Enhance leukocyte adhesion and promote monocyte emigration, contributing to the development of atherosclerosis. Moreover, BPA exposure could also induce various inflammation markers in the endothelial cells and increase the proinflammatory cytokines levels in the serum, all of which may cause the apoptosis of intimal smooth muscle cell and breakdown of matrix. Therefore, it will be necessary to investigate whether BPA can affect the rupture of atherosclerotic plaques. In addition to BPA’s direct effects on the arterial wall, enhanced atherosclerosis in BPA-treated WHHL rabbits may be attributed to other pathological actions induced by BPA. For example, we found that BPA exposure increased adiposity and induced hypertrophy in adipocytes in both subcutaneous and visceral adipose tissue but that body weight remained unchanged. It has been reported that adipose tissue is the primary target of BPA exposure and that perinatal or postnatal exposure to BPA induces adipocyte hypertrophy in mice and rats that is accompanied by lipogenic gene up-regulation. BPA, a lipophilic compound, can accumulate in adipose tissue, and detectable levels have been found in 50% of breast adipose tissue samples from women. Thus, BPA accumulation in adipose tissue may constitute a secondary source of internal BPA exposure. Moreover, BPA can affect adipocyte differentiation in cultured 3T3-L1 pre-adipocytes, leading to abnormal lipid metabolism. Furthermore, BPA exposure can affect some factors, such as adipokines and cytokines, which are secreted from adipose tissue and can influence the functions of endothelial cells, SMCs, and MQ in vessel walls. This may constitute another mechanism for BPA-induced enhancement of atherosclerosis. In addition to its effects on adipose tissue, BPA exposure could also impose toxic effects on the liver, including steatosis and inflammatory cell infiltration, but plasma hepatic-marker levels were not increased. BPA is rapidly catabolized in the liver within 24 hr, and so the accumulation of high levels of BPA in the liver is certainly detrimental to hepatocyte functions. The pathophysiological significance of BPA-induced amplification of genes related to ER stress, inflammation and lipid metabolism in the liver GS-5734 remains unknown; however, abnormal liver functions accompanied by increased adiposity could certainly contribute significantly to the development of atherosclerosis. An important observation in this study is cardiac damage in BPA-treated WHHL rabbits. Although they require verification, several possible mechanisms may be at play. First, BPA can directly change cardiac functions, as demonstrated by reports that BPA infusion causes ventricular arrhythmias in isolated rat hearts.