Effect Of Arsenic Trioxide On Germ Cell Cycle Arrest And Apoptosis In Caenorhabditis Elegans

With the development of science and technology, exploitation of a large number of mineral resources and unregulating use of pesticides, our living environment has been treated. Arsenic is recognized a worldwide environmental carcinogen, not only causes environmental pollution, but also endangers human’s health. Many studies have shown that arsenic seeps into the soil through a variety of ways and affects the metabolism of plants. At the same time, arsenic accumulates in human’s skins, hairs, bones and livers, damages liver and peripheral nervous system, increases the risk of liver cancer and skin cancer. Nevertheless, arsenic is also an effective means of cancer treatment. By changing the mitochondrial membrane potential, it can induce apoptosis and cell differentiation, influence cell cycle G2/M and the spindle checkpoint to control the expression and the activity of the protein. Because of the uncertainty of genetic toxic effects of arsenic, and the lack of high-dose concentration in vivo models, we can not accurately reflect the genetic mechanism of arsenic, and the concentration effects also need to continue to explore.Caenorhabditis elegans has been widely used in biological research, because of its short life, simple cells, fast breeding, the operability of the genetic and germ cells remains proliferating constant life. It is a good material for the study of cell signaling. C. elegans genome and the human genome are homologous so that the cell signaling pathway in C. elegans may reflect the signal transduction pathways in human’s.In this paper, we studied from life, cell proliferation and apoptosis of C. elegans, combined with RNA interference technology, to research gld-1gene regulation after arsenic exposure to C. elegans gonad cells. We found that expose with a high dose of arsenic in a short time on the C. elegans gld-1(q485) mutants, their lives were significantly extended. Further studies showed that exposure of arsenic inhibits cells proliferation and induces C. elegans wild-type and gld-1(q485) mutants germ cell cycle arrest, with significant time-dependent and dose-dependent. At the same time, arsenic can also significantly induce C. elegans germ cells apoptosis, with significant dose-dependent. By measuring germ cell apoptosis of the gld-1(q485), gld-1(op236), cep-1(the worm p53) gene knockout strains of C. elegans, the results shows that gld-1(q485) mutants does not appear apoptosis, gld-1(op236) significantly promotes the germ cells apoptosis with dose-dependent. cep-1plays an important role to promote arsenic-induced apoptosis and mediate gld-1(op236)-induced apoptosis. abl-1knockout strains of C. elegans significantly promote arsenic-induced apoptosis.