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      Effect of Oxidative Stress on Male Reproduction

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          Infertility affects approximately 15% of couples trying to conceive, and a male factor contributes to roughly half of these cases. Oxidative stress (OS) has been identified as one of the many mediators of male infertility by causing sperm dysfunction. OS is a state related to increased cellular damage triggered by oxygen and oxygen-derived free radicals known as reactive oxygen species (ROS). During this process, augmented production of ROS overwhelms the body's antioxidant defenses. While small amounts of ROS are required for normal sperm functioning, disproportionate levels can negatively impact the quality of spermatozoa and impair their overall fertilizing capacity. OS has been identified as an area of great attention because ROS and their metabolites can attack DNA, lipids, and proteins; alter enzymatic systems; produce irreparable alterations; cause cell death; and ultimately, lead to a decline in the semen parameters associated with male infertility. This review highlights the mechanisms of ROS production, the physiological and pathophysiological roles of ROS in relation to the male reproductive system, and recent advances in diagnostic methods; it also explores the benefits of using antioxidants in a clinical setting.

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          Strategies of antioxidant defense.

           H Sies (1993)
          Cellular protection against the deleterious effects of reactive oxidants generated in aerobic metabolism, called oxidative stress, is organized at multiple levels. Defense strategies include three levels of protection; prevention, interception, and repair. Regulation of the antioxidant capacity includes the maintenance of adequate levels of antioxidant and the localization of antioxidant compounds and enzymes. Short-term and long-term adaptation and cell specialisation in these functions are new areas of interest. Control over the activity of prooxidant enzymes, such as NADPH oxidase and NO synthases, is crucial. Synthetic antioxidants mimic biological strategies.
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            Role of reactive oxygen species in the pathophysiology of human reproduction.

            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.
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              Clinical relevance of oxidative stress in male factor infertility: an update.

              Male factor has been considered a major contributory factor to infertility. Along with the conventional causes for male infertility such as varicocele, cryptorchidism, infections, obstructive lesions, cystic fibrosis, trauma, and tumors, a new, yet important cause has been identified: oxidative stress. Oxidative stress (OS) is a result of the imbalance between reactive oxygen species (ROS) and antioxidants in the body, which can lead to sperm damage, deformity and eventually male infertility. This involves peroxidative damage to sperm membrane and DNA fragmentation at both nuclear and mitochondrial levels. OS has been implicated as the major etiological factor leading to sperm DNA damage. OS-induced DNA damage can lead to abnormalities in the offspring including childhood cancer and achondroplasia. In this article, we discuss the need of ROS in normal sperm physiology, the mechanism of production of ROS and its pathophysiology in relation to male reproductive system. The benefits of incorporating antioxidants in clinical and experimental settings have been enumerated. We also highlight the emerging concept of utilizing OS as a method of contraception and the potential problems associated with it.

                Author and article information

                World J Mens Health
                World J Mens Health
                The World Journal of Men's Health
                Korean Society for Sexual Medicine and Andrology
                April 2014
                25 April 2014
                : 32
                : 1
                : 1-17
                [1 ]Center for Reproductive Medicine, Cleveland Clinic, Cleveland, OH, USA.
                [2 ]Medical Physiology, Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg, South Africa.
                Author notes
                Correspondence to: Ashok Agarwal. Center for Reproductive Medicine & Andrology Center, Glickm an U rological and Kidney Institute, Cleveland Clinic, Desk X11, 10681 Carnegie Avenue, Cleveland, Ohio 44195, USA. Tel: +1-216-444-9485, Fax: +1-216-445-6049, agarwaa@
                Copyright © 2014 Korean Society for Sexual Medicine and Andrology

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Funded by: The Center for Reproductive Medicine, Glickman Urological & Kidney Institute, Cleveland Clinic (Cleveland, OH, USA)
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