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Endocrine disrupting chemicals (EDCs) including 17β-estradiol (E2) are widely distributed in the aquatic environment and are known to negatively affect the reproductive system of many animals, including fish. EDCs leading to feminization, altered sex ratio and reduced fecundity, it is possibly posing potential risks to the ecosystems. To investigate the potentially toxic effects of E2 exposure on little yellow croaker (Larimichthys polyactis, L. poliactis) who have a unique gonadal development pattern that males undergo a hermaphroditic stage. An experiment was set up where L. poliactis were maintained in tanks and exposed to E2 concentrations of 10 μg/L or no E2 exposure (the ethanol and control groups) from 30 to 90 days post-hatching (dph). After exposure, the E2 withdrawal and continual cultured to 150 and 365 dph. The morphological and histological analyses were used to compare the changes in the fish body and gonad under E2 exposure. The results showed that E2 exposure caused three major phenotypes at 30 and 60 days after treatment (dat), including ovary, ovotestis and gonadal development retardation compared with the control groups. The average ratio of these three phenotypes is 60.6%, 11.97% and 27.43%, respectively. The body length and weight of E2 exposure groups were repressed during the E2 exposure period, while it can recover after E2 withdrawal. However, the gonadal development (Gonadosomatic Index) of E2 exposure groups testis were retarded at 60 dat and doesn’t recover until 365 dph. The sex determination/differentiation-related genes erα, erβI, erβII, fshβ and cyp11b2 were significantly decreased in E2-exposure male fish. This research highlights the E2 leads to feminization, disrupts testis maturation and spermatogenesis, this effect persisted into the stage of sexual maturity. Collectively, our findings provide insights into the molecular mechanisms underlying E2 disturbance of a marine economic fish reproduction. |
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