Induction of Germline Cell Cycle Arrest and Apoptosis by Sodium Arsenite in Caenorhabditis elegans
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- 作者：Shunchang Wang ; Ye Zhao ; Lijun Wu ; Mingli Tang ; Caixing Su ; Tom K. Hei ; Zengliang Yu
- 刊名：Chemical Research in Toxicology
- 出版年：2007
- 出版时间：February 2007
- 年：2007
- 卷：20
- 期：2
- 页码：181 - 186
- 全文大小：142K
- 年卷期：v.20,no.2(February 2007)
- ISSN：1520-5010
文摘
The nematode Caenorhabditis elegans has been shown to be a model organism in studying aquatictoxicity. Although epidemiological studies have shown that arsenic is teratogenic and carcinogenic tohumans, the lethality assay indicated that C. elegans is less sensitive to inorganic arsenic than any otherorganisms that have been tested thus far. In the present study, we used the more malleable germline ofC. elegans as an in vivo system to investigate the genotoxic effects of arsenite. After animals wereexposed to sodium arsenite at concentrations ranging from 1 
M to 0.5 mM, mitotic germ cells andgermline apoptosis were scored after DAPI staining and acridine orange vital staining, respectively. DMSOrescue experiments were performed by exposing C. elegans to 0.01 mM arsenite in the presence ofDMSO (0.1%) for 24 h, and reactive oxygen species (ROS) were semiquantified by CM-H2DCFDAvital staining. The results indicated that arsenic exposure reduced the brood size of C. elegans and causedmitotic cell cycle arrest and germline apoptosis, which, to some extent, exhibited a concentration- andtime-dependent manner. The addition of 0.1% DMSO completely rescued arsenic-induced cell cyclearrest and partially suppressed germline apoptosis. Furthermore, treatment of animals with arsenite at adose of 0.01 mM significantly increased ROS production in the intestine, which could be reduced byDMSO treatment. The present study also indicated that C. elegans might be used as an in vivo modelsystem to study the mechanisms of arsenic-induced genotoxic effects.
M to 0.5 mM, mitotic germ cells andgermline apoptosis were scored after DAPI staining and acridine orange vital staining, respectively. DMSOrescue experiments were performed by exposing C. elegans to 0.01 mM arsenite in the presence ofDMSO (0.1%) for 24 h, and reactive oxygen species (ROS) were semiquantified by CM-H2DCFDAvital staining. The results indicated that arsenic exposure reduced the brood size of C. elegans and causedmitotic cell cycle arrest and germline apoptosis, which, to some extent, exhibited a concentration- andtime-dependent manner. The addition of 0.1% DMSO completely rescued arsenic-induced cell cyclearrest and partially suppressed germline apoptosis. Furthermore, treatment of animals with arsenite at adose of 0.01 mM significantly increased ROS production in the intestine, which could be reduced byDMSO treatment. The present study also indicated that C. elegans might be used as an in vivo modelsystem to study the mechanisms of arsenic-induced genotoxic effects.