Abstract
Exposure to 17α-ethynylestradiol (EE2, 5 μg/g food) impairs some reproductive events in the protandrous gilthead seabream and a short recovery period does not allow full recovery. In this study, spermiating seabream males in the second reproductive cycle (RC) were fed a diet containing 5 or 2.5 μg EE2/g food for 28 days and then a commercial diet without EE2 for the remaining RC. Individuals were sampled at the end of the EE2 treatment and then at the end of the RC and at the beginning of the third RC, 146 and 333 days after the cessation of treatment, respectively. Increased hepatic transcript levels of the gene coding for vitellogenin (vtg) and plasma levels of Vtg indicated both concentrations of EE2 caused endocrine disruption. Modifications in the histological organization of the testis, germ cell proliferation, plasma levels of the sex steroids and pituitary expression levels of the genes coding for the gonadotropin β-subunits, fshβ and lhβ were detected. The plasma levels of Vtg and most of the reproductive parameters were restored 146 days after treatments. However, although 50% of the control fish underwent sex reversal as expected at the third RC, male-to female sex change was prevented by both EE2 concentrations.
Highlights
Nowadays there is a broad variety of chemicals discharged from industrial and urban sources that have been described as endocrine disrupting chemicals (EDCs)
Exposure to 2.5 or 5 μg E E2/g food for 28 days had disruptive effects, since it caused a significant increase in the hepatic expression levels of vtg (Fig. 2a) and plasma levels of Vtg compared to the control fish (Fig. 2b)
Exposure to 5 μg E E2/g food for 25 or 28 days had a disruptive effect in male gilthead seabream, since it increased the hepatic expression of vtg and disrupted spermatogenesis and steroidogenesis
Summary
Nowadays there is a broad variety of chemicals discharged from industrial and urban sources that have been described as endocrine disrupting chemicals (EDCs). Alterations in reproductive endpoints such as plasma levels of steroid hormones[7,8,9,12,13], gonad morphology[6,7,8,9,13,14] and the expression levels of genes coding for estrogenic receptors or for steroidogenic e nzymes[8,9,10,13] help to assess the disruptive effects of this compound which vary according to dose, time of exposure, age and the stage in the reproductive cycle of the treated individuals[7,8,17]. When EE2 exposure was followed by a recovery period of 25 days when fish were fed a standard diet, reproductive parameters did not r ecover[35]
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