Ulva lactuca methanolic extract improves oxidative stress-related male infertility induced in experimental animals

2019 ◽  
pp. 1-9 ◽  
Author(s):  
Doaa A. Ghareeb ◽  
Alshimaa Abd-Elgwad ◽  
Nihal El-Guindy ◽  
Galila Yacout ◽  
Hala H. Zaatout
Keyword(s):  
Oxidative Stress ◽  
Male Infertility ◽  
Methanolic Extract ◽  
Ulva Lactuca ◽  
Experimental Animals

The mechanisms involved in obesity-induced male infertility

2020 ◽  
Vol 16 ◽  
Author(s):  
Hamed Heydari ◽  
Rafighe Ghiasi ◽  
Saber Ghaderpour ◽  
Rana Keyhanmanesh
Keyword(s):  
Oxidative Stress ◽  
Metabolic Disease ◽  
Male Infertility ◽  
Male Fertility ◽  
Reproductive Function ◽  
Disease Development ◽  
Significant Evidence ◽  
Male Reproductive Function ◽  
Negative Effect ◽  
And Oxidative Stress

Introduction: Obesity resulted by imbalance between the intake of energy and energy consumption can lead to growth and metabolic disease development in people. Both in obese men and animal models, several studies indicate that obesity leads to male infertility. Objective: This review has discussed some mechanisms involved in obesity-induced male infertility. Method: Online documents were searched through Science Direct, Pubmed, Scopus, and Google Scholar websites dating from 1959 to recognize studies on obesity, kisspeptin, leptin, and infertility. Results: Obesity induced elevated inflammatory cytokines and oxidative stress can affect male reproductive functions including spermatogenesis disorders, reduced male fertility power and hormones involved in hypothalamus-pituitarygonadal axis. Conclusion: There is significant evidence that obesity resulted in male infertility. obesity has negative effect on male reproductive function via several mechanisms such as inflammation and oxidative stress.

scholarly journals Oxidation of Sperm DNA and Male Infertility

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 97
Author(s):  
Leila Rashki Ghaleno ◽  
AliReza Alizadeh ◽  
Joël R. Drevet ◽  
Abdolhossein Shahverdi ◽  
Mojtaba Rezazadeh Valojerdi
Keyword(s):  
Oxidative Stress ◽  
Male Infertility ◽  
Oxidative Damage ◽  
Dna Fragmentation ◽  
Dna Bases ◽  
De Novo Mutation ◽  
Easy Access ◽  
Sperm Dna Fragmentation ◽  
Dna Base ◽  
Sperm Dna

One important reason for male infertility is oxidative stress and its destructive effects on sperm structures and functions. The particular composition of the sperm membrane, rich in polyunsaturated fatty acids, and the easy access of sperm DNA to oxidative damage due to sperm cell specific cytologic and metabolic features (no cytoplasm left and cells unable to mount stress responses) make it the cell type in metazoans most susceptible to oxidative damage. In particular, oxidative damage to the spermatozoa genome is an important issue and a cause of male infertility, usually associated with single- or double-strand paternal DNA breaks. Various methods of detecting sperm DNA fragmentation have become important diagnostic tools in the prognosis of male infertility and such assays are available in research laboratories and andrology clinics. However, to date, there is not a clear consensus in the community as to their respective prognostic value. Nevertheless, it is important to understand that the effects of oxidative stress on the sperm genome go well beyond DNA fragmentation alone. Oxidation of paternal DNA bases, particularly guanine and adenosine residues, the most sensitive residues to oxidative alteration, is the starting point for DNA damage in spermatozoa but is also a danger for the integrity of the embryo genetic material independently of sperm DNA fragmentation. Due to the lack of a spermatozoa DNA repair system and, if the egg is unable to correct the sperm oxidized bases, the risk of de novo mutation transmission to the embryo exists. These will be carried on to every cell of the future individual and its progeny. Thus, in addition to affecting the viability of the pregnancy itself, oxidation of the DNA bases in sperm could be associated with the development of conditions in young and future adults. Despite these important issues, sperm DNA base oxidation has not attracted much interest among clinicians due to the lack of simple, reliable, rapid and consensual methods of assessing this type of damage to the paternal genome. In addition to these technical issues, another reason explaining why the measurement of sperm DNA oxidation is not included in male fertility is likely to be due to the lack of strong evidence for its role in pregnancy outcome. It is, however, becoming clear that the assessment of DNA base oxidation could improve the efficiency of assisted reproductive technologies and provide important information on embryonic developmental failures and pathologies encountered in the offspring. The objective of this work is to review relevant research that has been carried out in the field of sperm DNA base oxidation and its associated genetic and epigenetic consequences.

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 Perbedaan Kadar Glutation (GSH) Hepar Tikus Putih Jantan (Rattus norvegicus) yang diinduksi Parasetamol Dosis Toksik dengan Pemberian Ekstrak Daun Kelor (Moringa oleifera)

2020 ◽  
Vol 20 (1) ◽  
pp. 247
Author(s):  
Nur Insani ◽  
H.M.T Kamaluddin ◽  
Swanny Swanny
Keyword(s):  
Oxidative Stress ◽  
Treatment Group ◽  
Leaf Extract ◽  
The Body ◽  
Control Group ◽  
Bb Rat ◽  
Toxic Dose ◽  
Experimental Animals ◽  
Significant Difference ◽  
Group Ii

Glutathione (GSH) transferase deficiency due to paracetamol exposure causes further oxidative stress to liver necrosis. To reduce oxidative stress that can cause damage to the liver of the body requires antioxidants. One plant to treat liver disease is the kelor leaf (because it has an active flavonoid material also has antioxidant activity). This study was conducted to determine the difference of glutathione hepar levels of male white rat induced paracetamol toxic dose by giving kelor leaf extract. The type of research is experimental laboratory in vivo with rancagan randomized post test only control group design. With the stages as follows 1.Leaf Extract Kelor with Ethanol 96%, 2.Perpeteration of experimental animals, 3.Treatment of experimental animals by giving extract of 3-dose of kelor leaf that is KP I 250 mg / 200 gr BB rat, KP II 500 mg / 200 gr BB rat, KP III 1000 mg / 200 gr BB rat  for 14 days combined with paracetamol dose 2 gr / 200 gr BB rat compared with the negative control group (group given only paracetamol dose 2 gr / 200 gr BB rat) and control group positif only fed regular feed for 14 days). The result showed that there was a significant difference mean of GSH levels between all treatment groups obtained p = 0,000 (p <α) p values smaller than 0.05. There was the highest increase of GSH in treatment group II (142,7525 μmol / mg) and lowest dose of GSH in positive control group (57,1812 μmol / mg), dose paracetamol toxic dosage and kelor leaf extract 500 mg / gr BB rat can increase GSH hepar p = 0,000 (p <α) p less than 0 , 05. The conclusion of the test results showed that giving of kelor leaf extract at dose of treatment group II can increase GSH hepar level significantly

scholarly journals Male Infertility: Pathogenetic Significance of Oxidative Stress and Antioxidant Defence (Review)

2021 ◽  
Vol 24 (6) ◽  
pp. 107-116
Author(s):  
Vsevolod Koshevoy ◽  
Svitlana Naumenko ◽  
Pavlo Skliarov ◽  
Serhiy Fedorenko ◽  
Lidia Kostyshyn
Keyword(s):  
Oxidative Stress ◽  
Male Infertility ◽  
Nitrosative Stress ◽  
Antioxidant Properties ◽  
Malonic Dialdehyde ◽  
The Body ◽  
Redox Activity ◽  
Enzymatic System ◽  
Male Body ◽  
Mitochondrial Potential

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 destruction of sperm DNA, reduced activity of acrosomal enzymes and mitochondrial potential of sperm, reduced overall antioxidant activity. This makes it impossible for an adequate response of the body. Multi component antioxidant defense system resists stress. It is represented by enzymatic and non-enzymatic links, which can neutralize harmful radicals and peroxidation products. It contributes to the full manifestation of reproductive function. The presence of powerful antioxidant properties of catalase, superoxide dismutase, and enzymes of the thiol-disulfide system, which form the enzymatic system of antioxidant protection, as well as selenium, zinc, copper, other trace elements, retinol, tocopherol, ascorbic acid, and vitamins as parts of the non-enzymatic system is shown. The efficiency of registration is substantiated thin biochemical shift detectors or complex methods, such as total antioxidant status of sperm or sperm plasma, mitochondrial membrane potential, etc along with simple markers of oxidative stress, such as diene conjugates, malonic dialdehyde, and metabolites of the Nitrogen Oxide cycle. Given the leading role of oxidative stress in the development of male hypofertility, the prospect of further research is the search for modern means for correction, especially among substances with pronounced redox activity

scholarly journals Effect of packing on changes in erythrocyte osmotic fragility and malondialdehyde concentration in donkeys administered with ascorbic acid

2012 ◽  
Vol 79 (1) ◽  
Author(s):  
Folashade Olaifa ◽  
Joseph O. Ayo ◽  
Suleiman F. Ambali ◽  
Peter I. Rekwot
Keyword(s):  
Oxidative Stress ◽  
Ascorbic Acid ◽  
Osmotic Fragility ◽  
Blood Samples ◽  
Experimental Animals ◽  
Erythrocyte Osmotic Fragility ◽  
Nacl Concentration ◽  
Experimental Subjects ◽  
Apparently Healthy

Experiments were performed with the aim of investigating the effect of packing on erythrocyte osmotic fragility (EOF) and malondialdehyde (MDA) concentration in donkeys, and the effect of ascorbic acid (AA). Twelve apparently healthy donkeys raised under the traditional extensive system served as experimental subjects. Six donkeys administered orally with AA (200 mg/kg) and subjected to packing were used as experimental animals, whilst six others not administered with AA served as controls. Blood samples were collected pre- and post-packing from all the donkeys for the determination of MDA and EOF. At 0.3% Sodium Chloride (NaCl) concentration, the percentage haemolysis was 93.69% ± 2.21% in the control donkeys and the value was significantly (P < 0.05) higher than the value of 71.31% ± 8.33%, recorded in the experimental donkeys. The post-packing MDA concentration obtained in the control donkeys was 39.62 µmol ± 4.16 µmol, and was not significantly different (P > 0.05) from the value of 35.97 µmol ± 2.88 µmol recorded in the experimental donkeys. In conclusion, the increase in haemolysis obtained in the donkeys suggested that packing induced oxidative stress, which was ameliorated by AA administration.

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