scholarly journals Riskometric assessment of factors affecting population health in situational analysis features of cytochemical indicators of activity circulating and tissue leukocytes and oxidative stress as a factor of chronic inflammation

2020 ◽  
Vol 8 (1) ◽  
pp. 43-57
Author(s):  
Irina Sokolovskaya ◽  
Alla Kutsak ◽  
Lyudmila Gordienko ◽  
Valerіі Bulanov ◽  
Tetiana Hryshyna ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Phagocytic Activity ◽  
Polymorphonuclear Leukocytes ◽  
Situational Analysis ◽  
Factors Affecting ◽  
Oxidative Protein Damage ◽  
Stress Oxidative ◽  
Dependent Processes ◽  
And Oxidative Stress ◽  
Dependent Mechanism

The study of the mechanism of oxidative stress and regulation of oxygen-dependent processes is important, as the establishment of a complex interaction between oxidative stress, oxidative protein damage and the body's antioxidant system makes it possible to clarify metabolic pathways of disease pathogenesis. In our study, we concluded that in patients with chronic non-specificinflammatory diseases of the genitals of men and women, the phagocytic activity of polymorphonuclear leukocytes is reduced mainly by the oxygen-dependent mechanism, and tissue - by the oxygen-independent. As an exception in patients with chlamydial infection, the phagocytic activity of tissue polymorphonuclear leukocytes was also reduced by an oxygen-dependent mechanism.

scholarly journals Neuronal Calcium Imaging, Excitability, and Plasticity Changes in the Aldh2–/– Mouse Model of Sporadic Alzheimer’s Disease

2020 ◽  
Vol 77 (4) ◽  
pp. 1623-1637
Author(s):  
Adam O. Ghoweri ◽  
Peter Gagolewicz ◽  
Hilaree N. Frazier ◽  
John C. Gant ◽  
R. David Andrew ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Long Term Potentiation ◽  
Calcium Dysregulation ◽  
Calcium Dependent ◽  
Term Potentiation ◽  
Dependent Processes ◽  
And Oxidative Stress

Background: Dysregulated signaling in neurons and astrocytes participates in pathophysiological alterations seen in the Alzheimer’s disease brain, including increases in amyloid-β, hyperphosphorylated tau, inflammation, calcium dysregulation, and oxidative stress. These are often noted prior to the development of behavioral, cognitive, and non-cognitive deficits. However, the extent to which these pathological changes function together or independently is unclear. Objective: Little is known about the temporal relationship between calcium dysregulation and oxidative stress, as some reports suggest that dysregulated calcium promotes increased formation of reactive oxygen species, while others support the opposite. Prior work has quantified several key outcome measures associated with oxidative stress in aldehyde dehydrogenase 2 knockout (Aldh2–/–) mice, a non-transgenic model of sporadic Alzheimer’s disease. Methods: Here, we tested the hypothesis that early oxidative stress can promote calcium dysregulation across aging by measuring calcium-dependent processes using electrophysiological and imaging methods and focusing on the afterhyperpolarization (AHP), synaptic activation, somatic calcium, and long-term potentiation in the Aldh2–/– mouse. Results: Our results show a significant age-related decrease in the AHP along with an increase in the slow AHP amplitude in Aldh2–/– animals. Measures of synaptic excitability were unaltered, although significant reductions in long-term potentiation maintenance were noted in the Aldh2–/– animals compared to wild-type. Conclusion: With so few changes in calcium and calcium-dependent processes in an animal model that shows significant increases in HNE adducts, Aβ, p-tau, and activated caspases across age, the current findings do not support a direct link between neuronal calcium dysregulation and uncontrolled oxidative stress.

scholarly journals Role of ςB in Heat, Ethanol, Acid, and Oxidative Stress Resistance and during Carbon Starvation inListeria monocytogenes

2001 ◽  
Vol 67 (10) ◽  
pp. 4454-4457 ◽  
Author(s):  
Adriana Ferreira ◽  
Conor P. O'Byrne ◽  
Kathryn J. Boor
Keyword(s):  
Oxidative Stress ◽  
Stationary Phase ◽  
Stress Resistance ◽  
Parent Strain ◽  
Acid Resistance ◽  
Carbon Starvation ◽  
Wild Type ◽  
Oxidative Stress Resistance ◽  
And Oxidative Stress ◽  
Dependent Mechanism

ABSTRACT To determine the contribution of sigma B (ςB) to survival of stationary-phase Listeria monocytogenescells following exposure to environmental stresses, we compared the viability of strain 10403S with that of an isogenic nonpolarsigB null mutant strain after exposure to heat (50°C), ethanol (16.5%), or acid (pH 2.5). Strain viabilities were also determined under the same conditions in cultures that had been previously exposed to sublethal levels of the same stresses (45°C, 5% ethanol, or pH 4.5). The ΔsigB and wild-type strains had similar viabilities following exposure to ethanol and heat, but the ΔsigB strain was almost 10,000-fold more susceptible to lethal acid stress than its parent strain. However, a 1-h preexposure to pH 4.5 yielded a 1,000-fold improvement in viability for the ΔsigB strain. These results suggest the existence in L. monocytogenes of both a ςB-dependent mechanism and a pH-dependent mechanism for acid resistance in the stationary phase. ςB contributed to resistance to both oxidative stress and carbon starvation inL. monocytogenes. The ΔsigB strain was 100-fold more sensitive to 13.8 mM cumene hydroperoxide than the wild-type strain. Following glucose depletion, the ΔsigB strain lost viability more rapidly than the parent strain. ςB contributions to viability during carbon starvation and to acid resistance and oxidative stress resistance support the hypothesis that ςB plays a role in protecting L. monocytogenes against environmental adversities.

scholarly journals Melatonin Inhibits Apoptosis and Oxidative Stress of Mouse Leydig Cells via a SIRT1-Dependent Mechanism

Molecules ◽  
2019 ◽  
Vol 24 (17) ◽  
pp. 3084 ◽  
Author(s):  
Gaoqing Xu ◽  
Jing Zhao ◽  
Hongyu Liu ◽  
Jun Wang ◽  
Wenfa Lu
Keyword(s):  
Oxidative Stress ◽  
Leydig Cells ◽  
B Cell Lymphoma ◽  
Nuclear Antigen ◽  
Protective Effects ◽  
Mrna And Protein Expression ◽  
Silent Information Regulator 1 ◽  
Proliferating Cell ◽  
And Oxidative Stress ◽  
Dependent Mechanism

The purpose of the present study is to examine the effects of melatonin on apoptosis and oxidative stress in mouse Leydig cells and to elucidate the mechanisms responsible for these effects. Our results indicated that 10 ng/mL of melatonin significantly promoted cell viability, the ratio of EdU-positive (5-Ethynyl-2′-deoxyuridine) cells, and increased the mRNA expression of proliferating cell nuclear antigen (PCNA), cyclin D1(CCND1), and cell division control protein 42 (CDC42) (p < 0.05). We also observed that melatonin inhibited apoptosis of mouse Leydig cells, accompanied with increased B-cell lymphoma-2 (BCL-2) and decreased BCL2 associated X (BAX) mRNA and protein expression. Moreover, addition of melatonin significantly decreased the reactive oxygen species (ROS) production and malondialdehyde (MDA) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels, while it increased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels (p < 0.05). In addition, we also found that melatonin increased the expression of SIRT1 (Silent information regulator 1) (p < 0.05). To explore the role of SIRT1 signaling in melatonin-induced cells, mouse Leydig cells were pretreated with EX527, an inhibitor of SIRT1. The protective effects of melatonin on mouse Leydig cells were reversed by EX527, as shown by decreased cell proliferation and increased cell apoptosis and oxidative stress. In summary, our results demonstrated that melatonin inhibited apoptosis and oxidative stress of mouse Leydig cells through a SIRT1-dependent mechanism.

scholarly journals hAMSC-CM Attenuates Paraquat-Induced A549 Cell Damage by Reducing Endoplasmic Reticulum Stress and Oxidative Stress

2021 ◽  
Author(s):  
Futuan Liao ◽  
Liming Gong ◽  
Lijing Jia ◽  
Jianhong Wang ◽  
Tongying Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cell Damage ◽  
Intervention Group ◽  
A549 Cells ◽  
Protective Effects ◽  
Stress Oxidative ◽  
Stress Damage ◽  
And Oxidative Stress

Abstract Acute paraquat (PQ) poisoning results in severe acute lung injury and pulmonary fibrosis, and there is no specific antidote; thus, the mortality rate of PQ poisoning is extremely high. The mechanism of poisoning may be associated with endoplasmic reticulum stress, oxidative stress damage and organ/tissue inflammation. Recent studies have reported that human amnion-derived mesenchymal stem cells (hAMSCs) secrete a variety of cytokines, and that hAMSC-conditioned medium (CM) has anti-inflammatory and immunomodulatory effects. The aim of the present study was to investigate whether hAMSC-CM exerts protective effects against PQ toxicity in A549 cells. The data demonstrated that the activity of A549 cells was decreased after 24 h of PQ exposure and that the cell viability of the hAMSC-CM intervention group was higher compared with the PQ-only group. hAMSC-CM intervention decreased cell damage, apoptosis rates, oxidative stress indexes, Bax/Bcl-2 ratios and CHOP expression levels in poisoned cells by CCK-8 experiment, apoptosis detection, ROS content detection, and Western blot analysis respectively. In conclusion, hAMSC-CM may attenuate the cell damage caused by PQ by reducing endoplasmic reticulum stress and oxidative stress.

scholarly journals Effects of Bene (Pistacia atlantica) on Histopathology of Testis, Sperm Chromatin Quality and Stress Oxidative in Busulfan-Induced Infertile Mice

2019 ◽  
Vol 25 (1) ◽  
pp. 24-30
Author(s):  
Hojat Norasteh ◽  
Shabnam Mohammadi ◽  
Mohammad Reza Nikravesh ◽  
Samaneh Broumand ◽  
Farimah Beheshti
Keyword(s):  
Oxidative Stress ◽  
Sperm Quality ◽  
Sperm Count ◽  
Sperm Parameters ◽  
Sperm Chromatin ◽  
Control Group ◽  
Mice Model ◽  
Pistacia Atlantica ◽  
Stress Oxidative ◽  
And Oxidative Stress

Background: Some plants stimulate spermatogenesis and increase fertility, while some cause spermatogenesis arrest. So far, the effects of bene (Pistacia atlantica) on male fertility have not been studied. The aim of this study was to investigate the effects of bene on sperm parameters, testicular histopathology, sperm quality, and oxidative stress in busulfan-induced infertile mice. Methods: Thirty-five male BALB/c mice were randomly assigned to control, sham, busulfan, bene, and bene + busulfan groups. The busulfan group received 10 mg/kg as a single dose and intraperitoneally. The bene group received pellets containing 10% of bene. Another group received 10 mg/kg busulfan and was fed with pellet containing 10% bene. Then, sperms, sperm chromatin quality, testicular histopathology, and oxidative stress levels were studied on the 35th day of the experiment. Results: Busulfan injection resulted in a significant reduction in sperm parameters compared to the control group (p<0.001); it decreased after bene administration (p<0.001). In addition, in the group treated with bene, the sperm count with damaged DNA was reduced and the level of malondialdehyde decreased compared to the busulfan group. A significant increase was observed in the mean level of superoxide dismutase and catalase enzymes in the bene + busulfan group compared to the busulfan group (p<0.001). The histopathological improvement of the testis was observed in the bene + busulfan group. Conclusion: The administration of 10 mg/kg of bene powder for 35 days reduced the oxidative stress, improved testicular histopathology, sperm chromatin quality, and sperm parameters in the infertile mice model.

scholarly journals Oxidative Stress and Bipolar Mood Disorder: An Important Yet Ambiguous Relationship

2022 ◽  
Author(s):  
Sara Rahsepar ◽  
Amirhooshang Mohammadpour
Keyword(s):  
Oxidative Stress ◽  
Bipolar Disorder ◽  
Thiobarbituric Acid ◽  
Bipolar Mood Disorder ◽  
Oxidative Markers ◽  
Stress Oxidative ◽  
Bipolar Patients ◽  
The Relationship ◽  
And Oxidative Stress

Bipolar disorder is a chronic psychological condition that disturbs many patients' lives around the world. The exact pathophysiology of bipolar disorder is yet unknown, but there are several hypotheses to explain this condition. One of the most challenging theories is the role of oxidative stress in the progression of bipolar disorder. Here, we conducted a narrative review to gather the studies that investigated the relationship between bipolar disorder and oxidative stress. We searched PubMed, Scopus, Web of science, and google scholar databases using the following keywords: “bipolar disorder,” “oxidative stress,” “oxidative markers,” and “bipolar patients.”     A majority of studies showed that oxidative markers such as Thiobarbituric acid reactive substances are significantly higher in bipolar patients compared to healthy subjects. Based on the included articles, bipolar disorder is associated with oxidative stress. Nevertheless, further well-established Cohorts are required to support these results.

scholarly journals NADPH oxidase links endoplasmic reticulum stress, oxidative stress, and PKR activation to induce apoptosis

2010 ◽  
Vol 191 (6) ◽  
pp. 1113-1125 ◽  
Author(s):  
Gang Li ◽  
Christopher Scull ◽  
Lale Ozcan ◽  
Ira Tabas
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Cellular Mechanisms ◽  
Apoptosis Pathway ◽  
Stress Oxidative ◽  
Induced Apoptosis ◽  
And Oxidative Stress

Endoplasmic reticulum (ER)–induced apoptosis and oxidative stress contribute to several chronic disease processes, yet molecular and cellular mechanisms linking ER stress and oxidative stress in the setting of apoptosis are poorly understood and infrequently explored in vivo. In this paper, we focus on a previously elucidated ER stress–apoptosis pathway whose molecular components have been identified and documented to cause apoptosis in vivo. We now show that nicotinamide adenine dinucleotide phosphate reduced oxidase (NOX) and NOX-mediated oxidative stress are induced by this pathway and that apoptosis is blocked by both genetic deletion of the NOX subunit NOX2 and by the antioxidant N-acetylcysteine. Unexpectedly, NOX and oxidative stress further amplify CCAAT/enhancer binding protein homologous protein (CHOP) induction through activation of the double-stranded RNA–dependent protein kinase (PKR). In vivo, NOX2 deficiency protects ER-stressed mice from renal cell CHOP induction and apoptosis and prevents renal dysfunction. These data provide new insight into how ER stress, oxidative stress, and PKR activation can be integrated to induce apoptosis in a pathophysiologically relevant manner.

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