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Aging is a natural process coupled with oxidative stress and chronic inflammation, gradually associated with losing organ function over time. Therefore, the objective of the current work was to peruse the protective effects of 8-week moderate-intensity interval training (MIIT) and ginger extract supplementation on some biomarkers of oxidative stress, inflammation, and lipid metabolism in the liver of elderly males Wistar rats (animal study with ethical code IR.BMSU.REC.1401.015). A total of thirty-two 22-month-aged male Wistar rats were randomly assigned to four groups: (1) control, (2) MIIT, (3) ginger, and (4) MIIT + ginger. After 8 weeks of treadmill training and ginger extract supplementation, the biochemical parameters (liver enzyme and lipid profile), inflammatory mediators (leucine-rich α-2 glycoprotein 1 (LRG1), tumor necrosis factor-alpha, and interleukin-6), pro-oxidant (malondialdehyde), antioxidant biomarkers (catalase, superoxide dismutase, total antioxidant capacity), some lipid metabolism regulators (carnitine palmitoyltransferase 1, adipose triglyceride lipase, acetyl-CoA carboxylase, CD36, and AMP-activated protein kinase), and liver histopathological changes were appraised. The acquired findings pointed out that MIIT combined with ginger extract appreciably diminished the serum levels of LRG1, liver enzymes, and lipid profile relative to the other groups after 8 weeks of intervention. Furthermore, ginger + MIIT caused a great improvement in the liver levels of antioxidant biomarkers, pro-oxidant, pro-inflammatory biomarkers, lipid metabolism regulators, and liver tissue impairment compared to the other groups. The findings suggested that MIIT + ginger was more effective in improving examined indices relative to the other groups., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Sulfur mustard (SM) is a chemical compound that preferentially targets ocular, cutaneous and pulmonary tissues. Although pathologic effect of SM has been extensively considered, molecular and cellular mechanism of its toxicity, especially at the chronic phase of injury is not well-understood. Excessive production of reactive oxygen species (ROS) and oxidative stress (OS) appears to be involved in SM-induced injuries. SM may trigger several molecular and cellular pathways linked to OS and inflammation that can subsequently result in cell death and apoptosis. At the acute phase of injury, SM can enhance ROS production and OS by reducing the activity of antioxidants, depletion of intercellular glutathione (GSH), decreasing the productivity of GSH-dependent antioxidants, mitochondrial deficiency, accumulation of leukocytes and pro-inflammatory cytokines. Overexpression of ROS producing enzymes and down-regulation of antioxidant enzymes are probably the major events by which SM leads to OS at the chronic phase of injury. Therefore, antioxidant therapy with potent antioxidants such as N-acetylcysteine and curcumin may be helpful to mitigate SM-induced OS damages. This review aims to discuss the proposed cellular and molecular mechanisms of acute and delayed SM toxicity, the importance of OS and mechanisms by which SM increases OS either at the acute or chronic phases of injuries along with research on antioxidant therapy as a suitable antidote.

Background: Semen hyperviscosity is a threatening cause of abnormal spermatozoa and infertility in men. We aimed to evaluate oxidative stress, antioxidants depletion and sperm apoptosis as main reasons for poor quality of spermatozoa in men with hyperviscous semen. Materials and Methods: In this cross-sectional study, ejaculate specimens were collected from fertile (n=102) and infertile men with hyperviscous semen (n=123) and without semen hyperviscosity (n=143). Total antioxidant capacity (TAC), glutathione (GSH), malondialdehyde (MDA), protein carbonyl (PC), 8-hydroxydeoxyguanosine (8-OHdG), and were measured in semen samples to estimate oxidative stress status. Gene expression pattern of BAX, CASPASE-9, CASPASE-3, and BCL2 was assessed to estimate sperm apoptosis. Results: The average of sperm count, normal morphology, normal motility, and sperm vitality in men with hyperviscous semen was significantly lower than infertile subjects without hyperviscous semen (P<0.01). Men with hyperviscous semen exhibited higher levels of PC (8.34 ± 1.03 nmol/mg vs. 6.01 ± 0.93 nmol/mg, P=0.008), MDA (1.14 ± 0.27 nmol/ ml vs. 0.89 ± 0.22 nmol/ml, P=0.031), 8-OHdG (259.71 ± 24.59 ng/ml vs. 197.13 ± 18.47 ng/ml, P=0.009), but lower TAC contents (1250.44 ± 66.23 μM/L vs. 1784.31 ± 89.87 μM/L, P=0.018) and GSH (3.82 ± 1.05 μM vs. 5.89 ± 0.87 μM, P=0.021) than men with non-viscous semen. The expression of BAX, CASPASE-3 and CASPASE-9 genes in men with hyperviscous semen was significantly increased by 1.39-fold (P=0.041), 1.47-fold (P=0.046), 1.29-fold (P=0.048), respectively, as compared with the infertile subjects without hyperviscous semen. However, BCL2 expression in infertile men without hyperviscous semen was higher compared to those with hyperviscous semen (1.36-fold, P=0.044). Conclusion: Hyperviscous semen is markedly associated with depletion of seminal plasma antioxidants, sperm membrane lipid peroxidation, DNA and protein oxidation, and sperm apoptosis. Antioxidant therapy might be considered as a valuable strategy to protect sperm cells against oxidative damage in cases with seminal fluid hyperviscosity. [ABSTRACT FROM AUTHOR]

Zinc (Zn) is necessary for the normal function of the male reproductive system and spermatozoa. Although influences of zinc deficiency on impaired spermatogenesis and male infertility have been widely considered, the molecular and cellular mechanisms of these abnormalities are not well understood. General abnormalities, including hypogonadism, Leydig cells damage, deficiency of sex hormone production and impaired spermatogenesis, as well as inflammation, antioxidant depletion, sperm death and male infertility can be observed during zinc deficiency. However, it is not obvious which pathways are relevant to the pathogenesis of zinc deficiency. Oxidative stress (OS) induced by reactive oxygen species is likely as the main mechanism of zinc deficiency which is associated with sperm DNA fragmentation, decrease in sperm membrane integrity, apoptosis, depletion of antioxidants, and consequently poor sperm quality and male infertility. Therefore, identification of these pathways will give valuable information regarding the mechanisms of zinc deficiency on the male reproductive system and the potential way for developing a better clinical approach. In this review, we aim to discuss the proposed cellular and molecular mechanisms of zinc deficiency on the male reproductive system, the importance of OS and mechanisms by which zinc deficiency induces OS and depletion of other antioxidants. [ABSTRACT FROM AUTHOR]

Context: Sulfur mustard (SM) is a lipophilic and reactive chemical compound that targets human airway system. Objective: Glutathione (GSH) depletion, oxidative stress (OS) status, and changes in expression of GSH-dependent antioxidant enzymes were considered in human mustard lungs. Materials and methods: Lung biopsies and bronchoalveolar lavage (BAL) were collected from non-exposed (n = 10) individuals and SM-exposed patients (n = 12). Alterations in expression of GSH-dependent enzymes were studied using RT2 Profiler™ PCR array. OS was evaluated by determining BAL fluid levels of total antioxidant capacity (TAC), malondialdehyde (MDA), and GSH. Results: Mean TAC (0.142 ± 0.027 µmol/l) and GSH (4.98 ± 1.02 nmol/l) in BAL fluids of control group was significantly higher (p < .05) than those in SM-exposed patients (TAC = 0.095 ± 0.018 µmol/l and GSH= 3.09 ± 1.02 nmol/l), while MDA level in BAL fluids of these patients (0.71 ± 0.06 nmol/l) was significantly (p = .001) higher than that in controls (0.49 ± 0.048 nmol/l). Glutathione peroxidases (GPXs), glutathione-s-transferases (GSTs), and glutathione synthetase (GSS) enzymes were overexpressed in mustard lung biopsies, while glutathione reductase (GSR) was significantly downregulated (14.95-fold). Conclusions: GSH depletion induced by GSR downregulation may be a major mechanism of SM toxicity on human lung. Despite overexpression of GSTs and GPXs genes, GSH depletion may decline the productivity of these enzymes and total antioxidants capacity, which is associated with OS. [ABSTRACT FROM AUTHOR]