Numerous studies have revealed that hypobaric hypoxia exposure elicited imbalance of homeostasis. However, the effects of intermittent hypobaric hypoxia (IHH) exposure on the female reproductive system have been rarely reported. This study aims to assess the effects of IHH on rat female reproductive system and explore the corresponding mechanism at the histological, endocrine and molecular levels.

The female rats were randomly divided into control and IHH groups. Multiple pathophysiological parameters, including body weight gain, organ coefficients, estrus cycle, and health signs were measured. Also, the reproductive hormones, hormone receptor mRNA expression and oxidant/antioxidant level were evaluated.

Significant increases of the heart, liver and lung coefficients were observed after IHH exposure. There were no statistically significant differences in ovarian and uterine coefficients, but changes were found in the morphology of the ovary and uterus. Additionally, the diestrus phase duration was significantly increased during IHH exposure. Furthermore, estrogen increased and the Luteinizing hormone and progesterone decreased after IHH exposure. Altered expression of ER, PR and LHR were also found in the IHH exposed rats. Importantly, IHH exposure significantly repressed the activities of GSH-Px and T-SOD and improved the contents of MDA.

Our results evince that IHH exposure caused estrus cycle irregularity. IHH induced oxidative stress along with ovarian and uterine structure damages, reproductive hormone disturbances and unusual expression of hormone receptors, thus suggesting a potential mechanism underlying IHH-induced reproductive system dysfunction.