Role of oxidative stress and antioxidant supplementation in Male fertility

2020 ◽  
Vol 20 ◽  
Author(s):  
Zahra Beygi ◽  
Sedighe Forouhari ◽  
Elahe Mahmoudi ◽  
Seyed Mohammad Gheibi Hayat ◽  
Firoozeh Nourimand
Keyword(s):  
Oxidative Stress ◽  
Life Style ◽  
Male Fertility ◽  
Treatment Strategies ◽  
Infertile Male ◽  
Dna Damages ◽  
Vitamins E And C ◽  
Anti Oxidant ◽  
Universal Health

: Nearly 15% of couples involve in infertility as a universal health issue. About 50% of infertility cases have been known to be associated with the male parameters. Oxidative stress (OS) represents an imbalance in the level of reactive ox-ygen species (ROS) and anti-oxidant. In fact, OS has been considered as one of the popular pathologies reported in about 50% of all infertile male. Therefore, the increased level of ROS may result in infertility via DNA damages or lipid peroxida-tion (LPO) as well as the enzymes inactivation and proteins oxidation in spermatozoa. Basically, OS results from the life-style variables. As the absence of antioxidant and the respective deficiencies in the semen cause OS, variations in the life-style and anti-oxidant regimes may be advantageous to treatment strategies for resolving such an issue. Actually, anti-oxidants like vitamins E and C, glutathione, coenzyme-Q10, carnitines, selenium, N-acetylcysteine, carotenoids, zinc, and pentoxifylline decline the OS-induced sperm damages.Therefore, the present review overviews the oxidative bio-chemistry associated with the sperm health and identifies which men would be most at risk of the oxidative infertility. Hence, the re-view would show the techniques provided to diagnose OS and diverse therapeutic options.

Platelet-rich plasma protects human melanocytes from oxidative stress and ameliorates melanogenesis induced by UVB irradiation

2021 ◽  
Author(s):  
Yongshi Ma ◽  
Min Xuan ◽  
Yunqing Dong ◽  
Hong Wang ◽  
Jianfang Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Platelet Rich Plasma ◽  
Protective Role ◽  
Dna Lesions ◽  
Dna Damages ◽  
Uvb Irradiation ◽  
Human Melanocytes ◽  
Anti Oxidant ◽  
Different Sources

Abstract To investigate the role of Platelet-rich plasma(PRP) from different sources in alleviating oxidative stress and ameliorating melanogenesis in UVB-irradiated PIG1 cells. PIG1 cells were irradiated with 80 mJ/cm2 UVB prior to 1% PRP application and the following experiments were taken: The viability of UVB-irradiated PIG1 cells, cellular malondialdehyde (MDA) and reactive oxygen species (ROS)content, and activities of anti-oxidant enzymes. Western blotting was utilized to detect the expression level of proteins associated with melanin synthesis, apoptosis and DNA lesions. We found that PRP intervention promoted cell proliferation, reduced MDA and ROS content, increased the activities of series of anti-oxidant enzymes and alleviated DNA damages in UVB-damaged PIG1 cells. Of notes, PRP treatment inhibited UVB-induced melanogenesis via PI3K/Akt/GSK3β signal pathway. Therefore, we suppose PRP treatment exerts protective role through their anti-oxidation effect on UVB-damaged PIG1 cells and hinders melanogenesis induced by UVB irradiation.

scholarly journals The Phosphoarginine Phosphatase PtpB from Staphylococcus aureus Is Involved in Bacterial Stress Adaptation during Infection

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 645
Author(s):  
Mohamed Ibrahem Elhawy ◽  
Sylvaine Huc-Brandt ◽  
Linda Pätzold ◽  
Laila Gannoun-Zaki ◽  
Ahmed Mohamed Mostafa Abdrabou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Treatment Strategies ◽  
Physiological Role ◽  
Aureus Strain ◽  
Stress Adaptation ◽  
Cellular Mechanisms ◽  
Host Interaction ◽  
Liver And Kidney

Staphylococcus aureus continues to be a public health threat, especially in hospital settings. Studies aimed at deciphering the molecular and cellular mechanisms that underlie pathogenesis, host adaptation, and virulence are required to develop effective treatment strategies. Numerous host-pathogen interactions were found to be dependent on phosphatases-mediated regulation. This study focused on the analysis of the role of the low-molecular weight phosphatase PtpB, in particular, during infection. Deletion of ptpB in S. aureus strain SA564 significantly reduced the capacity of the mutant to withstand intracellular killing by THP-1 macrophages. When injected into normoglycemic C57BL/6 mice, the SA564 ΔptpB mutant displayed markedly reduced bacterial loads in liver and kidney tissues in a murine S. aureus abscess model when compared to the wild type. We also observed that PtpB phosphatase-activity was sensitive to oxidative stress. Our quantitative transcript analyses revealed that PtpB affects the transcription of various genes involved in oxidative stress adaptation and infectivity. Thus, this study disclosed first insights into the physiological role of PtpB during host interaction allowing us to link phosphatase-dependent regulation to oxidative bacterial stress adaptation during infection.

scholarly journals The Protective Role of Sestrin2 in Atherosclerotic and Cardiac Diseases

2021 ◽  
Vol 22 (3) ◽  
pp. 1200
Author(s):  
Yoshimi Kishimoto ◽  
Kazuo Kondo ◽  
Yukihiko Momiyama
Keyword(s):  
Oxidative Stress ◽  
Protective Role ◽  
Chronic Inflammatory Disease ◽  
Atherosclerotic Disease ◽  
Cardiac Diseases ◽  
Compensatory Response ◽  
Age Related ◽  
Anti Oxidant ◽  
Progression Of Atherosclerosis

Atherosclerotic disease, such as coronary artery disease (CAD), is known to be a chronic inflammatory disease, as well as an age-related disease. Excessive oxidative stress produced by reactive oxygen species (ROS) contributes to the pathogenesis of atherosclerosis. Sestrin2 is an anti-oxidant protein that is induced by various stresses such as hypoxia, DNA damage, and oxidative stress. Sestrin2 is also suggested to be associated with aging. Sestrin2 is expressed and secreted mainly by macrophages, endothelial cells, and cardiomyocytes. Sestrin2 plays an important role in suppressing the production and accumulation of ROS, thus protecting cells from oxidative damage. Since sestrin2 is reported to have anti-oxidant and anti-inflammatory properties, it may play a protective role against the progression of atherosclerosis and may be a potential therapeutic target for the amelioration of atherosclerosis. Regarding the association between blood sestrin2 levels and atherosclerotic disease, the blood sestrin2 levels in patients with CAD or carotid atherosclerosis were reported to be high. High blood sestrin2 levels in patients with such atherosclerotic disease may reflect a compensatory response to increased oxidative stress and may help protect against the progression of atherosclerosis. This review describes the protective role of sestrin2 against the progression of atherosclerotic and cardiac diseases.

scholarly journals Curcumin and Endometriosis

2020 ◽  
Vol 21 (7) ◽  
pp. 2440 ◽  
Author(s):  
Alexandre Vallée ◽  
Yves Lecarpentier
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Uterine Cavity ◽  
Main Role ◽  
Oxygen Species ◽  
Inflammatory Agent ◽  
Gynecological Disorders ◽  
Anti Oxidant ◽  
Anti Inflammatory

Endometriosis is one of the main common gynecological disorders, which is characterized by the presence of glands and stroma outside the uterine cavity. Some findings have highlighted the main role of inflammation in endometriosis by acting on proliferation, apoptosis and angiogenesis. Oxidative stress, an imbalance between reactive oxygen species and antioxidants, could have a key role in the initiation and progression of endometriosis by resulting in inflammatory responses in the peritoneal cavity. Nevertheless, the mechanisms underlying this disease are still unclear and therapies are not currently efficient. Curcumin is a major anti-inflammatory agent. Several findings have highlighted the anti-oxidant, anti-inflammatory and anti-angiogenic properties of curcumin. The purpose of this review is to summarize the potential action of curcumin in endometriosis by acting on inflammation, oxidative stress, invasion and adhesion, apoptosis and angiogenesis.

scholarly journals Role of Anti-oxidants in the Treatment of Vitiligo

2019 ◽  
Vol 17 (1) ◽  
pp. 49-57
Author(s):  
Amit Kumar ◽  
Sudha Agrawal ◽  
Tapan Kumar Dhali ◽  
Shankar Kumr Majhi
Keyword(s):  
Oxidative Stress ◽  
Placebo Group ◽  
Vitamin E ◽  
Primary Outcome ◽  
Antioxidant Supplementation ◽  
Significant Difference ◽  
Anti Oxidant ◽  
And Oxidative Stress

Introduction: The role of free radicals and oxidative damage in the pathophysiology of vitiligo has been documented in recent studies. Antioxidant supplementation has been reported to be useful in the treatment of vitiligo. Objective: To evaluate the role of oral antioxidants supplementation therapy in the treatment of vitiligo by assessing the onset of repigmentation and oxidative stress. Materials and Methods: A total of 80 cases of vitiligo randomized into two groups: antioxidant and placebo comprising 40 patients each and were followed up for 8 weeks for the assessment of onset of repigmentation of vitiliginous lesions as primary outcome.  The activities of Malondialdehyde (MDA), Vitamin C, and Vitamin E in serum and of Catalase (CAT) in erythrocytes of patients at baseline and at end of eight weeks were also assessed by using the spectrophotometric assay. Results: The onset of repigmentation was noted significantly earlier among the anti-oxidant group as compared to the placebo group (p=0.015). At the baseline, between the two groups, no significant difference was found in the different biochemical parameters. However, at the end of 2 months the level of MDA (p<0.001) was found to be significantly lower and that of Vitamin E (p<0.001) and CAT (p=0.005) was significantly higher among the anti-oxidants group as compared to the placebo group. Conclusion: Antioxidant supplementation carried a better response in terms of early onset of repigmentation and significant decrease in the oxidative stress, in the short follow up of two months.

scholarly journals The role of oxidative stress and antioxidants in male fertility

2013 ◽  
Vol 65 ◽  
pp. 60-67 ◽  
Author(s):  
Renata Walczak–Jedrzejowska ◽  
Jan Karol Wolski ◽  
Jolanta Slowikowska–Hilczer
Keyword(s):  
Oxidative Stress ◽  
Male Fertility

Oxidative stress as a common pathway to chronic tubulointerstitial injury in kidney allografts

2007 ◽  
Vol 293 (2) ◽  
pp. F445-F455 ◽  
Author(s):  
Arjang Djamali
Keyword(s):  
Oxidative Stress ◽  
Interstitial Fibrosis ◽  
Treatment Strategies ◽  
Specific Treatment ◽  
Common Mechanism ◽  
Placebo Control ◽  
Tubulointerstitial Injury ◽  
Tubular Atrophy ◽  
Mesenchymal Transition

A major challenge for kidney transplantation is to dissect out the identifiable causes of chronic allograft tubulointerstitial fibrosis and to develop cause-specific treatment strategies. There has been a recent interest in the role of oxidative stress (OS) as a mediator of injury in chronic allograft tubular atrophy (TA) and interstitial fibrosis (IF). A review of the literature and data from my laboratory studying chronic allograft TA/IF in rat, rhesus monkey, and human kidneys suggests that OS is increased in graft-infiltrating macrophages, activated myofibroblasts, interstitium, and areas of tubular injury. Chronic allograft OS may be induced by inflammation, abnormal tissue oxygenation, immunosuppressant drugs, and comorbid clinical conditions including diabetes, hypertension, proteinuria, anemia, and dyslipidemia. Moreover, OS-induced chronic TA/IF is associated with signaling pathways including inflammation, apoptosis, hypoxia, and epithelial-to-mesenchymal transition. Most of these injury pathways participate in a self-perpetuating cycle with OS. In conclusion, evidence suggests that OS is a common mechanism of injury in chronic allograft TA/IF. However, most available data demonstrate a correlation and no causal relationship. Furthermore, the extent to which TA/IF is dependent on OS is unknown. These questions may be answered by prospective randomized placebo-control trials examining the role of select antioxidants in the prevention of chronic allograft TA/IF.

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