School of Environmental and Life Sciences, The University of Newcastle, Callaghan, NSW 2308, Australia; Department of Applied Chemistry and Chemical Engineering, Islamic University, Kushtia 7003, Bangladesh.
School of Environmental and Life Sciences, The University of Newcastle, Callaghan, NSW 2308, Australia.
Environ Pollut. 2020 Nov;266(Pt 1):114994. doi: 10.1016/j.envpol.2020.114994. Epub 2020 Jul 3.
Very little is currently known regarding the effects of estrogenic endocrine disrupting chemicals on embryonic and larval development in molluscs, nor the potential effects of parental (F) exposure on resultant F offspring. In this study, we assessed the embryotoxic impacts of exposure to environmentally relevant concentrations of the synthetic estrogen, 17α-ethinylestradiol (EE2), to male and female parents (50 ng/L) and their offspring (5 and 50 ng/L) in the native Australian Sydney rock oyster, Saccostrea glomerata. There were no detectable effects of parental exposure on fertilisation success, proportions of early larval (F) morphs and unfertilised eggs. Offspring impacts were evidenced in terms of developmental delays, with decreased percentages of D-veligers retained by 45 μm mesh, along with a reduction of swimming capabilities of larvae at 2 days post-fertilisation (dpf) when both parents had been exposed to 50 ng/L EE2. Although no significant parental effects were found on the survival of F larvae at 9 dpf, retardation of shell growth was observed on F larvae in treatments where both parents had been exposed to 50 ng/L EE2. Subsequent larval exposure from 2 to 9 dpf caused declines in survival and reduction of shell length in F larvae at both 5 and 50 ng/L EE2 across all parental exposure treatments. Collectively, parental EE2 imparts effects on offspring in terms of retardation of larval development, and subsequent offspring exposure to EE2 further exacerbates impacts to development. Future research should aim to understand the potential mechanisms of EE2 induced toxicity and its transmission resulting in altered phenotypes of the F generation.
目前，人们对雌激素内分泌干扰化学物质对贝类胚胎和幼虫发育的影响，以及亲代（F）暴露对后代 F 个体的潜在影响知之甚少。在这项研究中，我们评估了暴露于环境相关浓度的合成雌激素 17α-乙炔基雌二醇（EE2）对澳大利亚本土悉尼岩蚝（Saccostrea glomerata）雌雄亲代（50ng/L）及其后代（5 和 50ng/L）的胚胎毒性影响。亲代暴露对受精成功率、早期幼虫（F）形态比例和未受精卵均没有检测到影响。后代的影响表现为发育延迟，通过 45μm 筛网保留的 D 型幼体百分比降低，以及在亲代均暴露于 50ng/L EE2 时，孵化后 2 天（dpf）幼虫的游泳能力下降。尽管在 9 dpf 时，F 幼虫的存活率没有显著的亲代效应，但在亲代均暴露于 50ng/L EE2 的处理中，F 幼虫的壳生长受到了抑制。随后，从 2 至 9 dpf 对幼虫的后续暴露导致在所有亲代暴露处理中，F 幼虫在 5 和 50ng/L EE2 下的存活率下降和壳长减少。总的来说，EE2 对亲代的影响表现在幼虫发育的延迟上，随后对 EE2 的后代暴露进一步加剧了对发育的影响。未来的研究应旨在了解 EE2 诱导毒性的潜在机制及其传递，从而导致 F 代表型的改变。
