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 nu...

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Bibliographic Details
Published in:Toxicology and applied pharmacology 2013-12, Vol.273 (2), p.381-389
Main Authors: Zhang, Bingzhen, Shen, Chunzi, Yang, Liu, Li, Chunhui, Yi, Anji, Wang, Zhiping
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Animals
APOPTOSIS
Apoptosis - drug effects
Apoptosis - physiology
Biological and medical sciences
Blastocyst implantation
Carbon disulfide
Carbon Disulfide - toxicity
CARBON SULFIDES
DISULFIDES
DNA damage
DNA Damage - drug effects
DNA Damage - physiology
DNA DAMAGES
Embryo Loss - chemically induced
Embryo Loss - pathology
EMBRYOS
Endometrial cells
Endometrium - drug effects
Endometrium - pathology
Female
Medical sciences
MESSENGER-RNA
MICE
PREGNANCY
Prenatal Exposure Delayed Effects - chemically induced
Prenatal Exposure Delayed Effects - pathology
PROTEINS
Random Allocation
Toxicology
WOMEN
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Summary: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 (157.85mg/kg), 0.2 LD50 (315.7mg/kg) and 0.4 LD50 (631.4mg/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. •We built an animal model of CS2 exposure during blastocyst implantation.•Endometrial cells were used in the comet assay to detect DNA damage.•CS2 exposure caused DNA damage and endometrial cell apoptosis.•DNA damage and endometrial cell apoptosis were responsible for embryo loss.
ISSN:0041-008X
1096-0333
DOI:10.1016/j.taap.2013.09.013