Abstract
Bisphenol A (BPA) is a well-known endocrine-disrupting chemical that is ubiquitously present in the environment. In the present study, 4-h post-fertilization (hpf) zebrafish embryos were exposed to various environmentally relevant concentrations of BPA (0.1, 1, 10, 100, and 1000 μg/L) until 72 and 168 hpf, and the accumulation pattern of BPA and its potential to induce toxicity through apoptosis were determined. Compared to BPA concentrations in larvae at 168 hpf, BPA concentrations in embryos exposed until 72 hpf were at relatively higher levels (p < 0.05) with higher bioconcentration factor (BCF) values. The nonlinear fitting analysis indicated that the BCF values of BPA in fish embryos/larvae were significantly correlated to the log10-transformed BPA exposure concentrations in water in an inverse concentration-dependent manner. Fish accumulated more BPA as the exposure concentrations increased; however, their accumulation capacity of BPA declined and tended to be saturated in the high exposure groups of BPA. Moreover, caspase-3 activity was significantly induced upon BPA exposure at 0.1, 1, 10, and 100 μg/L BPA at 72 hpf, and also at 10 and 100 μg/L BPA at 168 hpf. Correspondingly, exposure to 10 and 100 μg/L of BPA significantly increased the DNA fragmentation in the extracted DNA at 168 hpf as determined by DNA ladder analysis. In addition, the expression patterns of four genes related to apoptosis including caspase-3, bax, p53, and c-jun were significantly up-regulated (p < 0.05) in fish embryos/larvae upon BPA exposure at 72 and 168 hpf. Our results revealed that low and environmentally relevant concentrations of BPA could be significantly accumulated in zebrafish and induced apoptosis with involvement of the regulation of caspase-3 and other apoptosis-related genes.
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