| Abstract: | Many investigations showed that cobalt exposure could induce apoptosis both in cells and tissues. However, appropriate in vivo animal models to assess the underlying mechanisms of cobalt-induced apoptosis are currently unavailable. The model organism, Caenorhabditis elegans, has been shown to be a good model for evaluating many biological processes. This study detected significant cobalt induced germline cell apoptosis after 12-h exposure; thus demonstrating that C. elegans could be a mammalian in vivo substitute model to study mechanisms of apoptosis. Then knockout gene C. elegans strains were utilized to investigate the relationship between cobalt-induced apoptosis and relevant signal pathways, which were involved in DNA damage and repair, apoptosis regulation, and damage signal transduction. The results presented here demonstrated that cobalt-induced apoptosis was independent of the DNA damage response gene, such as hus-1, p53/cep-1, and egl-1. The loss-of-function of the genes that related to JNK and p38 MAPK signaling cascades suppressed cobalt-induced germline apoptosis, while ERK signaling cascades have no effect on the cobalt-induced germline apoptosis. |
