Affiliations 

  • 1 Reproductive Biotechnology Research Center, Avicenna Research Institute, Academic Center for Education, Culture and Research, Tehran, Iran
  • 2 American Center for Reproductive Medicine, Cleveland Clinic, Cleveland, Ohio, 44195, USA. [email protected]
  • 3 Department of Physiology, Faculty of Medicine, MAHSA University, Jalan SP2, Bandar Saujana Putra, 42610, Jenjarom, Selangor, Malaysia
  • 4 Department of Physiology, Faculty of Medicine, Universiti Teknologi MARA, Sungai Buloh Campus, Jalan Hospital, 47000, Sungai Buloh, Selangor, Malaysia
  • 5 Department of Medical Biosciences, University of the Western Cape, Bellville, Cape Town, 7535, South Africa
  • 6 Reproductive Immunology Research Center, Avicenna Research Institute, Academic Center for Education, Culture and Research, Tehran, Iran
Reprod Biol Endocrinol, 2018 Sep 11;16(1):87.
PMID: 30205828 DOI: 10.1186/s12958-018-0406-2

Abstract

Reports of the increasing incidence of male infertility paired with decreasing semen quality have triggered studies on the effects of lifestyle and environmental factors on the male reproductive potential. There are numerous exogenous and endogenous factors that are able to induce excessive production of reactive oxygen species (ROS) beyond that of cellular antioxidant capacity, thus causing oxidative stress. In turn, oxidative stress negatively affects male reproductive functions and may induce infertility either directly or indirectly by affecting the hypothalamus-pituitary-gonadal (HPG) axis and/or disrupting its crosstalk with other hormonal axes. This review discusses the important exogenous and endogenous factors leading to the generation of ROS in different parts of the male reproductive tract. It also highlights the negative impact of oxidative stress on the regulation and cross-talk between the reproductive hormones. It further describes the mechanism of ROS-induced derangement of male reproductive hormonal profiles that could ultimately lead to male infertility. An understanding of the disruptive effects of ROS on male reproductive hormones would encourage further investigations directed towards the prevention of ROS-mediated hormonal imbalances, which in turn could help in the management of male infertility.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.