scholarly journals The Effect of Swimming Training on Serum Levels of Sex Hormones, Antioxidant Enzymes and Oxidative Damage of DNA Ovarian Tissue in Rats with Polycyclic Ovarian Syndrome

2020 ◽  
Vol 8 (4) ◽  
pp. 0-0
Author(s):  
Mehdi Noura ◽  
Samane Rafie ◽  
Seyed Ali Hosseini ◽  
Mohammad Amin Edalatmanesh ◽  
◽  
...  
Keyword(s):  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Sex Hormones ◽  
Ovarian Tissue ◽  
Serum Levels ◽  
Swimming Training ◽  
Ovarian Syndrome

scholarly journals Sexual Dimorphisms of Adrenal Steroids, Sex Hormones, and Immunological Biomarkers and Possible Risk Factors for Developing Rheumatoid Arthritis

2015 ◽  
Vol 2015 ◽  
pp. 1-13 ◽  
Author(s):  
Alfonse T. Masi ◽  
Azeem A. Rehman ◽  
Laura C. Jorgenson ◽  
Jennifer M. Smith ◽  
Jean C. Aldag
Keyword(s):  
Rheumatoid Arthritis ◽  
Risk Factors ◽  
Sexual Dimorphism ◽  
Sex Hormones ◽  
Inflammatory Diseases ◽  
Interleukin 2 ◽  
Tumor Necrosis Factor Receptor ◽  
Serum Levels ◽  
Amyloid A ◽  
Neuroendocrine Factors

Innate immunity and immunological biomarkers are believed to be interrelated with sex hormones and other neuroendocrine factors. Sexual dimorphism mechanisms may be operating in certain rheumatic and inflammatory diseases which occur more frequently in women than men, as rheumatoid arthritis (RA). Less data have been available on altered interrelations of the combined neuroendocrine and immune (NEI) systems as risk factors for development of certain diseases. In this study, serological interrelations of NEI biomarkers are analyzed before symptomatic onset of RA (pre-RA) versus control (CN) subjects, stratified by sex. Sexual dimorphism was found in serum levels of acute serum amyloid A (ASAA), soluble interleukin-2 receptor alpha (sIL-2Rα), and soluble tumor necrosis factor receptor 1 (sTNF-R1). Multiple steroidal and hormonal (neuroendocrine) factors also showed highly(p<0.001)significant sexual dimorphism in their assayed values, but less for cortisol(p=0.012), and not for 17-hydroxyprogesterone(p=0.176). After stratification by sex and risk of developing RA, differential NEI correlational patterns were observed in the interplay of the NEI systems between the pre-RA and CN groups, which deserve further investigation.

scholarly journals Active paraplegics are protected against exercise-induced oxidative damage through the induction of antioxidant enzymes

Spinal Cord ◽  
2016 ◽  
Vol 54 (10) ◽  
pp. 830-837 ◽  
Author(s):  
M Inglés ◽  
P Serra-Añó ◽  
J Gambini ◽  
F Abu-Sharif ◽  
M Dromant ◽  
...  
Keyword(s):  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Exercise Induced

scholarly journals Pharmaceutical Induction of PGC-1α Promotes Retinal Pigment Epithelial Cell Metabolism and Protects against Oxidative Damage

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Sangeeta Satish ◽  
Hannah Philipose ◽  
Mariana Aparecida Brunini Rosales ◽  
Magali Saint-Geniez
Keyword(s):  
Cell Death ◽  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Therapeutic Potential ◽  
Retinal Pigment Epithelial Cell ◽  
Cell Metabolism ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Age Related

Retinal pigment epithelium (RPE) dysfunction due to accumulation of reactive oxygen species and oxidative damage is a key event in the development of age-related macular degeneration (AMD). Here, we examine the therapeutic potential of ZLN005, a selective PGC-1α transcriptional regulator, in protecting RPE from cytotoxic oxidative damage. Gene expression analysis on ARPE-19 cells treated with ZLN005 shows robust upregulation of PGC-1α and its associated transcription factors, antioxidant enzymes, and mitochondrial genes. Energetic profiling shows that ZLN005 treatment enhances RPE mitochondrial function by increasing basal and maximal respiration rates, and spare respiratory capacity. In addition, ZLN005 robustly protects ARPE-19 cells from cell death caused by H2O2, ox-LDL, and NaIO3 without exhibiting any cytotoxicity under basal conditions. ZLN005 protection against H2O2-mediated cell death was lost in PGC-1α-silenced cells. Our data indicates that ZLN005 efficiently protects RPE cells from oxidative damage through selective induction of PGC-1α and its target antioxidant enzymes. ZLN005 may serve as a novel therapeutic agent for retinal diseases associated with RPE dystrophies.

scholarly journals Evaluation of the Relationship between the Level of DHEA-S and Sex Hormones in Some Infertile Iraqi Men

2021 ◽  
Vol 8 (5) ◽  
pp. 130-136
Author(s):  
Khaled S. Abd ◽  
Adnan F. AL-Azzawie
Keyword(s):  
Sex Hormones ◽  
Seminal Fluid ◽  
Age Groups ◽  
Serum Levels ◽  
Dehydroepiandrosterone Sulfate ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Infertile Men ◽  
The Relationship

This study aims to evaluate serum levels of the Dehydroepiandrosterone sulfate (DHEA-S) and its relationship with some sex hormones such as Follicle stimulating hormone (FSH), Luteinizing hormone (LH), prolactin and testosterone hormone and the infertility type in some infertile Iraqi men. Blood and seminal fluid samples from (60) idiopathic male infertile and (60) healthful individuals as a control group aged (18 to 60 year) were collected from private clinics. Serum hormones (DHEA-S, FSH, LH, prolactin and testosterone) were measurement using Enzyme Linked Immunosorbent Assay (ELISA). The levels of DHEA-S, FSH, LH and prolactin are significantly higher (P≤0.01) expect of the testosterone level was significantly decreased (P≤ 0.01) in the infertile men as compared with control group. High significant differences (P≤0.01) were recorded when comparing the hormonal levels (DHEA-S, FSH, LH, prolactin and testosterone) according to the age groups. There are significant differences (P≤ 0.01) in levels of (DHEA-S, FSH, LH, prolactin and testosterone) in the infertility period.  Smoker infertile men have high levels (P≤ 0.05) in the DHEA-S and LH while have low levels in the prolactin hormones compared with control. Patients with family history have shown significant differences (P≤0.05) in the levels of DHEA-S, FSH, LH and prolactin. In conclusion, this study revealed significantly increase in the DHEA-S levels in the infertile men and negative correlation between DHEA-S and FSH. Therefore, DHEA-S has important role in the diagnosis and follow up of the male infertility.

scholarly journals Clostridium butyricum Protects IPEC-J2 Cells from ETEC K88-Induced Oxidative Damage by Activating the Nrf2/ARE Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Caixia Dou ◽  
Zhiyuan Shang ◽  
Jiayun Qiao ◽  
Yimeng Wang ◽  
Haihua Li
Keyword(s):  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Signaling Pathway ◽  
Antioxidant Response ◽  
Clostridium Butyricum ◽  
Enterotoxigenic Escherichia Coli ◽  
Multiple Infection ◽  
Control Group ◽  
Related Factor ◽  
Viable Bacteria

Clostridium butyricum (CB) is a naturally occurring probiotic compound that can alleviate the oxidative damage induced by enterotoxigenic Escherichia coli K88 (ETEC K88) in porcine intestinal epithelial (IPEC-J2) cells. In this study, we investigate the molecular mechanism underlying this effect. Based on cell viability, malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPX) assessments, the optimal concentration of ETEC K88 was determined to be 1 × 10 3  cfu/mL. Viable bacteria counts in cells pretreated with CB and then infected with ETEC K88 show that CB can adhere to IPEC-J2 cells and that optimal adhesion is achieved at the multiple infection index (MOI) of 50 at 3 h of pretreatment. The results of qPCR indicate that although ETEC significantly decreases the expression levels of antioxidant enzymes regulated by NF-E2-related factor 2 (Nrf2) compared to the control group, CB reverses this effect. To confirm that Nrf2 is directly involved in the mechanism by which CB alleviates oxidative stress, siRNA was used to silence the expression of Nrf2 gene in IPEC-J2 cells. Compared to the NC+ETEC and siRNA+ETEC groups, the expressions of SOD1, SOD2, GPX1, and GPX2 in the NC+CB+ETEC and siRNA+CB+ETEC groups are significantly increased at 12 h and 24 h. This shows that CB can reduce ETEC K88-induced oxidative damage in IPEC-J2 cells by activating the expression of antioxidant enzymes implicated in the Kelch-like ECH-associated protein-1- (Keap1-) Nrf2/antioxidant response element (ARE) signaling pathway.

scholarly journals Oxidative stress and outcome of antioxidant supplementation in patients with polycystic ovarian syndrome (PCOS)

2018 ◽  
Vol 7 (5) ◽  
pp. 1667 ◽  
Author(s):  
Abubakar A. Panti ◽  
Constance E. Shehu ◽  
Yusuf Saidu ◽  
Karima A. Tunau ◽  
Emmanuel I. Nwobodo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Serum Levels ◽  
Clinical Pregnancy ◽  
Oxidative Stress Marker ◽  
Randomised Control Trial ◽  
Antioxidant Supplementation ◽  
Control Groups ◽  
Stress Marker ◽  
And Control

Background: PCOS is a condition with significant decrease in antioxidant with an increased risk of oxidative stress. Antioxidant supplementation has been shown to improve insulin sensitivity in PCOS and may improve outcome of management of PCOS. Objectives of this study were to determine the oxidative stress level of PCOS patients, to assess the effect of antioxidant supplementation on the outcome of management of PCOS and to compare with a control group.Methods: The study was a single blind randomised control trial involving 200 patients with PCOS. The study was conducted at Usmanu Danfodiyo University Teaching Hospital Sokoto. They were randomly divided into intervention and control groups and base line serum levels of oxidative stress marker, antioxidant enzymes, vitamins and minerals were determined. Antioxidant supplementation and placebo were given to the intervention and control groups respectively. All the patients had ovulation induction with clomiphene citrate and were followed up for 6 months. Outcome measures were clinical pregnancy or menstrual regularisation. Level of significance was <0.05.Results: There was statistical significance in the serum levels of oxidative stress marker, antioxidant enzymes, vitamins and minerals between the two groups (post intervention). Glutathione peroxidase (p = 0.001), superoxide dismutase (p = 0.0001), catalase (p= 0.0369), melondialdehyde (p= 0.007), Vitamin A, Vitamin C, Vitamin E (p = 0.0001), zinc and copper (p = 0.0001). The clinical pregnancy outcomes were 22 (22%) versus 2 (2%); live births 18 (18%) versus 2 (2%) and menstrual regularisation 48 (48%) versus 46 (46%) in the intervention and control groups respectively.Conclusions: Antioxidant supplementation in this study significantly affected pregnancy rate in patients with PCOS. Larger studies are suggested to revisit the conclusion of the Cochrane review that antioxidants supplementation had no significant role in female infertility.

scholarly journals Exercise protects against doxorubicin-induced oxidative stress and proteolysis in skeletal muscle

2011 ◽  
Vol 110 (4) ◽  
pp. 935-942 ◽  
Author(s):  
Ashley J. Smuder ◽  
Andreas N. Kavazis ◽  
Kisuk Min ◽  
Scott K. Powers
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Antioxidant Enzymes ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Oxidative Damage ◽  
Muscle Fibers ◽  
Muscular Exercise ◽  
Protease Activation ◽  
Exercise Induced

Doxorubicin (Dox) is a potent antitumor agent used in cancer treatment. Unfortunately, Dox is myotoxic and results in significant reductions in skeletal muscle mass and function. Complete knowledge of the mechanism(s) by which Dox induces toxicity in skeletal muscle is incomplete, but it is established that Dox-induced toxicity is associated with increased generation of reactive oxygen species and oxidative damage within muscle fibers. Since muscular exercise promotes the expression of numerous cytoprotective proteins (e.g., antioxidant enzymes, heat shock protein 72), we hypothesized that muscular exercise will attenuate Dox-induced damage in exercise-trained muscle fibers. To test this postulate, Sprague-Dawley rats were randomly assigned to the following groups: sedentary, exercise, sedentary with Dox, or exercise with Dox. Our results show increased oxidative stress and activation of cellular proteases (calpain and caspase-3) in skeletal muscle of animals treated with Dox. Importantly, our findings reveal that exercise can prevent the Dox-induced oxidative damage and protease activation in the trained muscle. This exercise-induced protection against Dox-induced toxicity may be due, at least in part, to an exercise-induced increase in muscle levels of antioxidant enzymes and heat shock protein 72. Together, these novel results demonstrate that muscular exercise is a useful countermeasure that can protect skeletal muscle against Dox treatment-induced oxidative stress and protease activation in skeletal muscles.

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