Methylparaben (MeP) is one of the most frequently used preservatives in our daily products. However, it is becoming an aquatic pollutant of emerging concern. To reveal the endocrine disruption mechanism and reproductive impairment of MeP, the present study exposed adult zebrafish to 0, 1, 3, and 10 μg/L (0, 6.6, 19.7, and 65.7 nM) of MeP for 28 days. The results showed that subchronic exposure to 10 μg/L of MeP significantly increased the gonadosomatic index in zebrafish. Spermatogenesis and oogenesis were blocked by MeP at concentrations as low as 1 μg/L. Furthermore, parental exposure to MeP induced developmental deficits in offspring larvae, by increasing mortality, stimulating precocious hatching, and elevating heart rate. Blood concentrations of estradiol, testosterone, and 11-keto-testosterone were consistently lowered in MeP exposure groups. Transcriptional results evidenced that the disturbance in steroidogenesis and feedback regulation mechanisms along the hypothalamic-pituitary-gonadal axis underlay the imbalance of sex hormones. In line with the low estradiol level, hepatic production of vitellogenin (VTG) was significantly down-regulated, subsequently leading to a deficiency of VTG supply during oogenesis. To our knowledge, this is the first study to provide systemic insight about the antiestrogenic activity and reproductive toxicity of MeP.
Keywords: Endocrine disruption; Gametogenesis; Methylparaben; Reproduction; Vitellogenesis; Zebrafish.
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