## 1 Introduction  
Emerging evidence suggests that prenatal exposure to endocrine-disrupting chemicals (EDCs), whether of natural or synthetic origin, increases the susceptibility to cardiovascular diseases in adulthood [1]. Bisphenol A (BPA) is one of the ubiquitously manufactured EDCs, and is most widely used in various plastic-related consumer products. BPA is able to leach from consumer products and its contaminants are detected in water, food, and dust, etc. [2]. Its presence was also identified in biological solutions, including urine, placenta, breast milk, amniotic fluid, blood, tissues, and cord blood [3]. Although the United States Environmental Protection Agency (EPA) guidelines consider BPA exposure at a concentration of 50 \(\upmu\)g/kg/day to be safe, some studies have shown various adverse health effects even at this concentration [4; 5; 6; 7; 8]. Humans are exposed to higher concentrations of BPA than the reference dose, Ref. [9] particularly industrial workers and children, where significant urinary BPA levels were noted [10]. The presence of BPA with higher concentrations than 11.2 ng/mL was associated with teratogenic effects in human embryos [11].  
BPA could reach the fetus through the placenta and affect the development of various systems of the human body [12; 13; 14; 15]. A recent study, in support of [PERSON]'s hypothesis, has demonstrated that prenatal exposure to BPA triggers the onset of atherosclerosis in the adult progeny [16]. Furthermore, a few studies have investigated the direct impact of prenatal BPA exposure on cardiovascular structure and function in sheep, rodents, and monkeys. Perinatal BPA exposure significantly increased the ventricular wall thickness in the offspring of rodents [17; 18; 19]. Fetal hearts of BPA-exposed rats showed signs of fibrosis [20] and abnormal development by enhancing ferrotposis [21]. It has been demonstrated that prenatal BPA exposure affects fetal liver maturation [13], contributes to hepatic steatosis development [22; 23], and alters nephrogenesis in adult offspring [24]. Epidemiological investigations have indicated that BPA exposure during critical periods of fetal development correlates with elevated blood pressure levels in children [25; 26]. Various natural compounds have been investigated to ameliorate BPA exposure-induced adverse effects in various body systems [27]. However, the therapeutic potential of natural compounds against perinatal BPA exposure-induced cardiovascular alterations and hepatic steatosis is yet to be explored.  
Rsv is a popular nutritional phytoalexin, commonly found in pistachios, red wine, dark chocolate, berry fruits, etc. Figure 1 illustrates the structures of Rsv and BPA. Potential health-beneficial effects of Rsv include its anti-obesogenic, anti-inflammatory, anti-atherosclerotic, antioxidant properties, anti-carcinogenic activity, platelet aggregation inhibition, and promotion of endothelial function, etc. [28]. The consumption of a reference dose of 5 g/day is considered to be safe [29]. Rsv is known to cross the placental barrier [30] and reduce fetal oxidative stress by improving fetal oxygen delivery and acting on fetal tissues to regulate the genes of the redox system [31]. In our previous study, Rsv exposure significantly prevented BPA exposure-induced atherosclerotic lesion formation in the offspring mice in adulthood [32]. The beneficial effects of Rsv treatment on cardiovascular health in adults have also been reported [33]. In this study, we sought to explore how perinatal Rsv exposure affects the adverse cardiovascular changes and hepatic steatosis induced by BPA in adult offspring.