Early developmental exposure to pentachlorophenol causes alterations on mRNA expressions of caspase protease family in zebrafish embryos

- PCP caused distinct developmental abnormality in zebrafish embryos.
- The caspase genes more than caspase-3 could be affected by PCP exposure.
- The changes of casp9 indicated PCP possibly induced intrinsic apoptosis pathway.

Caspase proteases play an essential role in cell apoptosis and inflammation, thus matter greatly in animal development and other biological processes. As a ubiquitous environmental pollutant, pentachlorophenol (PCP) is considered to have adverse effects on animal apoptosis during embryonic development, yet the evidence that PCP interfere with caspase genes was seldom reported. To uncover the effects of PCP on caspases expression in early embryos of zebrafish, two concentrations of PCP (5 μg/L and 200 μg/L) were chosen and 14 types of caspase genes at two different developmental stages, 8 h post-fertilization (hpf) and 24 hpf were analyzed. Lower survival and hatching rates, distinct developmental delay and morphological deformities of head and tail were observed. PCP, especially in the high concentration, significantly altered the expressions of most caspase genes. At 8 hpf, PCP had the most significant inductive effects on gene casp8l2 with fold changes (FCs) of 6.87 at 5 μg/L and 4.48 at 200 μg/L, and casp6l1 (with FCs of 3.15/3.69), and inhibitory effects on caspa (with FCs of 0.93/0.53) and caspb (with FCs of 0.99/0.57). At 24 hpf, PCP had the most significant effects on casp6l2, casp9, and caspc. PCP exposure possibly disrupted intrinsic apoptosis pathway considering its effects on casp9 expression. In addition, most caspase genes exhibited higher levels at 24 hpf than 8 hpf except caspc. Our results suggested that PCP had different effects on varied caspase genes, which probably resulting in a profound impact on caspase proteins and apoptosis processes and, ultimately, developmental abnormality.