Environmental relevant concentrations of triclosan affected developmental toxicity, oxidative stress, and apoptosis in zebrafish embryos.

Abstract

Triclosan (TCS), as a broad-spectrum antibacterial agent, is widely used in various pharmaceutical and personal care products. However, the details of ecological environmental health risks of TCS are not clear. In this study, zebrafish embryos/larval were exposed to environmentally relevant concentrations of TCS to evaluate the developmental toxicity. Four-hour post-fertilization (hpf) zebrafish embryos were exposed to 0, 2, 10, 50, and 250μg/L TCS until 96 h. The heart beats at 72 hpf were significantly increased in 2μg/L TCS group, while significantly decreased in 250μg/L TCS treated group compared with control. The results of acridine orange staining, terminal deoxynucleotide transferase-mediated UTPnick end labeling assay, and detection of mitochondrial membrane potential showed that 50 and 250μg/L TCS resulted in apoptosis. Meanwhile, reactive oxygen species (ROS) and DNA damage were induced, but SOD activity was significantly decreased in 250μg/L TCS treated group. In addition, SOD(Mn) and GPx gene mRNA expressions were significantly down-regulated in 50 and 250μg/L TCS treated groups, while Casp3, Casp9, Puma, Casp8, Apaf1, and Bid genes in 250μg/L TCS and Mdm2 gene in 50μg/L treated groups were significantly up-regulated. P53 protein was significantly up-regulated in 250μg/L TCS treated group. The overall results showed that TCS can cause oxidative stress and result in apoptosis via the involvement of ROS-p53-caspase-dependent apoptotic pathway in zebrafish embryos. The present findings suggest the potential mechanisms of TCS-induced developmental toxicity appears to be the generation of ROS and the consequent triggering of apoptosis genes.