Department of Epidemiology and Health Statistics, School of Public Health, Shandong University, Jinan, China.
Toxicol Appl Pharmacol. 2013 Dec 1;273(2):381-9. doi: 10.1016/j.taap.2013.09.013. Epub 2013 Sep 29.
Carbon disulfide (CS2) may lead to spontaneous abortion and very early pregnancy loss in women exposed in the workplace, but the mechanism remains unclear. We designed an animal model in which gestating Kunming strain mice were exposed to CS2 via i.p. on gestational day 4 (GD4). We found that the number of implanted blastocysts on GD8 was significantly reduced by each dose of 0.1 LD50 (157.85 mg/kg), 0.2 LD50 (315.7 mg/kg) and 0.4 LD50 (631.4 mg/kg). In addition, both the level of DNA damage and apoptosis rates of endometrial cells on GD4.5 were increased, showed definite dose-response relationships, and inversely related to the number of implanted blastocysts. The expressions of mRNA and protein for the Bax and caspase-3 genes in the uterine tissues on GD4.5 were up-regulated, while the expressions of mRNA and protein for the Bcl-2 gene were dose-dependently down-regulated. Our results indicated that DNA damage and apoptosis of endometrial cells were important reasons for the loss of implanted blastocysts induced by CS2.
二硫化碳（CS2）可能导致职业暴露的女性发生自然流产和极早期妊娠丢失，但机制尚不清楚。我们设计了一种动物模型，使昆明种孕鼠在妊娠第 4 天（GD4）通过腹腔注射暴露于 CS2。我们发现，每个剂量的 0.1LD50（157.85mg/kg）、0.2LD50（315.7mg/kg）和 0.4LD50（631.4mg/kg）均显著减少了 GD8 的着床胚泡数量。此外，GD4.5 的子宫内膜细胞的 DNA 损伤水平和细胞凋亡率均增加，呈现出明确的剂量-反应关系，且与着床胚泡的数量呈负相关。GD4.5 的子宫组织中 Bax 和 caspase-3 基因的 mRNA 和蛋白表达上调，而 Bcl-2 基因的 mRNA 和蛋白表达则呈剂量依赖性下调。我们的结果表明，子宫内膜细胞的 DNA 损伤和凋亡是 CS2 导致着床胚泡丢失的重要原因。
