55
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Role of reactive oxygen species in the pathophysiology of human reproduction

      , ,
      Fertility and Sterility
      Elsevier BV

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          To summarize the role of reactive oxygen species (ROS) in the pathophysiology of human reproduction. Review of literature. Fertility research center and obstetrics and gynecology department in a tertiary care facility. ROS plays an essential role in the pathogenesis of many reproductive processes. In male-factor infertility. oxidative stress attacks the fluidity of the sperm plasma membrane and the integrity of DNA in the sperm nucleus. Reactive oxygen species induced DNA damage may accelerate the process of germ cell apoptosis, leading to the decline in sperm counts associated with male infertility. ROS mediated female fertility disorders share many pathogenic similarities with the ones on the male side. These similarities include a potential role in the pathophysiology of endometriosis and unexplained infertility. High follicular fluid ROS levels are associated with negative IVF outcomes, particularly in smokers. Moreover, oxidative stress may be responsible in hydrosalpingeal fluid mediated embryotoxicity as well as poor in vitro embryonic development. High levels of ROS are detrimental to the fertility potential both in natural and assisted conception states.

          Related collections

          Author and article information

          Journal
          Fertility and Sterility
          Fertility and Sterility
          Elsevier BV
          00150282
          April 2003
          April 2003
          : 79
          : 4
          : 829-843
          Article
          10.1016/S0015-0282(02)04948-8
          12749418
          ebd0d76b-964d-483b-bcca-3d42b4b719bf
          © 2003

          https://www.elsevier.com/tdm/userlicense/1.0/

          History

          Comments

          Comment on this article