Parental exposure to the synthetic estrogen 17α-ethinylestradiol (EE2) affects offspring development in the Sydney rock oyster, Saccostrea glomerata

Islam, Rafiquel; Kit Yu, Richard Man; O’Connor, Wayne A.; Anh Tran, Thi Kim; Andrew-Priestley, Megan; Leusch, Frederic D.L.; MacFarlane, Geoff R.

Parental exposure to the synthetic estrogen 17α-ethinylestradiol (EE2) affects offspring development in the Sydney rock oyster, Saccostrea glomerata

2020

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 (F₀) exposure on resultant F₁ 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 (F₁) 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 F₁ larvae at 9 dpf, retardation of shell growth was observed on F₁ 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 F₁ 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 F₁ generation.

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