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Effect of Chronic Ethanol Exposure on Female Rat Reproductive Cyclicity and Hormone Secretion
Author(s) -
Emanuele N. V.,
LaPaglia N.,
Steiner J.,
Kirsteins L.,
Emanuele M. A.
Publication year - 2001
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.2001.tb02312.x
Subject(s) - estrous cycle , medicine , endocrinology , estrogen , hormone , ethanol , biology , biochemistry
Background : Ethanol exposure impairs mammalian reproductive function. However, the mechanisms are not fully understood. Methods: Adult female rats were given an ethanol or a calorically matched control diet. A third group was given a liquid nonethanol diet. Half the animals 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 disruption was prolongation of diestrous, with an increased time interval between proestrous surges. In four ethanol‐fed rats, there was complete cessation of the estrous cycle. However, ethanol did not decrease ovarian or uterine weight. 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 ethanol exposure was disruption of the estrous regularity, leading to a decreased number of proestrous surges. Part of the mechanism of this disruption might be a transient estrogen increase or a decrease in circulating insulin‐like growth factor.