Effects of adrenergic α-antagonists on the early life stages of Japanese medaka (Oryzias latipes).

The occurrence of pharmaceuticals in the aquatic environment has stimulated considerable research efforts into their potential ecotoxicological consequences. There are a number of pharmaceuticals targeting adrenergic receptors; however, relatively few studies have explored the effects of adrenergic α-antagonists (or α-blockers) on fish. In this study, moxisylyte was selected as a representative α-blocker, and Japanese medaka embryos were exposed to moxisylyte (1-625 µg/L) for 44 days. Moxisylyte caused no significant or only marginal effects on the mortality, development, and growth; however, most genes involved in detoxification and antioxidant were transcriptionally upregulated, and antioxidant enzymes activities were induced as well. Moxisylyte exposure resulted in transcriptional downregulation of most of the steroidogenesis genes, and accordingly, the mRNA levels of steroid hormone receptors and vitellogenin decreased, particularly in males, indicating that moxisylyte disrupts the hypothalamic-pituitary-gonadal (HPG) axis in a gender-specific manner. Therefore, the risk of α-blockers on fish should not be overlooked and deserves further investigation.

Inhibitory effects of estrogenic endocrine disrupting chemicals on fin regeneration in zebrafish are dependent on estrogen receptors.

For fish and other aquatic organisms, disrupting their capacity for repair and regeneration will reduce their quality of life and survivorship in the wild. Studies have shown that 17α-ethinylestradiol (EE2), a synthetic estrogenic endocrine disrupting chemical (EEDC), can inhibit caudal fin regeneration in larval zebrafish following fin amputation. However, whether the inhibitory effects of EE2 are dependent on estrogen receptor (ER) remains unknown. Therefore, in this study, amputated zebrafish larvae were exposed to the ER agonist EE2 alone and in combination with the ER antagonist ICI 182,780 (ICI), and the change in regenerative capacity was determined. The inhibition of fin regeneration caused by EE2 alone (100 ng/L) was ameliorated after combination with ICI (30-300 µg/L), and these changes in regeneration-related signaling and the immune system corresponded with morphological observations, implying that the effects of EE2 on regeneration were possibly initiated by the activation of ER. Furthermore, the role of ER was confirmed with a natural ligand of ER, namely, 17ß-estradiol (E2), and as expected, the effects of E2 (10, 100 and 1000 ng/L) paralleled those of EE2. In conclusion, EEDCs can disrupt the regenerative capacity in zebrafish, possibly due to the binding and activation of ERs and the consequent alteration of signaling pathways that regulate fin regeneration and immune competence. Given that EEDCs appear to be ubiquitous in the aquatic environment, the risk of these chemicals might be readdressed regarding their potential effects on tissue repair and regeneration.