Ovarian dysfunction after ischemia-reperfusion of the ovarian blood vessel in experimental rats

K. Nariai, R. Fukumoto, Shin Onota, Ken Watanabe, H. Uchiyama, K. Kanayama, Kahei Sato
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Abstract

Excessive production of reactive oxygen species (ROS) lead to oxidative stress in tissue or organ dysfunction. To confirm ovarian dysfunction by ROS, ischemia-reperfusion (I/R) treatment of the ovarian blood vessels was performed using experimental rats in this study. Preventive effect of superoxide dismutase (SOD) as a radical scavenger against ovarian I/R injury was also examined. Hormonal sensitivities to equine chorionic gonadotropin (eCG) and human chorionic gonadotropin (hCG) in the ovary decreased after the I/R. Ovarian tissue and ovum destruction were also observed. These changes could be prevented by SOD administration. Our data suggest that I/R injury related to ROS production causes ovarian dysfunction. The dysfunction is prevented by administration of a radical scavenger.
实验大鼠卵巢血管缺血再灌注后的卵巢功能障碍
活性氧(ROS)的过量产生导致组织或器官的氧化应激功能障碍。为了证实ROS对卵巢功能障碍的影响,本研究采用实验大鼠对卵巢血管进行缺血再灌注(I/R)处理。研究了超氧化物歧化酶(SOD)作为自由基清除剂对卵巢I/R损伤的预防作用。卵巢对马绒毛膜促性腺激素(eCG)和人绒毛膜促性腺激素(hCG)的激素敏感性在I/R后下降。卵巢组织和卵子也被破坏。这些变化可以通过SOD来预防。我们的数据表明,与ROS产生相关的I/R损伤导致卵巢功能障碍。这种功能障碍可以通过使用根治性清除剂来预防。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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