Evaluation of sodium arsenite exposure on reproductive competence in pregnant and postlactational dams and their offspring
•Arsenic reduced BW and increased T and E2 in pregnancy without hindering gestation.•Arsenic compromises postlactational estrous cycle resumption.•Arsenite decreases preovulatory follicles and serum E2 and increases cysts and FSH levels.•Young arsenic-exposed litters show altered GnRH and FSH expres...
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Veröffentlicht in: | Reproductive toxicology (Elmsford, N.Y.) N.Y.), 2017-04, Vol.69, p.1-12 |
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Sprache: | eng |
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Zusammenfassung: | •Arsenic reduced BW and increased T and E2 in pregnancy without hindering gestation.•Arsenic compromises postlactational estrous cycle resumption.•Arsenite decreases preovulatory follicles and serum E2 and increases cysts and FSH levels.•Young arsenic-exposed litters show altered GnRH and FSH expression.
We investigated arsenite exposure on the reproductive axis of dams (during pregnancy and at cyclicity resumption) and their offspring.
Pregnant rats were exposed to 5 (A5) or 50ppm (A50) of sodium arsenite in drinking water from gestational day 1 (GD1) until sacrifice at GD18 or two months postpartum. Offspring were exposed to the same treatment as their mothers from weaning to adulthood.
A50-pregnant rats gained less weight, showed increased testosterone and estradiol but pregnancy was unaffected. After lactation, arsenic-exposed dams presented compromised cyclicity, decreased estradiol, increased follicle-stimulating hormone (FSH), less preovulatory follicles and presence of ovarian cysts, suggesting impaired reproduction. A50-offspring presented lower body weight; A50-female-offspring showed elevated gonadotropin releasing hormone (GnRH), FSH and testosterone, while A50-males showed diminished GnRH/FSH, but normal testosterone.
We conclude that arsenite at the present exposure levels did not compromise pregnancy outcome while it negatively affected reproductive physiology in postpartum dams and their offspring. |
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ISSN: | 0890-6238 1873-1708 |
DOI: | 10.1016/j.reprotox.2017.01.002 |