Fessional phagocytes, such as LixisenatideMedChemExpress Lixisenatide neutrophils, contain NADPHoxidase that generates huge amounts of superoxide for microbicidal purposes. Nitrogen oxide species (RNOS) are mainly derived from nitric oxide (NO) and also play various roles in reproductive organs [6]. Nitric oxide synthase (NOS), which is encoded by three different genes, NOS I, NOS II, and NOSAntioxide/redox systemMany low molecular weight antioxidants, such as antioxidative vitamins and polyphenols, are ordinarily present in nutrients. Although ROS are scavenged by these compounds, enzymatic detoxification is more efficient [1]. The following major antioxidative enzymes are present in our body.Superoxide dismutase (SOD) The superoxide anion is produced by a one-electron reduction of an oxygen molecule and initiates a radical chain reaction. It is believed that SOD, which dismutates the superoxide anion to hydrogen peroxide, plays a central part in antioxidative reactions. Three isozymes are produced by mammalians.SOD1 encodes Cu,Zn-SOD that contains Cu and Zn as metal cofactors and is largely cytosolic, while SOD2encoding Mn-SOD is a mitochondrial isoform containing Mn. SOD3, which encodes the extracellular form (ECSOD), is structurally similar to CuZn-SOD, and also contains Cu and Zn as metal cofactors. Since a mutation in SOD1 causes amyotrophic lateral sclerosis, extensive studies have been carried out in neuronal cells. One of thePage 2 of2005, :http://www.rbej.com/content/3/1/striking phenotypes of SOD1-deficient mice is female infertility and this is discussed below. Mn-SOD is a mitochondrial isoform but its gene, SOD2, is encoded by nuclear DNA. SOD2 is inducible under various oxidative stress and inflammatory conditions and, hence, the regulatory mechanism of the gene has been a subject of extensive study. Homozygous SOD2-deficient mice suffer severe cardiovascular damage and die soon after birth [8]. Although no PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/25636517 abnormality in the genital tract has been reported for heterozygous mice, transgenic male mice that express higher levels of Mn-SOD are infertile but the mechanism for this is unknown [9]. EC-SOD is present at high levels in the epididymis as well as the lung [10]. EC-SOD is also localized in the nuclei in the seminiferous tubules of the testis [11]. Superoxide decreases levels of NO by converting it to peroxinitrite. Thus, scavenging superoxide in vasculature extends the half-life of nitric oxide (NO), which results in an increase in cGMP levels. It is probable that elevated levels of cGMP relax vascular smooth muscle and supports erectile responses. Erectile function is improved by transferring the SOD3 gene to the penis in aged rats [12]. However, no recognizable phenotype in the reproductive system has yet been reported in SOD3 knockout mice [13].Peroxidases Glutathione peroxidase (GPx) plays a central role in the detoxification of peroxides using the reduced form of glutathione (GSH) as an electron donor. Many enzymes that are classified into different family of proteins exhibit GSH-dependent peroxidase activity. Conventional GPx contains selenocysteine (Sec) at its active center and appears to play a pivotal role in detoxification of peroxides. At least four selenium-containing GPx isozymes are produced in mammalians. The cytosolic form, GPX1, is widely distributed in tissues and has been the most extensively investigated form. However, GPX1-knockout mice show no abnormality in phenotype including reproductive capability [14]. GPX2 encodes a gastrointes.
