Meeting Abstract
Bisphenol A is an estrogen mimic that also disrupts the hypoxia-inducible factor (HIF-1α) which mediates the cardiovascular system’s response to hypoxia via angiogenesis and erythropoiesis. The purpose of this study was to determine if BPA compromises the typical cardiovascular response to hypoxia in zebrafish (Danio rerio). Cardiovascular response was assessed by measuring cardiac and vascular parameters including caudal vessel diameter, cardiac output (Q), peak arterial and venous RBC velocity, and vascular branching in hypoxia and BPA treatments. With hypoxia exposure alone, arterial and venous vessel diameters decreased by 23% and 29%, respectively while RBC velocity decreased by 35% and 28%. Arterial and venous diameter decreased with BPA exposure alone, but simultaneous exposure to BPA and hypoxia compounded to further decrease diameter and red blood cell velocity. Heart rate (ƒH), which was unaffected by hypoxia, had a 17% decrease with BPA alone at the highest concentration. BPA and hypoxia synergized to decrease ƒH by 51 and 87% in the 1 mg/L and 5 mg/L BPA treatments, respectively. Q, a product of ƒH and stroke volume (SV) was also unaffected by hypoxia alone, but decreased by 54 and 74% in the highest BPA concentrations with co-exposure. Co-exposed embryos at the highest concentration of BPA took 146% times longer to reach 50% hatching compared to 86% longer with hypoxia alone. BPA alone did not delay development. Mortality rates were highest in the 5 mg/L BPA and hypoxia exposure. Our results indicate that simultaneous exposure to BPA and hypoxia synergistically compromises the cardiovascular system’s response to hypoxia, slows development, and increases mortality.