Effects of dibutylphthalate and ethynylestradiol on liver peroxisomes, reproduction, and development of zebrafish (Danio rerio)

Abstract

The aim of the present work was to study the effects of the peroxisome proliferator dibutylphthalate (DBP) and the xenoestrogen 17alpha-ethynylestradiol (EE2) on liver peroxisomes, reproduction, and development of zebrafish (Danio rerio). In experiment 1, newly fertilized zebrafish eggs were exposed for five weeks, covering the entire period of sexual determination, to nominal concentrations of 25 and 100 microg/L of DBP and 5 microg/L of EE2. In experiment 2, adult female zebrafish were exposed for 15 d to 100 and 500 microg/L of DBP and 5 microg/L of EE2, and afterward, they were paired with untreated males to study the effects in the resultant offspring. Ethynylestradiol provoked marked mortality (approximately 50%) and delayed development of larvae as well as sterility of adult females, possibly related to alterations in aromatase gene expression. Ethynylestradiol up-regulated vitellogenin expression in the early life stages and increased vitellogenin synthesis and accumulation in adult females. Ethynylestradiol caused liver peroxisome proliferation in early life stages but not in adult females. Dibutylphthalate caused teratogenic effects in early life stages and mortality of the larvae obtained from exposed females. Dibutylphthalate provoked liver peroxisome proliferation and up-regulation of cytochrome P450A1 in early life stages at the end of the exposure and in adult females. Dibutylphthalate also up-regulated the expression of aromatase genes. In conclusion, the xenoestrogen EE2 caused liver peroxisome proliferation in early life stages of zebrafish, but the peroxisome proliferator DBP did not behave as a typical xenoestrogen. Overall, changes in gene expression were more marked during early life stages than in adult female zebrafish.