scholarly journals Molecular Changes Induced by Oxidative Stress that Impair Human Sperm Motility

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 134 ◽  
Author(s):  
Karolina Nowicka-Bauer ◽  
Brett Nixon
Keyword(s):  
Oxidative Stress ◽  
Sperm Motility ◽  
Reproductive Tract ◽  
Therapeutic Interventions ◽  
Antioxidant Defenses ◽  
Ros Production ◽  
Paternal Genome ◽  
Male Reproductive Tract ◽  
Ability To Act ◽  
The Impact

A state of oxidative stress (OS) and the presence of reactive oxygen species (ROS) in the male reproductive tract are strongly correlated with infertility. While physiological levels of ROS are necessary for normal sperm functioning, elevated ROS production can overwhelm the cell’s limited antioxidant defenses leading to dysfunction and loss of fertilizing potential. Among the deleterious pleiotropic impacts arising from OS, sperm motility appears to be particularly vulnerable. Here, we present a mechanistic account for how OS contributes to altered sperm motility profiles. In our model, it is suggested that the abundant polyunsaturated fatty acids (PUFAs) residing in the sperm membrane serve to sensitize the male germ cell to ROS attack by virtue of their ability to act as substrates for lipid peroxidation (LPO) cascades. Upon initiation, LPO leads to dramatic remodeling of the composition and biophysical properties of sperm membranes and, in the case of the mitochondria, this manifests in a dissipation of membrane potential, electron leakage, increased ROS production and reduced capacity for energy production. This situation is exacerbated by the production of cytotoxic LPO byproducts such as 4-hydroxynonenal, which dysregulate molecules associated with sperm bioenergetic pathways as well as the structural and signaling components of the motility apparatus. The impact of ROS also extends to lesions in the paternal genome, as is commonly seen in the defective spermatozoa of asthenozoospermic males. Concluding, the presence of OS in the male reproductive tract is strongly and positively correlated with reduced sperm motility and fertilizing potential, thus providing a rational target for the development of new therapeutic interventions.

scholarly journals Male Infertility, Oxidative Stress and Antioxidants

2021 ◽  
Author(s):  
Vegim Zhaku ◽  
Ashok Agarwal ◽  
Sheqibe Beadini ◽  
Ralf Henkel ◽  
Renata Finelli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Male Infertility ◽  
Male Fertility ◽  
Reproductive Tract ◽  
Healthy Lifestyle ◽  
Free Radical Scavengers ◽  
Semen Parameters ◽  
Ros Production ◽  
Modus Operandi ◽  
Male Reproductive Tract

Within the male reproductive system, oxidative stress (OS) has been identified as prevailing etiology of male infertility. The effects of reactive oxygen species (ROS) on male fertility depend on the dimensions, “modus operandi” of the ROS and the oxido-reduction potential (ORP) of the male reproductive tract. Hereupon, for an adequate response to OS, the cells of our body are endowed with a well-sophisticated system of defense in order to be protected. Various antioxidant enzymes and small molecular free radical scavengers, maintain the delicate balance between oxidants and reductants (antioxidants), crucial to cellular function and fertility. Therapeutic use of antioxidants is an optimal and coherent option in terms of mitigating OS and improving semen parameters. Therefore, recognizing and managing OS through either decreasing ROS levels or by increasing antioxidant force, appear to be a requesting approach in the management of male infertility. However, a clear defined attitude of the experts about the clinical efficacy of antioxidant therapy is still deprived. Prominently, antioxidant such as coenzyme Q10, vitamin C and E, lycopene, carnitine, zinc and selenium have been found useful in controlling the balance between ROS production and scavenging activities. In spite of that, healthy lifestyle, without smoke and alcohol, everyday exercise, reduction of psychological stress and quality well-designed meals, are habits that can overturn male infertility.

scholarly journals Oxidative Stress, Testicular Inflammatory Pathways and Male Reproduction

2021 ◽  
Vol 22 (18) ◽  
pp. 10043
Author(s):  
Sulagna Dutta ◽  
Pallav Sengupta ◽  
Petr Slama ◽  
Shubhadeep Roychoudhury
Keyword(s):  
Oxidative Stress ◽  
Male Infertility ◽  
Reproductive Tract ◽  
Inflammatory Responses ◽  
Male Reproduction ◽  
Male Reproductive Tract ◽  
Proinflammatory Mediators ◽  
Global Issue ◽  
Causative Factors ◽  
Infertility Patients

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. Both processes may be simultaneously found in the pathogenesis of male infertility. Thus, the present article aims to explain the role of inflammation and OS in male infertility in detail, as well as to show the mechanistic pathways that link causative factors of male reproductive tract inflammation, OS induction, and oxidant-sensitive cellular cascades leading to male infertility.

scholarly journals Proteomics and metabolomics in cow fertility: a systematic review

Reproduction ◽  
2020 ◽  
Vol 160 (5) ◽  
pp. 639-658
Author(s):  
Nicolas Aranciaga ◽  
James D Morton ◽  
Debra K Berg ◽  
Jessica L Gathercole
Keyword(s):  
Oxidative Stress ◽  
Systematic Review ◽  
Large Scale ◽  
Reproductive Tract ◽  
Early Embryo ◽  
Female Reproductive Tract ◽  
Full Potential ◽  
Technical Standards ◽  
The Impact

Cow subfertility is a multi-factorial problem in many countries which is only starting to be unravelled. Molecular biology can provide a substantial source of insight into its causes and potential solutions, particularly through large scale, untargeted omics approaches. In this systematic review, we set out to compile, assess and integrate the latest proteomic and metabolomic research on cow reproduction, specifically that on the female reproductive tract and early embryo. We herein report a general improvement in technical standards throughout the temporal span examined; however, significant methodological limitations are also identified. We propose easily actionable avenues for ameliorating these shortcomings and enhancing the reach of this field. Text mining and pathway analysis corroborate the relevance of proteins and metabolites related to the triad oxidative stress-inflammation-disease on reproductive function. We envisage a breakthrough in cattle reproductive molecular research within the next few years as in vivo sample techniques are improved, omics analysis equipment becomes more affordable and widespread, and software tools for single- and multi-omics data processing are further developed. Additional investigation of the impact of local oxidative stress and inflammation on fertility, both at the local and systemic levels, is key towards realising the full potential of this field.

scholarly journals Zika virus in rhesus macaque semen and reproductive tract tissues: a pilot study of acute infection†

2020 ◽  
Vol 103 (5) ◽  
pp. 1030-1042 ◽  
Author(s):  
Jenna K Schmidt ◽  
Katherine D Mean ◽  
Riley C Puntney ◽  
Eric S Alexander ◽  
Ruth Sullivan ◽  
...  
Keyword(s):  
Pilot Study ◽  
Rhesus Macaque ◽  
Zika Virus ◽  
Reproductive Tract ◽  
Acute Infection ◽  
Viral Rna ◽  
Viral Reservoir ◽  
Computer Assisted ◽  
Male Reproductive Tract ◽  
The Impact

Abstract Although sexual transmission of Zika virus (ZIKV) is well-documented, the viral reservoir(s) in the male reproductive tract remains uncertain in humans and immune-intact animal models. We evaluated the presence of ZIKV in a rhesus macaque pilot study to determine persistence in semen, assess the impact of infection on sperm functional characteristics, and define the viral reservoir in the male reproductive tract. Five adult male rhesus monkeys were inoculated with 105 PFU of Asian-lineage ZIKV isolate PRVABC59, and two males were inoculated with the same dose of African-lineage ZIKV DAKAR41524. Viremia and viral RNA (vRNA) shedding in semen were monitored, and a cohort of animals were necropsied for tissue collection to assess tissue vRNA burden and histopathology. All animals exhibited viremia for limited periods (1–11 days); duration of shedding did not differ significantly between viral isolates. There were sporadic low levels of vRNA in the semen from some, but not all animals. Viral RNA levels in reproductive tract tissues were also modest and present in the epididymis in three of five cases, one case in the vas deferens, but not detected in testis, seminal vesicles or prostate. ZIKV infection did not impact semen motility parameters as assessed by computer-assisted sperm analysis. Despite some evidence of prolonged ZIKV RNA shedding in human semen and high tropism of ZIKV for male reproductive tract tissues in mice deficient in Type 1 interferon signaling, in the rhesus macaques assessed in this pilot study, we did not consistently find ZIKV RNA in the male reproductive tract.

scholarly journals Circulating Leukocytes and Oxidative Stress in Cardiovascular Diseases: A State of the Art

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Speranza Rubattu ◽  
Maurizio Forte ◽  
Salvatore Raffa
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Diseases ◽  
Stress Level ◽  
Mononuclear Cells ◽  
Pathological Condition ◽  
Clinical Manifestations ◽  
Therapeutic Interventions ◽  
Oxidative Stress Level ◽  
The Impact

Increased oxidative stress from both mitochondrial and cytosolic sources contributes to the development and the progression of cardiovascular diseases (CVDs), and it is a target of therapeutic interventions. The numerous efforts made over the last decades in order to develop tools able to monitor the oxidative stress level in patients affected by CVDs rely on the need to gain information on the disease state. However, this goal has not been satisfactorily accomplished until now. Among others, the isolation of circulating leukocytes to measure their oxidant level offers a valid, noninvasive challenge that has been tested in few pathological contexts, including hypertension, atherosclerosis and its clinical manifestations, and heart failure. Since leukocytes circulate in the blood stream, it is expected that they might reflect quite closely both systemic and cardiovascular oxidative stress and provide useful information on the pathological condition. The results of the studies discussed in the present review article are promising. They highlight the importance of measuring oxidative stress level in circulating mononuclear cells in different CVDs with a consistent correlation between degree of oxidative stress and severity of CVD and of its complications. Importantly, they also point to a double role of leukocytes, both as a marker of disease condition and as a direct contributor to disease progression. Finally, they show that the oxidative stress level of leukocytes reflects the impact of therapeutic interventions. It is likely that the isolation of leukocytes and the measurement of oxidative stress, once adequately developed, may represent an eligible tool for both research and clinical purposes to monitor the role of oxidative stress on the promotion and progression of CVDs, as well as the impact of therapies.

scholarly journals Chronic Kidney Disease and Disproportionally Increased Cardiovascular Damage: Does Oxidative Stress Explain the Burden?

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Anila Duni ◽  
Vassilios Liakopoulos ◽  
Karolos-Pavlos Rapsomanikis ◽  
Evangelia Dounousi
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Left Ventricular ◽  
Antioxidant Defenses ◽  
Pon1 Activity ◽  
Pathophysiological Mechanism ◽  
Ros Production ◽  
Cardiovascular Damage

Chronic kidney disease (CKD) patients are among the groups at the highest risk for cardiovascular disease and significantly shortened remaining lifespan. CKD enhances oxidative stress in the organism with ensuing cardiovascular damage. Oxidative stress in uremia is the consequence of higher reactive oxygen species (ROS) production, whereas attenuated clearance of pro-oxidant substances and impaired antioxidant defenses play a complementary role. The pathophysiological mechanism underlying the increased ROS production in CKD is at least partly mediated by upregulation of the intrarenal angiotensin system. Enhanced oxidative stress in the setting of the uremic milieu promotes enzymatic modification of circulating lipids and lipoproteins, protein carbamylation, endothelial dysfunction via disruption of nitric oxide (NO) pathways, and activation of inflammation, thus accelerating atherosclerosis. Left ventricular hypertrophy (LVH) and heart failure are hallmarks of CKD. NADPH oxidase activation, xanthine oxidase, mitochondrial dysfunction, and NO-ROS are the main oxidative pathways leading to LVH and the cardiorenal syndrome. Finally, a subset of antioxidant enzymes, the paraoxonases (PON), deserves special attention due to abundant clinical evidence accumulated regarding reduced serum PON1 activity in CKD as a contributor to the increased burden of cardiovascular disease. Future, meticulously designed studies are needed to assess the effects of antioxidant therapy on patients with CKD.

scholarly journals Gallic acid enhances reproductive function by modulating oxido-inflammatory and apoptosis mediators in rats exposed to aflatoxin-B1

2020 ◽  
Vol 245 (12) ◽  
pp. 1016-1028 ◽  
Author(s):  
Solomon E Owumi ◽  
Isaac A Adedara ◽  
Ayomide P Akomolafe ◽  
Ebenezer O Farombi ◽  
Adegboyega K Oyelere
Keyword(s):  
Oxidative Stress ◽  
Gallic Acid ◽  
Aflatoxin B1 ◽  
Reproductive Function ◽  
Interleukin 10 ◽  
Antioxidant Defenses ◽  
The Impact ◽  
Hormonal Levels

Aflatoxin B1 (AFB1) is reported to elicit adverse reproductive outcomes in animals. Gallic acid (GA) is known to exhibit antioxidant and inflammatory bioactivities. The impact of GA on AFB1-facilitated reproductive dysfunction is nonexistent in literature. This investigation elucidated GA protective effect on AFB1-induced reproductive toxicities in rats, exposed for 28 consecutive days to AFB1 (75 µg/kg), or co-treated with GA (20 or 40 mg/kg) body weight. AFB1 significantly (p  <  0.05) reduced testicular function biomarkers, serum hormonal levels, and functional sperm characteristics in experimental animals. GA abated AFB1-induced increases (p  <  0.05) in lipid peroxidation and reactive oxygen and nitrogen species, suppressed myeloperoxidase, interleukin-1β, nitric oxide, and tumor necrosis factor-α levels—inflammatory biomarkers—in testes, epididymis, and hypothalamus. Furthermore, GA improved antioxidant defenses and alleviated reduction in interleukin-10, caspase-3 activation, and histological variations in epididymis, testes, and hypothalamus of rats dosed with AFB1. Conclusively, GA enhanced reproductive function in AFB1-exposed rats by modulating inflammatory, oxidative stress, and apoptosis mediators. Impact statement Infertility resulting from reproductive deficiency can be stressful. Exposure to aflatoxin B1, a dietary mycotoxin prevalent in improperly stored grains, is reported to elicit reproductive insufficiencies and infertility. We, therefore, examined the likely beneficial effect of gallic acid (GA) a phytochemical, recognized to exhibit in vitro and in vivo pharmacological bioactivities against oxidative stress and related inflammatory damages in rats, since AFB1 toxicities are predicated on oxidative epoxide formation, in a bid to proffer new evidence to advance the field of nutriceutical application from plant-derived chemopreventive agents. Our findings will advance the field of chemoprevention by presenting data absent in the literature on GA. Our results demonstrate further evidence for GA conferred protection against AFB1-mediated histological lesions in testes, epididymis, and hypothalamus of treated rats; suppresses oxidative damages, relieved inflammatory and apoptotic responses, restored sperm functional characteristics, and hormonal levels relevant for reproductive integrity and function.

scholarly journals Cyclopentenone Prostaglandins as Potential Inducers of Intracellular Oxidative Stress

2001 ◽  
Vol 276 (15) ◽  
pp. 12076-12083 ◽  
Author(s):  
Mitsuhiro Kondo ◽  
Tomoko Oya-Ito ◽  
Takeshi Kumagai ◽  
Toshihiko Osawa ◽  
Koji Uchida
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Antioxidant Defenses ◽  
Ros Production ◽  
Cell Degeneration ◽  
Lipid Peroxidation Products ◽  
Ubiquitinated Proteins ◽  
Cyclopentenone Prostaglandins ◽  
Oxidant Effect ◽  
Intracellular Oxidative Stress

In the present study, we find that cyclopentenone prostaglandins (PGs) of the J2series, naturally occurring derivatives of PGD2, are potential inducers of intracellular oxidative stress that mediates cell degeneration. Based on an extensive screening of diverse chemical agents on induction of intracellular production of reactive oxygen species (ROS), we found that the cyclopentenone PGs, such as PGA2, PGJ2, Δ12-PGJ2, and 15-deoxy-Δ12,14-PGJ2, showed the most potent pro-oxidant effect on SH-SY5Y human neuroblastoma cells. As the intracellular events that mediate the PG cytotoxicity, we observed (i) the cellular redox alteration represented by depletion of antioxidant defenses, such as glutathione and glutathione peroxidase; (ii) a transient decrease in the mitochondrial membrane potential (Δψ); (iii) the production of protein-bound lipid peroxidation products, such as acrolein and 4-hydroxy-2-nonenal; and (iv) the accumulation of ubiquitinated proteins. These events correlated well with the reduction in cell viability. In addition, the thiol compound,N-acetylcysteine, could significantly inhibit the PG-induced ROS production, thereby preventing cytotoxicity, suggesting that the redox alteration is closely related to the pro-oxidant effect of cyclopentenone PGs. More strikingly, the lipid peroxidation end products, acrolein and 4-hydroxy-2-nonenal, detected in the PG-treated cells potently induced the ROS production, which was accompanied by the accumulation of ubiquitinated proteins and cell death, suggesting that the membrane lipid peroxidation products may represent one of the causative factors that potentiate the cytotoxic effect of cyclopentenone PGs by accelerating intracellular oxidative stress. These data suggest that the intracellular oxidative stress, represented by ROS production/lipid peroxidation and redox alteration, may underlie the well documented biological effects, such as antiproliferative and antitumor activities, of cyclopentenone PGs.

Obesity, asthma, and oxidative stress

2010 ◽  
Vol 108 (3) ◽  
pp. 754-759 ◽  
Author(s):  
Fernando Holguin ◽  
Anne Fitzpatrick
Keyword(s):  
Oxidative Stress ◽  
Inhaled Corticosteroids ◽  
Inflammatory Diseases ◽  
Therapeutic Interventions ◽  
Antioxidant Defenses ◽  
Oxidative Stress Biomarkers ◽  
Public Health Policies ◽  
Asthma Patients ◽  
Nonalcoholic Hepatic Steatosis ◽  
And Oxidative Stress

Obesity is associated with increased systemic and airway oxidative stress, which may result from a combination of adipokine imbalance, comorbidities, and reduced antioxidant defenses. While obesity-mediated increased oxidative stress plays an important role in the pathogenesis of vascular disease and nonalcoholic hepatic steatosis, little is known of how it may affect the lung. Contrary to what has previously been thought, the combination of obesity and asthma, both chronic inflammatory diseases, does not necessarily result in a synergistic effect, leading to even greater oxidative stress. However, most available studies have compared the levels of oxidative stress biomarkers on stable asthma patients, and it is possible that the interaction of oxidative stress between obesity and asthma is not readily detectable under basal conditions. We propose that obesity-mediated oxidative stress, which may affect the lung function of asthmatic subjects by increasing airway inflammation and reducing the effectiveness of inhaled corticosteroids, may become evident during exposure to an aggravating factor or during periods of asthma exacerbation. Understanding whether obesity-mediated oxidative stress has a mechanistic role in the association between obesity and asthma will help in the formation of public health policies and increase our capacity to develop therapeutic interventions that improve the life of obese asthmatic subjects.

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