17-α-ethinylestradiol (EE2) is one of the most potent endocrine disrupting compounds found in the aquatic environments, and is known to strongly alter fish reproduction and fitness. While the effects of direct exposure to EE2 are well studied in adults, there is an increasing need to assess the impacts of exposure during early life stages. Sensitivity to pollutants during this critical window can potentially affect the phenotype later in life or in subsequent generations. This study investigated phenotypic outcome of early-life exposure to 17-α-ethinylestradiol during development and in adults of the mangrove rivulus, Kryptolebias marmoratus. Being one of the only two known self-fertilizing hermaphroditic vertebrates, this fish makes it possible to work with genetically identical individuals. Therefore, using rivulus makes it possible to examine, explicitly, the phenotypic effects of environmental variance while eliminating the effects of genetic variance. Genetically identical rivulus were exposed for the first 28days post hatching (dph) to 0, 4 or 120ng/L of EE2, and then were reared in uncontaminated water until 168dph. Growth, egg laying and steroid hormone levels (estradiol, cortisol, 11-ketotestosterone, testosterone) were measured throughout development. Exposed fish showed a reduction in standard length directly after exposure (28dph), which was more pronounced in the 120ng/L group. This was followed by compensatory growth when reared in clean water: all fish recovered a similar size as controls by 91dph. There was no difference in the age at maturity and the proportions of mature, non-mature and male individuals at 168dph. At 4ng/L, fish layed significantly fewer eggs than controls, while, surprisingly, reproduction was not affected at 120ng/L. Despite a decrease in fecundity at 4ng/L, there were no changes in hormones levels at the lower concentration. In addition, there were no significant differences among treatments immediately after exposure. However, 120ng/L exposed fish exhibited significantly higher levels of testosterone at 91 and 168dph and 11-ketotestosterone at 168dph, up to 140days after exposure. These results indicate that early-life exposure to EE2 had both immediate and delayed impacts on the adult's phenotype. While fish growth was impaired during exposure, compensatory growth, reduced fecundity and modification of the endocrine status were observed after exposure ceased.
Keywords: 17-α-ethinylestradiol; Delayed response; Endocrine disruption; Fish; Growth; Steroid hormones.
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