The role of oxidative stress and antioxidants in male fertility

Abstract

Oxidative stress results from the imbalance between production of the reactive oxygen species (ROS) and the protective effect of the antioxidant system responsible for their neutralization and removal. An excess of ROS causes a pathological reaction resulting in damage to cells and tissues. Spermatozoa are particularly vulnerable to the harmful effects of ROS. Oxidative stress affects their activity, damages DNA structure, and accelerates apoptosis, all of which consequently decrease their numbers, hinders motility and development of normal morphology, and impairs function. This leads to disturbances in fertility or embryo development disorder. The main cellular source of ROS in the semen are immature sperm cells and white blood cells. The increase in the number of leukocytes may be due to infection and inflammation, but can also be secondary to harmful environmental factors, long sexual abstinence, or varicocele. The protective antioxidant system in the semen is composed of enzymes, as well as nonenzymatic substances, which closely interact with each other to ensure optimal protection against ROS. Non–enzymatic antioxidants include vitamins A, E, C, and B complex, glutathione, pantothenic acid, coenzyme Q10 and carnitine, and micronutrients such as zinc, selenium, and copper. It seems that a deficiency of any of them can cause a decrease in total antioxidant status. In vitro and in vivo that studies demonstrate many antioxidants possess a beneficial effect on fertility and, therefore, their use is recommended as supportive therapy for the treatment of infertility in men.

Role of Antioxidants in the Treatment of Male Infertility

“…), and micronutrients (Selenium, Zinc, & Copper) which interact each other to ensure an optimal protection against the oxidative stress. A deficiency of one of them may result in a decrease of total plasma antioxidant capacity [18]. The main antioxidants will be discussed below.…”

“…It is encoded by the SOD1 gene and it is mainly localized in the cytoplasm. The other intracellular form is manganese SOD (MnSOD) that acts in the mitochondrial matrix [18]. Its gene, SOD2, is inducible under various inflammatory conditions and the nuclear factor kappa B (NF-kB) appears to be the main factor responsible for its induction.…”

“…Under physiological conditions, catalase plays a role in the nitric oxide-induced sperm capacitation [18]. Its activity has been associated with low sperm quality [26].…”

“…GPXs protect sperm DNA from oxidative damage, playing a role in the chromatin condensation and mainly in the mitochondrial matrix [18]. GPX-defective expression in human spermatozoa has been reported to be associated with OAT [29].…”

“…GSH participates in preserving the intracellular milieu in a reduced state and, in addition, it is an electron donator to GPX. GSH displays its antioxidant activity by the reconstruction of thiol groups (-SH) in proteins and preventing cell membrane from lipid oxidation [18].…”