Life Sciences Division, Graduate School at Shenzhen, Tsinghua University, Shenzhen, PR China.
Chemosphere. 2011 Jan;82(3):443-50. doi: 10.1016/j.chemosphere.2010.09.056. Epub 2010 Oct 20.
The effects of bisphenol A (BPA) on abalone (Haliotis diversicolor supertexta) embryonic development were investigated by exposing the fertilized eggs to four different concentrations of BPA (0.05, 0.2, 2 and 10 μg mL(-1)). Toxicity endpoints including the embryo development parameters, the physiological features and the expression profile of several reference genes (prohormone convertase 1, PC1; cyclin B, CB; and cyclin-dependent kinase 1, CDK1) were assessed. The results showed that BPA could markedly reduce embryo hatchability, increase developmental malformation, and suppress the metamorphosis behavior of larvae. The possible toxicological mechanisms hidden behind of these effects (i.e. disturbing the embryogenesis) might result from three aspects: (1) BPA disturbance the cellular ionic homeostasis and osmoregulation of abalone embryos by changing the Na+-K+-ATPase and Ca2+-Mg2+-ATPase levels; (2) BPA induced oxidative damage of embryos by significantly altering the peroxidase (POD) activities and the malondialdehyde (MDA) production; and (3) the RT-PCR analysis further demonstrated that BPA perturbed the cellular endocrine regulation and cell cycle progression by down-regulating the PC1 gene, as well as over-expressing the CB and CDK1 genes. This is the first comprehensive study on the developmental toxicity of BPA to the marine abalone at morphological, physiological and molecular levels. The results in this study also indicated that the embryo tests can contribute to the ecological risk assessment of the endocrine disruptors in marine environment.
双酚 A（BPA）对皱纹盘鲍（Haliotis diversicolor supertexta）胚胎发育的影响，通过暴露受精卵于四种不同浓度的 BPA（0.05、0.2、2 和 10μg mL(-1))进行研究。毒性终点包括胚胎发育参数、生理特征和几个参考基因（前激素转化酶 1，PC1；细胞周期蛋白 B，CB；和细胞周期蛋白依赖性激酶 1，CDK1）的表达谱。结果表明，BPA 能显著降低胚胎孵化率，增加发育畸形，并抑制幼虫变态行为。这些影响背后的可能毒理学机制（即干扰胚胎发生）可能来自三个方面：（1）BPA 通过改变 Na+-K+-ATPase 和 Ca2+-Mg2+-ATPase 水平，干扰鲍胚胎的细胞离子稳态和渗透调节；（2）BPA 通过显著改变过氧化物酶（POD）活性和丙二醛（MDA）产生，诱导胚胎氧化损伤；（3）RT-PCR 分析进一步表明，BPA 通过下调 PC1 基因以及过表达 CB 和 CDK1 基因，干扰细胞内分泌调节和细胞周期进程。这是首次在形态、生理和分子水平上全面研究 BPA 对海洋鲍的发育毒性。本研究结果还表明，胚胎试验有助于评估海洋环境中内分泌干扰物的生态风险。
