DNA damage and apoptosis of endometrial cells cause loss of the early embryo in mice exposed to carbon disulfide.
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.
Department of Epidemiology and Health Statistics, School of Public Health, Shandong University, Jinan, China.
Bingzhen
B
Zhang
Chunzi
C
Shen
Liu
L
Yang
Chunhui
C
Li
Anji
A
Yi
Zhiping
Z
Wang
D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D002246:Carbon Disulfide / Q000633:toxicity*; D004249:DNA Damage / Q000187:drug effects / Q000502:physiology*; D020964:Embryo Loss / Q000139:chemically induced* / Q000473:pathology*; D004717:Endometrium / Q000187:drug effects / Q000473:pathology*; D005260:Female; D051379:Mice; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000139:chemically induced / Q000473:pathology; D011897:Random Allocation
D002246:Carbon Disulfide
Apoptosis; Blastocyst implantation; Carbon disulfide; DNA damage; Endometrial cells