Effects of the bioconcentration and parental transfer of environmentally relevant concentrations of difenoconazole on endocrine disruption in zebrafish (Danio rerio).

Difenoconazole, a typical triazole fungicide, inhibits lanosterol-14R-demethylase (CYP51) to prevent fungal sterol synthesis and its residues are frequently detected in the environment due to its wide application. Previous studies have demonstrated that difenoconazole altered the triglyceride levels, and gene expression relevant to cholesterol biosynthesis in zebrafish. However, endocrine-disruption in the hypothalamus-pituitary-gonadal-liver (HPGL) axis, the effects of transferring to offspring, and the underlying mechanisms of difenoconazole in aquatic organisms are still unknown. In this study, we defined the effects of difenoconazole at environmental concentrations on endocrine disturbance using zebrafish as an experimental model. The results indicated that difenoconazole induced a significant change in the somatic index, and pathological variations in tissues, and steroid hormone levels. RT-PCR experiments further confirmed that difenoconazole significantly induced expression alteration of lhr, hsd3β, hsd11β, cyp19a in the ovary and star, cyp19a, cyp3c1 in the testis, and erα genes in livers. In addition, difenoconazole exposure in parental zebrafish affected the hatchability and length of its offspring. Moreover, the burdens of difenoconazole and difenoconazole alcohol in females were higher than in males. These findings highlighted that difenoconazole exposure at environmentally relevant concentrations elicited estrogenic endocrine-disruption effects via altering homeostasis of sex steroid hormones in the HPGL axis and the adverse effects can be transferred to the offspring.

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