scholarly journals Effects of electromagnetic radiations on the male reproductive system

2018 ◽  
Vol 7 (1) ◽  
pp. 1152-1161
Author(s):  
A.S. Adah ◽  
D.I. Adah ◽  
K.T. Biobaku ◽  
A.B. Adeyemi
Keyword(s):  
Oxidative Stress ◽  
Electromagnetic Radiation ◽  
Natural Environment ◽  
Reproductive System ◽  
Electromagnetic Waves ◽  
Living Organism ◽  
Testicular Tissue ◽  
The Body ◽  
Male Reproductive System ◽  
Electromagnetic Radiations

Electromagnetic radiation (EMR) emitting from the natural environment, as well as from the use of industrial and everyday appliances, constantly influences the body of the animal. It is expected that the interactions between electromagnetic radiation and the living organism would depend on the amount and parameters of the transmitted energy and type of tissue exposed. Electromagnetic waves exert an influence on the male reproductive system causing spermatozoa to have decreased motility, morphometric abnormalities, increased peroxidation due to oxidative stress, histological aberrations in the testes and in some cases atrophy of the testicular tissue. This review presents from literature some of effects of electromagnetic radiations on the male reproductive system.Keywords: Electromagnetic Radiations, Male Reproductive System, Animals, Humans

scholarly journals Power Failure of Mitochondria and Oxidative Stress in Neurodegeneration and Its Computational Models

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 229
Author(s):  
JunHyuk Woo ◽  
Hyesun Cho ◽  
YunHee Seol ◽  
Soon Ho Kim ◽  
Chanhyeok Park ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Computational Models ◽  
Neuronal Damage ◽  
Living Organism ◽  
The Body ◽  
Mitochondrial Functions ◽  
A Cell ◽  
The Brain ◽  
And Oxidative Stress

The brain needs more energy than other organs in the body. Mitochondria are the generator of vital power in the living organism. Not only do mitochondria sense signals from the outside of a cell, but they also orchestrate the cascade of subcellular events by supplying adenosine-5′-triphosphate (ATP), the biochemical energy. It is known that impaired mitochondrial function and oxidative stress contribute or lead to neuronal damage and degeneration of the brain. This mini-review focuses on addressing how mitochondrial dysfunction and oxidative stress are associated with the pathogenesis of neurodegenerative disorders including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. In addition, we discuss state-of-the-art computational models of mitochondrial functions in relation to oxidative stress and neurodegeneration. Together, a better understanding of brain disease-specific mitochondrial dysfunction and oxidative stress can pave the way to developing antioxidant therapeutic strategies to ameliorate neuronal activity and prevent neurodegeneration.

Hippocampal Oxidative Stress Induced by Radiofrequency Electromagnetic Radiation and the Neuroprotective Effects of Aerobic Exercise in Rats: A Randomized Control Trial

2021 ◽  
pp. 1-7
Author(s):  
Mina Rasouli Mojez ◽  
Abbas Ali Gaeini ◽  
Siroos Choobineh ◽  
Mohsen Sheykhlouvand
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Aerobic Exercise ◽  
Electromagnetic Radiation ◽  
Antioxidant Capacity ◽  
Electromagnetic Waves ◽  
Control Group ◽  
And Control ◽  
Radiofrequency Electromagnetic Radiation

Background: The present study determined whether 4 weeks of moderate aerobic exercise improves antioxidant capacity on the brain of rats against oxidative stress caused by radiofrequency electromagnetic radiation emitted from cell phones. Methods: Responses of malondialdehyde, catalase, glutathione peroxidase, and superoxide dismutase, as well as the number of hippocampal dead cells, were examined. Male Wistar rats (10–12 wk old) were randomly assigned to 1 of 4 groups (N = 8): (1) moderate aerobic exercise (EXE) (2 × 15–30 min at 1215 m/min speed with 5 min of active recovery between sets), (2) exposure to 900/1800 MHz radiofrequency electromagnetic waves 3 hours per day (RAD), (3) EXE + RAD, and (4) exposure to an experimental phone without battery. Results: Following the exposure, the number of the hippocampal dead cells was significantly higher in group RAD compared with groups EXE, EXE + RAD, and control group. Malondialdehyde concentration in group RAD was significantly higher than that of groups EXE, EXE + RAD, and control group. Also, the activity of catalase, glutathione peroxidase, and superoxide dismutase in groups EXE, EXE + RAD, and control group was significantly higher compared with those of the exposure group. Conclusion: This study demonstrated that moderate aerobic exercise enhances hippocampal antioxidant capacity against oxidative challenge in the form of radiofrequency electromagnetic waves.

Mancozeb induces testicular dysfunction through oxidative stress and apoptosis: Protective role of N-acetylcysteine antioxidant

2018 ◽  
Vol 34 (11) ◽  
pp. 798-811 ◽  
Author(s):  
Mohaddeseh Mohammadi-Sardoo ◽  
Ali Mandegary ◽  
Mohammad Nabiuni ◽  
Seyed-Noureddin Nematollahi-Mahani ◽  
Bagher Amirheidari
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Reproductive System ◽  
Histopathological Examination ◽  
Antioxidant Property ◽  
Testicular Tissue ◽  
Protective Role ◽  
Protein Carbonyl ◽  
Mrna Levels ◽  
Nadph Oxidase 4

Mancozeb (MZB) is one of the fungicides used in pest control programs that might affect human health including reproductive system. The aim of this study was to demonstrate the mechanisms through which MZB induces testicular tissue damage and the probable protective effect of N-acetylcysteine (NAC), a modified amino acid, with antioxidant property, against MZB toxicity in an animal model. Male albino mice ( n = 8) were exposed to different doses of MZB (250 and 500 mg/kg/day) by oral gavage without or with NAC (200 mg/kg, twice/week) for 40 days. Sub-chronic MZB dose-dependently decreased sperm motility and count. Exposure to MZB increased lipid peroxidation and protein carbonyl, while it reduced antioxidant enzymes activities, total antioxidant capacity, and glutathione content. The histopathological examination clearly showed deleterious changes in the testicular structure. At the molecular levels, the results of quantitative real time-poly chain reaction (qRT-PCR) showed that MZB upregulated oxidative stress markers inducible nitric oxide synthase (iNOS) and NADPH oxidase 4 (NOX4) and downregulated expression of the glutathione peroxidase 1 (Gpx1) gene as one of the most important antioxidant enzymes. MZB also induced apoptosis dose-dependently in the testes as determined by the terminal dUTP nick-end labeling assay and immunoblotting. NAC administration decreased the mRNA levels of both iNOS and NOX4 with a concomitant increase in Gpx1 expression. It also significantly decreased MZB-induced oxidative stress and apoptosis. Collectively, the present study showed MZB-induced oxidative damage in testes leading to apoptosis. It revealed that antioxidants such as NAC can mitigate oxidant injury induced by the dithiocarbamate pesticides in the reproductive system.

scholarly journals Sperm oxidative stress: clinical significance and management

2021 ◽  
pp. 19-27
Author(s):  
S. I. Gamidov ◽  
T. V. Shatylko ◽  
A. Yu. Popova ◽  
N. G. Gasanov ◽  
R. S. Gamidov
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reproductive System ◽  
Molecular Mechanisms ◽  
Assisted Reproductive Technologies ◽  
Reactive Oxygen ◽  
Reproductive Technologies ◽  
Male Reproductive System ◽  
Antioxidant Systems ◽  
Oxygen Species

Oxidative stress is one of the leading causes of sperm dysfunction. Excessive amounts of reactive oxygen species can damage sperm membranes and disrupt their DNA integrity, which affects not only the likelihood of getting pregnant naturally, but also the clinical outcomes of assisted reproductive technologies and the risk of miscarriage. Sperm cells are extremely vulnerable to oxidative stress, given the limited functional reserve of their antioxidant systems and the DNA repair apparatus. Lifestyle factors, most of which are modifiable, often trigger generation of reactive oxygen species.  Both the lifestyle modification and use of antioxidant dietary supplements are adequate and compatible ways to combat male oxidative stress-associated infertility. The search for other internal and external sources of reactive oxygen species, the identification of the etiology of oxidative stress and treatment of respective diseases are necessary for the successful regulation of redox processes in the male reproductive system in clinical practice, which is required not only to overcome infertility, but also to prevent induced epigenetic disorders in subsequent generations. The article presents the analysis of the molecular mechanisms of male idiopathic infertility. The authors provide an overview of how to prevent oxidative stress as one of the causes of subfebrile fever. The article provides an overview of modern therapeutics, as well as the options for eliminating the consequences of the effect of reactive oxygen species on spermatogenesis and male reproductive system in general.

scholarly journals Pyrethroids Toxicity to Male Reproductive System and Offspring as a Function of Oxidative Stress Induction: Rodent Studies

2021 ◽  
Vol 12 ◽  
Author(s):  
Xu Zhang ◽  
Tongtong Zhang ◽  
Xiaohan Ren ◽  
Xinglin Chen ◽  
ShangQian Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Sperm Motility ◽  
Reproductive System ◽  
Sperm Quality ◽  
Sperm Count ◽  
Meta Analysis ◽  
Serum Testosterone ◽  
Male Reproductive System ◽  
Serum Testosterone Level ◽  
Testis Weight

Pyrethroids may be related to male reproductive system damage. However, the results of many previous studies are contradictory and uncertain. Therefore, a systematic review and a meta-analysis were performed to assess the relationship between pyrethroid exposure and male reproductive system damage. A total of 72 articles were identified, among which 57 were selected for meta-analysis, and 15 were selected for qualitative analysis. Pyrethroid exposure affected sperm count (SMD= -2.0424; 95% CI, -2.4699 to -1.6149), sperm motility (SMD=-3.606; 95% CI, -4.5172 to -2.6948), sperm morphology (SMD=2.686; 95% CI, 1.9744 to 3.3976), testis weight (SMD=-1.1591; 95% CI, -1.6145 to -0.7038), epididymal weight (SMD=-1.1576; 95% CI, -1.7455 to -0.5697), and serum testosterone level (SMD=-1.9194; 95% CI, -2.4589 to -1.3798) in the studies of rats. We found that gestational and lactational exposure to pyrethroids can reduce sperm count (SMD=1.8469; 95% CI, -2.9010 to -0.7927), sperm motility (SMD=-2.7151; 95% CI, -3.9574 to -1.4728), testis weight (SMD=-1.4361; 95% CI, -1.8873 to -0.9848), and epididymal weight (SMD=-0.6639; 95% CI, -0.9544 to -0.3733) of F1 offspring. Exposure to pyrethroids can increase malondialdehyde (SMD=3.3451; 95% CI 1.9914 to 4.6988) oxide in testes and can reduce the activities of glutathione (SMD=-2.075; 95% CI -3.0651 to -1.0848), superoxide dismutase (SMD=-2.4856; 95% CI -3.9612 to -1.0100), and catalase (SMD=-2.7564; 95% CI -3.9788 to -1.5340). Pyrethroid exposure and oxidative stress could damage male sperm quality. Gestational and lactational pyrethroid exposure affects the reproductive system of F1 offspring.

scholarly journals Bacterial Infections Affect Male Fertility: A Focus on the Oxidative Stress-Autophagy Axis

2021 ◽  
Vol 9 ◽  
Author(s):  
Sutian Wang ◽  
Kunli Zhang ◽  
Yuchang Yao ◽  
Jianhao Li ◽  
Shoulong Deng
Keyword(s):  
Oxidative Stress ◽  
Reproductive System ◽  
Bacterial Infections ◽  
Reproductive Organs ◽  
Innate Immune ◽  
Male Reproductive System ◽  
Pathogenic Microorganisms ◽  
Immune Functions ◽  
Molecular Patterns ◽  
Multiple Signaling

Numerous factors trigger male infertility, including lifestyle, the environment, health, medical resources and pathogenic microorganism infections. Bacterial infections of the male reproductive system can cause various reproductive diseases. Several male reproductive organs, such as the testicles, have unique immune functions that protect the germ cells from damage. In the reproductive system, immune cells can recognize the pathogen-associated molecular patterns carried by pathogenic microorganisms and activate the host’s innate immune response. Furthermore, bacterial infections can lead to oxidative stress through multiple signaling pathways. Many studies have revealed that oxidative stress serves dual functions: moderate oxidative stress can help clear the invaders and maintain sperm motility, but excessive oxidative stress will induce host damage. Additionally, oxidative stress is always accompanied by autophagy which can also help maintain host homeostasis. Male reproductive system homeostasis disequilibrium can cause inflammation of the genitourinary system, influence spermatogenesis, and even lead to infertility. Here, we focus on the effect of oxidative stress and autophagy on bacterial infection in the male reproductive system, and we also explore the crosslink between oxidative stress and autophagy during this process.

scholarly journals Effects of monosodium glutamate on testicular structural and functional alterations induced by quinine therapy in rat: An experimental study

2021 ◽  
Author(s):  
Davoud Kianifard ◽  
Seyyed Maysam Mousavi Shoar ◽  
Morteza Fallah Karkan ◽  
Ahmed Aly
Keyword(s):  
Reproductive System ◽  
Monosodium Glutamate ◽  
Serum Testosterone ◽  
Testicular Tissue ◽  
Male Reproductive System ◽  
Control Group ◽  
High Dose ◽  
Sperm Analysis ◽  
High Doses ◽  
The Impact

Background: Quinine (QU) as an anti-malarial drug induces alterations in testicular tissue. Toxic effects of monosodium glutamate (MSG) on the male reproductive system have been recognized. Objective: To investigate the impact of MSG administration on the intensity of gonadotoxicity of QU. Materials and Methods: Sixty eight-wk old Wistar rats weighing 180-200 gr were divided into six groups (n = 10/each): the first group as a control; the second and third groups received low and high doses of MSG (2 & 4 gr/kg i.p.), respectively, for 28 days; the fourth group received QU for seven days (25 mg/kg); and in the fifth and sixth groups, QU was gavaged following the MSG administration (MSG + QU) from day 22 to day 28. Serum testosterone and malondialdehyde (MDA) levels were measured. Testes samples were prepared for tissue MDA levels, histomorphometry, and immunohistochemistry of p53. Sperm analysis was performed on cauda epididymis. Results: Serum and tissue MDA levels were increased in treated groups compared to the control group. This increment was higher in the MSG + QU groups. The testosterone levels were reduced significantly (p < 0.0001) in all treated groups. In addition, histomorphometric indices and tubular epithelium population were reduced significantly (p < 0.0001) in QU, MSG + QU, and consequently in high-dose MSG, QU, MSG + QU groups. All spermatogenic indices were reduced in the treated groups, particularly in the MSG + QU groups. Sperm motility and viability indices were reduced significantly (p = 0.003) in the MSG + QU groups. Finally, the overexpression of p53 was observed in the MSG + QU groups. Conclusion: The administration of MSG before and during QU therapy may intensify testicular tissue alterations. Key words: Male reproductive system, Monosodium glutamate, Quinine hydrochloride, Rat.

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