,035 ± 70 vs. 484 ± 48 mg/dL, p = 0.02) although body weight and blood glucose levels were not different between groups. Human umbilical vein endothelial cells (HUVECs) were treated with 0.1-10 nM BPA but BPA did not affect HUVEC proliferation or migration. BPA could accelerate atherosclerosis in ApoE(-/-) mice, which may have resulted from an increase in non-HDL cholesterol levels.

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