Effect of chronic ethanol exposure on female rat reproductive cyclicity and hormone secretion

Citation
Nv. Emanuele et al., Effect of chronic ethanol exposure on female rat reproductive cyclicity and hormone secretion, ALC CLIN EX, 25(7), 2001, pp. 1025-1029
Citations number
22
Categorie Soggetti
Clinical Psycology & Psychiatry","Neurosciences & Behavoir
Journal title
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
ISSN journal
01456008 → ACNP
Volume
25
Issue
7
Year of publication
2001
Pages
1025 - 1029
Database
ISI
SICI code
0145-6008(200107)25:7<1025:EOCEEO>2.0.ZU;2-J
Abstract
Background: Ethanol exposure impairs mammalian reproductive function. Howev er, the mechanisms are not fully understood. Methods: Adult female rats were given an ethanol or a calorically matched c ontrol diet. A third group was given a liquid nonethanol diet. Half the ani mals were killed at 2 weeks (short chronic) and the other half at 2 months (long chronic), all on the day of proestrous on the basis of daily vaginal smears. Results: The major effect of ethanol feeding was disruption in the estrous cycle. Although all of the pair-fed animals continued to cycle, 40% of the ethanol rats in the short chronic study had disruption of their cycles. In the long chronic study, 83% of the ethanol animals had abnormal cycling, in contrast to 16% of the pair-fed controls. The nature of the cycle disrupti on was prolongation of diestrous, with an increased time interval between p roestrous surges. In four ethanol-fed rats, there was complete cessation of the estrous cycle. However, ethanol did not decrease ovarian or uterine we ight. Ethanol significantly increased serum estradiol in the short chronic but not long chronic study, whereas progesterone was unchanged. Ethanol did cause a significant reduction in circulating insulin-like growth factor. Conclusions: The major effect of both short chronic and long chronic ethano l exposure was disruption of the estrous regularity, leading to a decreased number of proestrous surges. Part of the mechanism of this disruption migh t be a transient estrogen increase or a decrease in circulating insulin-lik e growth factor.