## 4 Discussion  
Our previous study findings indicate that perinatal exposure to BPA in ApoE mice results in the formation of atherosclerotic lesions in the aorta of adult offspring [32]. Similar findings were observed in a study of a PXR-Humanized mouse animal model [33]. In this study, we explored the lesion characteristics, arterial wall thickness, and elastic preservation of BPA-exposed offspring mice. Histo-morphometric analysis of the brachiocephalic artery revealed increased elastic breaks and intima-to-media thickness ratio in BPA-exposed mice. Indeed, elastin fibers are crucial for maintaining the structural integrity of blood vessels and regulating the proliferation and migration of smooth muscle cells [39]. During the development of atherosclerosis, the fragmentation and degradation of elastic laminae can occur, which enables SMC penetration into the intima layer. This process contributes to the formation of atheomatous plaques [40]. Increased disruption of elastin lamellae is typically observed in atherosclerosis progression [38; 39]. Hence, the increased number of elastic breaks in BPA-exposed mice indicate its role in atherosclerosis progression. This is further evidenced by the increased intima-to-media thickness ratio and the presence of cholesterol clefts and calcium deposits in the intimal lesion in BPA-exposed mice. Studies have explored the adverse effects of BPA exposure on fetal heart development and cardiac structure/function in adult offspring [17; 18; 20]. In an in vitro study, BPA exposure altered the normal function of the in vitro model of the fetal heart [20]. In a study by [PERSON] et al., sex-specific effects on cardiac structure/function were observed in BPA-exposed adult male offspring mice [17]. The concentric remodeling of cardiac muscle and increased relative wall thickness were noted in male mice. Findings of the study also suggested that the altered structure is due to the direct action of BPA on the heart, as there was no pathological increase in blood pressure [17]. In a study by [PERSON] et al., prenatal BPA exposure significantly increased heart weight, LVW thickness, and perivascular and interstitial fibrosis in adult male offspring mice [18]. The possible mechanisms behind the BPA-induced adverse effects on heart development were studied. According to the study conducted by [PERSON] et al., maternal exposure to BPA was found to cause changes in the transcript expression profile in the fetal heart [41]. The same study findings revealed that the regulation of two genes (Myh6 and Adam12) in the left ventricle is shown to be related to cardiac hypertrophy. Another study revealed that developmental BPA exposure in pregnant rats alters miR-17-5p,-208-3p, and-210-3p expressions in fetal hearts [20]. In our study, the observed histo-morphometric changes in the heart support the previous in vitro and in vivo study findings that demonstrate the cardiotoxic effects of perinatal BPA exposure on adult offspring. However, contrary to most previous studies, we did not observe a sexually dimorphic effect of BPA on the rodent heart. These sex-specific differences could be due to different animal models used in these studies. The worldwide reported pooled prevalence of non-alcoholic fatty liver disease (NAFLD) is 25.24%, with the highest prevalence rates in South American and Middle Eastern countries [42]. Current evidence suggests that reprogramming of the liver during the critical periods of gestation increases the risk of developing NAFLD [43], in addition to other factors, including obesity and a sedentary lifestyle. Experimental studies have reported BPA-induced hepatic steatosis in the liver without altering its weight [22; 44; 45]. In agreement with these studies, we observed sex-specific BPA-induced hepatic steatosis in adult female offspring. However, in a study by [PERSON] et al., BPA exposure had no effect on fetal liver morphology [20].