Reproductive tract infection, inflammation and male infertility (original) (raw)
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Role of oxidative stress, infection and inflammation in male infertility
Andrologia, 2018
Oxidative stress (OS), defined as an overabundance of reactive oxygen species (ROS) or a deficiency of antioxidants, has been linked to sperm damage and male infertility. There are many sources of OS and inflammation including varicocele, tobacco usage, alcohol, obesity/metabolic syndrome, leukocytospermia, sexually transmitted disease (i.e., Neisseria gonorrhoeae, Chlamydia trachomatis, Treponema pallidum), bacterial prostatitis, microorganism mutations leading to more OS, and viral infections (i.e., human immunodeficiency virus, hepatitis). This review is focusing on infection and inflammation-mediated OS, the inflammatory markers underlying pathology, clinical significance in male infertility, and a brief description of the recommended treatment modalities.
Oxidative Stress, Testicular Inflammatory Pathways and Male Reproduction
International Journal of Molecular Sciences
Inflammation is among the core causatives of male infertility. Despite male infertility being a serious global issue, “bits and pieces” of its complex etiopathology still remain missing. During inflammation, levels of proinflammatory mediators in the male reproductive tract are greater than usual. According to epidemiological research, in numerous cases of male infertility, patients suffer from acute or chronic inflammation of the genitourinary tract which typically occurs without symptoms. Inflammatory responses in the male genital system are inextricably linked to oxidative stress (OS). OS is detrimental to male fertility parameters as it causes oxidative damage to reproductive cells and intracellular components. Multifarious male infertility causative factors pave the way for impairing male reproductive functions via the common mechanisms of OS and inflammation, both of which are interlinked pathophysiological processes, and the occurrence of any one of them induces the other. Bo...
Impact of Inflammation on Male Reproductive Tract
Fertility in the male is dependent on the proper production of sperm cells. This process , called spermatogenesis is very complex and involves the synchronization of numerous factors. The presence of pro–inflammatory cytokines, tumor necrosis factor alpha (TNF–α), interleukin–1 alpha (IL–1 α) and interleukin 1 beta (IL–1 β) cy-tokines in the male reproductive tract (testis, epididymis and sperm) may have certain physiological functions. However, when the levels of these cytokines are higher than normal, as seen in conditions of inflammation, they become very harmful to sperm production. Moreover, inflammation is also associated with oxidative stress and the latter is well known to impair sperm function. Epidemiological studies regarding male infertility have revealed that more and more infertile men suffer from acute or chronic inflammation of the genitourinary tract, which often occurs without any symptoms. The inflammatory reactions within the male genital tract are inevitably connected with oxidative stress. Oxidative stress, especially in sperm, is harmful because it damages sperm DNA and causes apoptosis in sperm. This article reviewed the suggested mechanisms and contribution of inflammation to male infertility. In addition, the review was further strengthened by discussing how inflammation affects both fertility and assisted reproductive technologies (ART).
Role of leucocytes in reproductive tract infections and male infertility
Chemical Biology Letters, 2020
Oxidative stress (OS), occurring as a result of redox imbalance, have been considered a leading cause of male infertility. Redox imbalance is mediated by excessive production of reactive oxygen species (ROS) exceeding the antioxidant capacity. In seminal plasma, the main contributor of ROS are the infiltrated and resident leukocytes, although modest seminal levels of ROS are always maintained by spermatozoa and other testicular cells. Leukocytes are common constituents of seminal plasma even in healthy and fertile men. However, it has been suggested that during an inflammatory process the number of seminal leucocytes increases and activated leading to leukocytospermia. It is usually associated with reproductive tract infections, and subsequently, its impact on male infertility should not be overlooked. In such condition, leukocyte mediated ROS production and induction of OS can significantly deteriorate sperm morphology and functions through lipid peroxidation. This chain of oxidative damage disrupts the sperm membrane, intracellular components, as well as damages sperm nuclear and mitochondrial DNA. These may account for reduced semen quality and lead to male infertility, although further detailed interventions are needed to draw conclusive remark on the association of seminal leukocytes with male infertility. Thus, the present review article aims to provide a precise overview of the exact roles and sources of seminal leukocytes, the mechanism by which they operate during an inflammatory and healthy microenvironment and their association with male infertility.
The mechanisms by which Oxidative Stress and Free Radical Damage produces Male infertility
In a healthy body, ROS (reactive oxygen species) and antioxidants remain in balance. When the balance is disrupted towards an overabundance of ROS, oxidative stress (OS) occurs. OS results from an imbalance between prooxidants (free radical species) and the body's scavenging ability (antioxidants). ROS are a double-edged swordthey serve as key signal molecules in physiological processes but also have a role in pathological processes. The production of ROS is a normal physiological event in various organs including the testis. Overproduction of ROS can be detrimental to sperm and being associated with male infertilities. The excessive generation of ROS by abnormal spermatozoa, contaminating leukocytes and by a various type of pollutants has been identified as detrimental etiologies for male infertilities Free radicals are substances with one or more unpaired electrons, which are formed as a results of many physiological and pathological cellular metabolic processes, especially in mitochondria. Enzymatic (Catalase, superoxide dismutase) and non enzymatic (vitamins A and E) natural antioxidant defense mechanisms exist; however, these mechanisms may be overcome, causing lipid peroxidation to take place. For example, breakdown in the cells results in the formation of molecules whose further metabolism in the cell leads to ROS production. Thus increased OS stimulates the activity of enzymes called cytochrome P450, which contribute to ROS production. . Oxidative stress index (OSI) was calculated as ([TOS/TAS] x 100). TOS and OSI were significantly higher and PON-1 activity and TAS were significantly lower in subfertile male with abnormal semen parameters than in male with idiopathic subfertility and fertile donors. PON-1 activity was also strongly correlated with sperm concentration, motility, and morphology in the overall group. The receiver operating characteristic curve analysis revealed a high diagnostic value for PON-1 activity with respect to male-factor sub fertility. ROS may cause infertility by two principal mechanisms, first ROS damage the sperm membrane which in turn reduces the sperm motility and ability to fuse with the oocyte secondly, and ROS directly damage sperm DNA, compromising the paternal genomic contribution to the embryo. Oxidative stress due to excessive production of ROS, impaired antioxidant defense mechanisms, or both precipitates a range of pathologies that are currently believed to negatively affect the male reproductive function. Oxidative stress-induced damage to sperm may be mediated by lipid peroxidation of the sperm plasma membrane, reduction of sperm motility, and damage to the DNA in the sperm nucleus, as the production of ROS is one of the principal mechanisms by which neutrophils destroy pathogens, it is not surprising that seminal leukocytes have the potential to cause oxidative stress. Despite the established role of OS in the pathogenesis of male infertility, there is a lack of consensus as to the clinical utility of seminal OS testing in an infertility clinic. One important reason for the inability to utilize the OS test in clinical practice is related to the lack of a standard protocol for assessment of seminal OS. Antioxidants are powerful and there are few trials investigating antioxidant supplementation in male reproduction. Several researches indicate that the diagnostic and prognostic capabilities of the seminal OS test are beyond those of conventional tests of sperm quality and function. The OS test can accurately discriminate between fertile and infertile male and identify male with a clinical diagnosis of male-factor infertility that are likely to initiate a pregnancy when followed over a period of time. We strongly believe that incorporating such a test into the routine andrology workup is an important step for the future of the male infertility practice. The resulting state of the cell, known as (OS) can lead to cell injury. ROS production and Lipid peroxidation, free radical and oxidative stress in relation to fertility are the aim of this review [Magda M El-Tohamy. The mechanisms by which Oxidative Stress and Free Radical Damage produces Male infertility.
Reactive Oxygen Species in Seminal Plasma as a Cause of Male Infertility
Journal of gynecology obstetrics and human reproduction, 2018
Male factor is responsible for 40-50% of infertility cases, contributing equally as a female factor. Oxidative stress has now emerged as one of the major causes of unexplained male infertility, as it leads to increased risk of Deoxyribonucleic acid (DNA) fragmentation, decreased sperm motility, concentration and abnormal morphology. Though a certain amount of reactive oxygen species (ROS) activity is essential for normal functioning of sperms, an excess lead to pathological effects on semen parameters, ultimately resulting in male sub-fertility or infertility. Furthermore, oxidative stress affected sperm cells with damaged DNA result in increased risk of birth defects, neuropsychiatric problems and cancers in off-springs of such fathers due to increased risk of de-novo mutations in the germline and post-fertilization. Hence, present review helps in highlighting the facts about ROS, their production, physiological functions and pathological effects on sperm dysfunction and DNA damage...
Journal of Personalized Medicine
Oxidative and inflammatory damage underlie several conditions related to male infertility, including varicocele. Free light chains of immunoglobulins (FLCs) are considered markers of low-grade inflammation in numerous diseases. Coenzyme Q10 (CoQ10), a lipidic antioxidant and anti-inflammatory compound, is involved in spermatozoa energy metabolism and motility. We aimed to evaluate FLCs’ seminal levels in patients with varicocele in comparison to control subjects and to correlate them with CoQ10 and Total Antioxidant Capacity (TAC) in human semen. Sixty-five patients were enrolled. Semen analysis was performed; patients were divided into three groups: controls, 12 normozoospermic patients, aged 34 (33–41) years; varicocele (VAR), 29 patients, aged 33 (26–37) years; and idiopathic, 24 oligo-, astheno- and oligoasthenozoospermic patients aged 37 (33.5–40.5) years. FLCs (κ and λ) were assayed by turbidimetric method; CoQ10 by HPLC; TAC by spectrophotometric method. λ FLCs showed a trend...
Male Infertility: Pathogenetic Significance of Oxidative Stress and Antioxidant Defence (Review)
Scientific Horizons
The basis of the pathogenesis of male infertility is the processes of peroxide oxidation of biological substrates, especially lipids and proteins. By destroying the sperm membrane, toxic peroxidation products reduce its motility and ability to fertilize the egg, which is determined by a decrease in the number of motile sperm in the ejaculate. These changes lead to complete or partial male infertility. The authors of the review found that is accompanied by a damaging effect on the structural and functional activity of the gonads and is manifested, in particular, by an imbalance in the hormonal background of the male body. Similar effects are characteristic of an increase in the content of reactive Nitrogen species and its metabolites, which cause nitrosative stress, which is also the cause of male hypofertility and is inseparable from the state of oxidative stress. In scientific work it is determined that the accumulation of harmful peroxidation products leads to damage and destructi...