Suppression of uterine decidualization correlated with reduction in serum progesterone levels as a cause of preimplantation embryonic loss induced by diphenyltin in rats.
In our previous study, diphenyltin dichloride (DPTCl) at 16.5 mg/kg and higher on days 0-3 of pregnancy was found to induce preimplantation embryonic loss in rats. In the present study, the effects of DPTCl on uterine decidualization in pseudopregnant rats, effects of ovarian hormones on uterine decidualization in ovariectomized rats, and effects of progesterone on the DPTCl-induced preimplantation embryonic loss in pregnant rats were determined. Female rats were given DPTCl by gastric intubation at 4.1, 8.3, 16.5, or 24.8 mg/kg on days 0-3 of pseudopregnancy and the decidual cell response was induced on day 4 of pseudopregnancy. The uterine weight on day 9 of pseudopregnancy served as an index of uterine decidualization. A significant decrease in uterine weight, which indicates suppression of uterine decidualization, was detected at 16.5 and 24.8 mg/kg. Ovarian weight and number of corpora lutea in the DPTCl-treated groups were comparable to the controls. A significant decrease in the serum progesterone levels was found at 16.5 and 24.8 mg/kg in pseudopregnant rats. The hormonal regimen consisting of progesterone and estrone-supported decidual development in ovariectomized rats given DPTCl. Pregnancy rate and number of implantations were significantly lower in the intact mated groups given DPTCl at 16.5 and 24.8 mg/kg on days 0-3 of pregnancy than in the control group and significantly higher in the groups given DPTCl plus progesterone than in the groups given DPTCl alone. These results show that reduction in serum progesterone levels is correlated with suppression of uterine decidualization and progesterone protects against preimplantation embryonic loss induced by DPTCl.[1]References
- Suppression of uterine decidualization correlated with reduction in serum progesterone levels as a cause of preimplantation embryonic loss induced by diphenyltin in rats. Ema, M., Miyawaki, E. Reprod. Toxicol. (2002) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
