Abstract
Spermatozoon is a cell with a precious message to deliver: the paternal DNA. Its motility machinery must be working perfectly and it should be able to acquire fertilizing ability in order to accomplish this mission. Infertility touches 1 in 6 couples worldwide and in half of the cases the causes can be traced to men. A variety of conditions such as infections of the male genital tract, varicocele, drugs, environmental factors, diseases, smoking, etc., are associated with male infertility and a common feature among them is the oxidative stress in semen that occurs when reactive oxygen species (ROS) are produced at high levels and/or when the antioxidant systems are decreased in the seminal plasma and/or spermatozoa. ROS-dependent damage targets proteins, lipids, and DNA, thus compromising sperm function and survival. Elevated ROS in spermatozoa are associated with DNA damage and decreased motility. Paradoxically, ROS, at very low levels, regulate sperm activation for fertilization. Therefore, the regulation of redox signaling in the male reproductive tract is essential for fertility. Peroxiredoxins (PRDXs) play a central role in redox signaling being both antioxidant enzymes and modulators of ROS action and are essential for pathological and physiological events. Recent studies from our lab emphasize the importance of PRDXs in the protection of spermatozoa as infertile men have significant low levels of PRDXs in semen and with little enzymatic activity available for ROS scavenging. The relationships between sperm DNA damage, motility and lipid peroxidation and high levels of thiol-oxidized PRDXs suggest the enhanced susceptibility of spermatozoa to oxidative stress and further support the importance of PRDXs in human sperm physiology. This review aims to characterize PRDXs, hidden players of the sperm antioxidant system and highlight the central role of PRDXs isoforms in the protection against oxidative stress to assure a proper function and DNA integrity of human spermatozoa.
Highlights
Infertility is an important human health problem that affects ~15% of couples worldwide and the underlying cause in half of these cases can be traced to men [1]
In somatic cells, elevated levels of reactive oxygen species (ROS) are prevented by the presence of a complex enzymatic antioxidant system involving superoxide dismutase (SOD) that removes O2− and catalase (CAT; restricted to peroxisomes), glutathione peroxidases (GPXs) and peroxiredoxins (PRDXs) that remove
31 kDa [84]; the p27 form is found in the plasma membrane, cytosol and acrosome of human spermatozoa, whereas p31 is found in the head fraction, in the acrosome (Figure 2, Table 1) [85]
Summary
Infertility is an important human health problem that affects ~15% of couples worldwide and the underlying cause in half of these cases can be traced to men [1]. The antioxidant system present in semen [21,22] is not sufficient to protect sperm from ROS-dependent damage such as peroxidation of membrane lipids [23], DNA fragmentation and oxidation of bases [24,25], low mitochondrial membrane potential [26,27] and inactivation of enzymes associated with motility [28,29]. These inhibitors are removed from the spermatozoa to allow a rise of ROS that will trigger the phosphorylation events that ultimate will allow the spermatozoon to achieve the capacitated state [48,49,50] It is not known how the spermatozoon controls the levels of ROS to avoid the production of an excess of this reactive substances and promoting toxicity. PRDX4 is present in testis as two isoforms of 27
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