Previous studies have shown that prenatal ethanol exposure can partially masculinize or defeminize neurobehavioral development of female rats. An early age of onset of anovulation is one of the primary characteristics of partial defeminization. Consequently, we examined the occurrence of anovulation in fetal alcohol-exposed (FAE) female rats at 2, 6, and 12 months of age using both vaginal cytology as well as wheel-running behavior. We assessed the ability of estrogen and progesterone to elicit proprioceptive behaviors and lordosis at 2 and 17 months of age. Female subjects were derived from Sprague-Dawley dams administered an ethanol liquid diet (35% ethanol-derived calories), a pair-fed isocaloric liquid diet, or fed lab chow from days 14 to 22 of gestation. Litter representatives were placed in a computer-monitored wheel-running apparatus under a 12-hr lighting schedule from 49 to 60 days of age. Vaginal smears were taken from littermates during this same period. This same procedure was conducted again from 180 to 196 and from 380 to 396 days of age, except that vaginal cytology was examined in the same animals immediately after wheel-running behavior was studied. At approximately 2 months of age, a normal cyclical pattern of wheel-running, characteristic of 4- to 5-day estrus cycles, was observed in all animals. No differences were detected in mean activity levels during the wheel-running period. This was accompanied by normal cyclic vaginal cytology and normal proprioceptive behaviors and lordosis. At 6 months of age, FAE females exhibited significantly reduced wheel-running.(ABSTRACT TRUNCATED AT 250 WORDS)
Pregnant T-O mice were exposed to 50 ATA He-O2 pressure for 4 days at different stages of gestation: 4-7, 6-9, and 9-12 days gestation. Controls were exposed to 1 atmosphere absolute (ATA) air. After the exposure period, pregnancy continued until 18 days gestation when the mice were killed and autopsied. Data were collected relating to the litters and placentas (Litter size, percent resorptions, placental weight, fetal-to-placental ratio) and fetuses (weight, crown-rump length, sex, skeletal abnormalities) and analyzed using analysis of variance. Results showed a small but significant increase in the percent resorptions in the pressure group and also a decrease in crown-rump length and placental weight. None of these changes were related to the stage of gestation in which the mice were exposed. No teratogenic effects of pressure were seen. We conclude that exposure to 50 ATA He-O2 during pregnancy in mice produces a small nonselective effect on fetal growth and development but does not affect any specific event taking place during these stages of embryogenesis.
Objective: To investigate the association between duration of ovarian torsion and levels of serum inhibin B in an animal model. Materials and Methods: An animal model prospective study was conducted in a tertiary referral hospital and chemical pathology institute. Nineteen female Lewis rats were divided to four groups. In the first group, the control group, laparotomies alone were performed. In groups 2-4 laparotomies and right ovarian torsion for 720 degrees with fixation of the adnexa to the parietal peritoneum were performed. Blood samples were taken from the rat groups at 12, 24, and 36 hours after laparotomy. Inhibin B levels were measured by ELISA. Results: Serum mean ± SD inhibin B level in the control rats during the beginning of the metesterus, 12, 24, and 36 hours later were 108.4 ± 43.6, 129.5 ± 49.3, 99.07 ± 60.50, and 91.58 ± 27.74 pg/ml, respectively. Inhibin B levels in the control group increased 12 hours after the beginning of the metesterus, whereas in the study group, a decline in inhibin B levels was found at the same time. This difference was significant (p = 0.05). Inhibin B levels at 24 and 36 hours from the beginning of the metestrus did not show statistical difference. Conclusions: Unilateral ovarian torsion in rats changed the pattern of inhibin B secretion at the beginning of the metesterus and was associated with a significant decrease in inhibin B serum levels. This observation, following acute ovarian vascular occlusion, is probably due the effects of ischemia on hormonal regulation during the early follicular phase.
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