424. Polyunsaturated fatty acids and mitochondrial reactive oxygen species production in human spermatozoa and male infertility

2008 ◽  
Vol 20 (9) ◽  
pp. 104
Author(s):  
A. J. Koppers ◽  
R. J. Aitken
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Fatty Acids ◽  
Male Infertility ◽  
Polyunsaturated Fatty Acids ◽  
Sperm Motility ◽  
Human Spermatozoa ◽  
Ros Generation ◽  
Oxygen Species ◽  
Mitochondrial Ros

Reactive oxygen species (ROS) are traditionally considered detrimental by-products of cellular metabolism. However, ROS have conflicting roles in human spermatozoa, either as a functional mediator of sperm capacitation or generating a state of oxidative stress that is associated with male infertility. Using the probe MitoSOX Red, we have shown that defective human spermatozoa generate mitochondrial ROS in manner that was negatively correlated with motility (R2 = 0.8048). Previous research has shown higher levels of polyunsaturated fatty acids (PUFAs) in defective spermatozoa. However, the addition of PUFA to normal human spermatozoa results in increased mitochondrial ROS production (P < 0.001) and lipid peroxidation (P < 0.001) determined by MitoSOX Red and BODIPY C11 assays, as a consequence human spermatozoa also exhibited decreased sperm motility (P < 0.001). Ongoing research is currently evaluating the relationship between cellular levels of PUFAs in human spermatozoa and mitochondrial ROS generation and decreased sperm motility. This research demonstrates that mitochondrial ROS generation in human spermatozoa may have significant consequences for their function and we propose that elevated PUFA content may be a primary cause of increased oxidative stress and therefore male infertility.

scholarly journals Significance of Mitochondrial Reactive Oxygen Species in the Generation of Oxidative Stress in Spermatozoa

2008 ◽  
Vol 93 (8) ◽  
pp. 3199-3207 ◽  
Author(s):  
Adam J. Koppers ◽  
Geoffry N. De Iuliis ◽  
Jane M. Finnie ◽  
Eileen A. McLaughlin ◽  
R. John Aitken
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Complex I ◽  
Mitochondrial Membrane ◽  
Reactive Oxygen ◽  
Human Spermatozoa ◽  
Ros Generation ◽  
Oxygen Species ◽  
Mitochondrial Ros ◽  
Sperm Movement

Abstract Context: Male infertility has been linked with the excessive generation of reactive oxygen species (ROS) by defective spermatozoa. However, the subcellular origins of this activity are unclear. Objective: The objective of this study was to determine the importance of sperm mitochondria in creating the oxidative stress associated with defective sperm function. Method: Intracellular measurement of mitochondrial ROS generation and lipid peroxidation was performed using the fluorescent probes MitoSOX red and BODIPY C11 in conjunction with flow cytometry. Effects on sperm movement were measured by computer-assisted sperm analysis. Results: Disruption of mitochondrial electron transport flow in human spermatozoa resulted in generation of ROS from complex I (rotenone sensitive) or III (myxothiazol, antimycin A sensitive) via mechanisms that were independent of mitochondrial membrane potential. Activation of ROS generation at complex III led to the rapid release of hydrogen peroxide into the extracellular space, but no detectable peroxidative damage. Conversely, the induction of ROS on the matrix side of the inner mitochondrial membrane at complex I resulted in peroxidative damage to the midpiece and a loss of sperm movement that could be prevented by the concomitant presence of α-tocopherol. Defective human spermatozoa spontaneously generated mitochondrial ROS in a manner that was negatively correlated with motility. Simultaneous measurement of general cellular ROS generation with dihydroethidium indicated that 68% of the variability in such measurements could be explained by differences in mitochondrial ROS production. Conclusion: We conclude that the sperm mitochondria make a significant contribution to the oxidative stress experienced by defective human spermatozoa.

A Study of Role of Reactive Oxygen Species in Idiopathic Male Infertility & Its Management by Antioxidant Therapy in Uttar Pradesh (U.P.)

2021 ◽  
Vol 8 (32) ◽  
pp. 3023-3027
Author(s):  
Namrata Shrivastava ◽  
Vaibhav Shrivastava ◽  
Manish Pandey
Keyword(s):  
Reactive Oxygen Species ◽  
Male Infertility ◽  
Reactive Oxygen ◽  
Antioxidant Therapy ◽  
Semen Parameters ◽  
Control Group ◽  
P Value ◽  
Ros Generation ◽  
Variable Degree ◽  
Oxygen Species

BACKGROUND Infertility is defined as the inability to conceive after at 1 year of regular unprotected intercourse. Male contributes to almost half of infertility cases and in almost 30 % of cases, no definite aetiology is identified, and hence, male infertility is labelled idiopathic in these cases. Oxidative energy production mechanisms are almost always accompanied by reactive oxygen species (ROS), generation whose too much concentrations can lead to extensive protein damage and cytoskeletal modifications and inhibit cellular mechanisms. A number of laboratory techniques have been developed to evaluate oxidative stress by measuring ROS level in the semen. In recent times antioxidant supplements have been proposed as useful agents to increase the scavenging capacity of seminal plasma, controversy still surrounds their actual clinical utility. METHODS 34 male patients were included in this study. Reactive oxygen species detection was done by Flowcytometry using dichloroflurosecindiacetate (DCFH-DA). RESULTS The ROS in the patient group was found to be significantly higher 29.821 (5.6300 than the control group 22.162 (1.6331 having p value < 0.001). The ROS (29.821 ± 5.6300) was found to be significantly reduced after 3 months of antioxidant therapy which got reduced to 19.893 ± 4.2299 respectively. CONCLUSIONS Our study demonstrates that infertile men have significantly higher level of ROS (as measured by flowcytometry) & lower sperm count (oligospermia), decreased progressive & total motility and increased immotile sperms as compared to healthy fertile men. This study further proves that antioxidant therapy based on a combination of carnitine, zinc, coq10, lycopene and vitamin C & E for 3 months is associated with a decrease of ROS as measured by flowcytometry & a variable degree of improvement in above mentioned semen parameters. KEYWORDS Reactive Oxygen Species, Male Infertility

scholarly journals Impacts of Oxidative Stress and Antioxidants on Semen Functions

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Amrit Kaur Bansal ◽  
G. S. Bilaspuri
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Sperm Quality ◽  
Reactive Oxygen ◽  
The Body ◽  
Atp Depletion ◽  
Contributory Factor ◽  
Ros Generation ◽  
Oxygen Species ◽  
High Concentrations

Oxidative stress (OS) has been considered a major contributory factor to the infertility. Oxidative stress is the result of imbalance between the reactive oxygen species (ROS) and antioxidants in the body which can lead to sperm damage, deformity, and eventually male infertility. Although high concentrations of the ROS cause sperm pathology (ATP depletion) leading to insufficient axonemal phosphorylation, lipid peroxidation, and loss of motility and viability but, many evidences demonstrate that low and controlled concentrations of these ROS play an important role in sperm physiological processes such as capacitation, acrosome reaction, and signaling processes to ensure fertilization. The supplementation of a cryopreservation extender with antioxidant has been shown to provide a cryoprotective effect on mammalian sperm quality. This paper reviews the impacts of oxidative stress and reactive oxygen species on spermatozoa functions, causes of ROS generation, and antioxidative strategies to reduce OS. In addition, we also highlight the emerging concept of utilizing OS as a tool of contraception.

scholarly journals Interactions between Cytosolic Phospholipase A2 Activation and Mitochondrial Reactive Oxygen Species Production in the Development of Ventilator-Induced Diaphragm Dysfunction

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Xian-Long Zhou ◽  
Xiao-Jun Wei ◽  
Shao-Ping Li ◽  
Rui-Ning Liu ◽  
Ming-Xia Yu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Phospholipase A2 ◽  
Cytosolic Phospholipase A2 ◽  
Ros Generation ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Diaphragm Dysfunction ◽  
Cytosolic Phospholipase ◽  
Mitochondrial Ros ◽  
Cpla2 Activation

Cytosolic phospholipase A2 (cPLA2) has been reported to be critical for infection-induced mitochondrial reactive oxygen species (ROS) production and diaphragm dysfunction (DD). In the present study, we aim to investigate whether cPLA2 was involved in ventilator-induced diaphragm dysfunction (VIDD). Our results showed that mechanical ventilation (MV) induced cPLA2 activation in the diaphragm with excessive mitochondrial ROS generation and muscle weakness. Specific inhibition of cPLA2 with CDIBA resulted in decreased mitochondrial ROS levels and improved diaphragm forces. In addition, mitochondria-targeted antioxidant MitoTEMPO attenuated ventilator-induced mitochondrial oxidative stress and downregulated cPLA2 activation in vivo. Both CDIBA and MitoTEMPO were able to attenuate protein degradation, muscle atrophy, and weakness following prolonged MV. Furthermore, laser Doppler imaging showed that MV decreased diaphragm tissue perfusion and induced subsequent hypoxia. An in vitro study also demonstrated a positive association between cPLA2 activation and mitochondrial ROS generation in C2C12 cells cultured under hypoxic condition. Collectively, our study showed that cPLA2 activation positively interacts with mitochondrial ROS generation in the development of VIDD, and ventilator-induced diaphragm hypoxia serves as a possible contributor to this positive feedback loop.

scholarly journals Guilingji Protects Against Spermatogenesis Dysfunction From Oxidative Stress via Regulation of MAPK and Apoptotic Signaling Pathways in Immp2l Mutant Mice

2022 ◽  
Vol 12 ◽  
Author(s):  
Zhenqing Wang ◽  
Yun Xie ◽  
Haicheng Chen ◽  
Jiahui Yao ◽  
Linyan Lv ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Male Infertility ◽  
Mapk Pathway ◽  
Reactive Oxygen ◽  
Mutant Mice ◽  
Mitogen Activated Protein Kinase ◽  
Seminiferous Tubules ◽  
Oxygen Species ◽  
Inner Mitochondrial Membrane

Male infertility is a major health issue with an estimated prevalence of 4.2% of male infertility worldwide. Oxidative stress (OS) is one of the main causes of male infertility, which is characterized by excessive reactive oxygen species (ROS) or lack of antioxidants. Meanwhile, it is reported that oxidative stress plays an important role in the spermatogenic impairment in Inner mitochondrial membrane peptidase 2-like (Immp2l) mutant mice. In this study, we focused on the potential mechanism of Guilingji in protecting the spermatogenic functions in Immp2l mutant mice. The results revealed that Immp2l mutant mice exhibit impaired spermatogenesis and histology shows seminiferous tubules with reduced spermatogenic cells. After administration of Guilingji [150 mg/kg per day intragastric gavage], however, alleviated spermatogenesis impairment and reversed testis histopathological damage and reduced apoptosis. What’s more, western blotting and the levels of redox classic markers revealed that Guilingji can markedly reduce reactive oxygen species. Moreover, Guilingji treatment led to inhibition of the phosphorylation of mitogen-activated protein kinase (MAPK), regulated apoptosis in the cells. In summary, Guilingji can improve spermatogenesis in Immp2l mutant mice by regulating oxidation-antioxidant balance and MAPK pathway. Our data suggests that Guilingji may be a promising and effective antioxidant candidate for the treatment of male infertility.

scholarly journals Survival Signaling by C-RAF: Mitochondrial Reactive Oxygen Species and Ca2+ Are Critical Targets

2008 ◽  
Vol 28 (7) ◽  
pp. 2304-2313 ◽  
Author(s):  
Andrey V. Kuznetsov ◽  
Julija Smigelskaite ◽  
Christine Doblander ◽  
Manickam Janakiraman ◽  
Martin Hermann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Mitochondrial Ros ◽  
Survival Signaling ◽  
First Time

ABSTRACT Survival signaling by RAF occurs through largely unknown mechanisms. Here we provide evidence for the first time that RAF controls cell survival by maintaining permissive levels of mitochondrial reactive oxygen species (ROS) and Ca2+. Interleukin-3 (IL-3) withdrawal from 32D cells resulted in ROS production, which was suppressed by activated C-RAF. Oncogenic C-RAF decreased the percentage of apoptotic cells following treatment with staurosporine or the oxidative stress-inducing agent tert-butyl hydroperoxide. However, it was also the case that in parental 32D cells growing in the presence of IL-3, inhibition of RAF signaling resulted in elevated mitochondrial ROS and Ca2+ levels. Cell death is preceded by a ROS-dependent increase in mitochondrial Ca2+, which was absent from cells expressing transforming C-RAF. Prevention of mitochondrial Ca2+ overload after IL-3 deprivation increased cell viability. MEK was essential for the mitochondrial effects of RAF. In summary, our data show that survival control by C-RAF involves controlling ROS production, which otherwise perturbs mitochondrial Ca2+ homeostasis.

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