The Effect Of Intrauterine Hypoxia On Testicular Reproductive Function

• Published in: Russian open medical journal Vol. 10; no. 2
• Main Authors: Palatova, Tatiana V., Bucharskaya, Alla B., Medvedeva, Anna V., Voronina, Elena S., Pakhomy, Svetlana S., Maslyakova, Galina N.
• Format: Journal Article
• Language: English
• Published: 01.06.2021
• ISSN: 2304-3415; 2304-3415
• DOI: 10.15275/rusomj.2021.0204

Goal — to assess the effect of antenatal hypoxia of various origins on the morphology and reproductive function of the testes of newborn and mature rats in experiment. Material and Methods — In experiments 15 white outbred female rats aged 4 to 10 months with a weight of 200±30 g were used. Laboratory animals were randomly divided into 2 experimental and 1 control groups, 5 females each. The first group underwent normobaric hypoxia throughout pregnancy (21 days). Hypoxia modeling was conducted in accordance with the method of N.N. Karkishchenko (2010). The second group underwent hemic hypoxia during the second and third week of pregnancy, in accordance with the method of L.M. Sosedova (2012). The third (control) group was not exposed to any effect throughout pregnancy. Results — in the testicles of newborn rats of the experimental groups, the decrease of tubule diameter was observed, the increase of stroma area and development of interstitial edema were noted. In the group of hemic hypoxia, a significant decrease in the number of Leydig cells was noted. In the tissues of the testicles of mature rats, who underwent antenatal hypoxia, a decrease of tubule diameter, a significant decrease in the spermatogenesis index and a decrease of spermatogonia number were noted. The developed damage of spermatogenic epithelium in experimental groups of newborns and mature rats was confirmed by marked expression of the apoptosis marker (Bax), weak expression of proliferation markers (Ki-67) and receptor of receptor of fibroblast growth factor (FGFR). Conclusion — in animals with chronic hypoxia of various origins, there is an inhibition of spermatogenesis and a violation of the spermatogenetic function of the testicular seminiferous tubules.