scholarly journals Adverse effects of microplastics and oxidative stress-induced MAPK/Nrf2 pathway-mediated defense mechanisms in the marine copepod Paracyclopina nana

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Chang-Bum Jeong ◽  
Hye-Min Kang ◽  
Min-Chul Lee ◽  
Duck-Hyun Kim ◽  
Jeonghoon Han ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adverse Effects ◽  
Defense Mechanisms ◽  
Nrf2 Pathway ◽  
Marine Copepod ◽  
And Oxidative Stress

scholarly journals Apigenin Protects Against Renal Tubular Epithelial Cell Injury and Oxidative Stress by High Glucose via Regulation of NF-E2-Related Factor 2 (Nrf2) Pathway

2019 ◽  
Vol 25 ◽  
pp. 5280-5288 ◽  
Author(s):  
Jichen Zhang ◽  
Xuemei Zhao ◽  
Hongling Zhu ◽  
Jingnan Wang ◽  
Junhua Ma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
High Glucose ◽  
Cell Injury ◽  
Tubular Epithelial Cell ◽  
Related Factor ◽  
Renal Tubular Epithelial Cell ◽  
Nrf2 Pathway ◽  
Renal Tubular ◽  
And Oxidative Stress

scholarly journals Hyperbaric Oxygen Treatment: Effects on Mitochondrial Function and Oxidative Stress

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1827
Author(s):  
Nofar Schottlender ◽  
Irit Gottfried ◽  
Uri Ashery
Keyword(s):  
Oxidative Stress ◽  
Hyperbaric Oxygen ◽  
Mitochondrial Function ◽  
Defense Mechanisms ◽  
Term Treatment ◽  
Mitochondrial Activity ◽  
Hyperbaric Oxygen Treatment ◽  
Oxygen Treatment ◽  
Long Term Treatment ◽  
And Oxidative Stress

Hyperbaric oxygen treatment (HBOT)—the administration of 100% oxygen at atmospheric pressure (ATA) greater than 1 ATA—increases the proportion of dissolved oxygen in the blood five- to twenty-fold. This increase in accessible oxygen places the mitochondrion—the organelle that consumes most of the oxygen that we breathe—at the epicenter of HBOT’s effects. As the mitochondrion is also a major site for the production of reactive oxygen species (ROS), it is possible that HBOT will increase also oxidative stress. Depending on the conditions of the HBO treatment (duration, pressure, umber of treatments), short-term treatments have been shown to have deleterious effects on both mitochondrial activity and production of ROS. Long-term treatment, on the other hand, improves mitochondrial activity and leads to a decrease in ROS levels, partially due to the effects of HBOT, which increases antioxidant defense mechanisms. Many diseases and conditions are characterized by mitochondrial dysfunction and imbalance between ROS and antioxidant scavengers, suggesting potential therapeutic intervention for HBOT. In the present review, we will present current views on the effects of HBOT on mitochondrial function and oxidative stress, the interplay between them and the implications for several diseases.

scholarly journals Curcumin Attenuates Oxaliplatin-Induced Liver Injury and Oxidative Stress by Activating the Nrf2 Pathway

2020 ◽  
Vol Volume 14 ◽  
pp. 73-85 ◽  
Author(s):  
Yulei Lu ◽  
Shengming Wu ◽  
Bangde Xiang ◽  
Lequn Li ◽  
Youzhi Lin
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Nrf2 Pathway ◽  
And Oxidative Stress

Adverse effects of low occupational cadmium exposure on renal and oxidative stress biomarkers in solderers

2012 ◽  
Vol 70 (2) ◽  
pp. 108-113 ◽  
Author(s):  
Ramona Hambach ◽  
Dominique Lison ◽  
Patrick D'Haese ◽  
Joost Weyler ◽  
Guido François ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adverse Effects ◽  
Cadmium Exposure ◽  
Oxidative Stress Biomarkers ◽  
Stress Biomarkers ◽  
And Oxidative Stress

scholarly journals Cardioprotective Effect of Quercetin in 5/6-Nephrectomized Rats: Focus on Myocardial fibrosis and Oxidative Stress

2017 ◽  
Vol 2 (3) ◽  
pp. 87-95
Author(s):  
Tri Yuliani ◽  
Melva Louisa ◽  
Wawaimuli Arozal ◽  
Vivian Soetikno ◽  
Nafrialdi Nafrialdi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Fibrosis ◽  
Defense Mechanisms ◽  
Chronic Administration ◽  
Cardioprotective Effect ◽  
Sprague Dawley ◽  
Antioxidant Mechanism ◽  
Uremic Cardiomyopathy ◽  
And Oxidative Stress ◽  
Gpx Activity

Uremic cardiomyopathy is the leading cause of death in patients with chronic kidney disease. Fluid overload and oxidative stress play important roles in its pathogenesis. This study aims to determine the effect of quercetin on uremic cardiomyopathy in 5/6-nephrectomized rats. To our knowledge, its cardioprotective effect on uremic cardiomyopathy induced in rats by 5/6 nephrectomy has not been investigated yet. Uremia was induced surgically in male Sprague-Dawley rats via 5/6 nephrectomy. Quercetin was administered per orally at a dose of 100 mg/kg/day for 8 weeks prior to sacrifice. Meanwhile, captopril was administered at a dose of 10 mg/kg/day. Lipid peroxidation was assessed using TBARS reaction, while GPX activity was determined to explore the endogen antioxidant mechanism. Myocardial fibrosis was analyzed using Massons’ Trichrome staining and the level of NT-proBNP in plasma was measured as a marker of cardiac dysfunction. Nephrectomy 5/6 had no effects on plasma NT– proBNP levels, cardiac and plasma MDA levels, but induced mild myocardial fibrosis and significant increase in cardiac GPX activity in comparison with normal rat (p<0.05). However, administration of quercetin or captopril did not ameleriote those mild myocardial fibrosis and increased GPX activity. Uremic cardiomyopathy induced by 5/6 nephrectomy demonstrated mild myocardial fibrosis but preservation of cardiac function demonstrated by NT-proBNP levels. Increased of GPX activity in the nephrectomized-rats compared to the control rats (p<0.05) suggests induction of antioxidant defense mechanisms that might not be exhausted yet. This condition highlighted a compensatory phase which was unchanged following chronic administration of either quercetin or captopril.

scholarly journals Therapeutic Influence on Important Targets Associated with Chronic Inflammation and Oxidative Stress in Cancer Treatment

Cancers ◽  
2021 ◽  
Vol 13 (23) ◽  
pp. 6062
Author(s):  
Margarita Neganova ◽  
Junqi Liu ◽  
Yulia Aleksandrova ◽  
Sergey Klochkov ◽  
Ruitai Fan
Keyword(s):  
Oxidative Stress ◽  
Chronic Inflammation ◽  
Defense Mechanisms ◽  
Cell Transformation ◽  
Oncogenic Signaling ◽  
Predisposing Factor ◽  
Tumor Spread ◽  
Chronic Inflammatory Response ◽  
Cell Defense ◽  
And Oxidative Stress

Chronic inflammation and oxidative stress are the interconnected pathological processes, which lead to cancer initiation and progression. The growing level of oxidative and inflammatory damage was shown to increase cancer severity and contribute to tumor spread. The overproduction of reactive oxygen species (ROS), which is associated with the reduced capacity of the endogenous cell defense mechanisms and/or metabolic imbalance, is the main contributor to oxidative stress. An abnormal level of ROS was defined as a predisposing factor for the cell transformation that could trigger pro-oncogenic signaling pathways, induce changes in gene expression, and facilitate accumulation of mutations, DNA damage, and genomic instability. Additionally, the activation of transcription factors caused by a prolonged oxidative stress, including NF-κB, p53, HIF1α, etc., leads to the expression of several genes responsible for inflammation. The resulting hyperactivation of inflammatory mediators, including TNFα, TGF-β, interleukins, and prostaglandins can contribute to the development of neoplasia. Pro-inflammatory cytokines were shown to trigger adaptive reactions and the acquisition of resistance by tumor cells to apoptosis, while promoting proliferation, invasion, and angiogenesis. Moreover, the chronic inflammatory response leads to the excessive production of free radicals, which further aggravate the initiated reactions. This review summarizes the recent data and progress in the discovery of mechanisms that associate oxidative stress and chronic inflammation with cancer onset and metastasis. In addition, the review provides insights for the development of therapeutic approaches and the discovery of natural substances that will be able to simultaneously inhibit several key oncological and inflammation-related targets.

Hypoxia. 1. Intracellular sensors for oxygen and oxidative stress: novel therapeutic targets

2011 ◽  
Vol 300 (2) ◽  
pp. C226-C231 ◽  
Author(s):  
Toshio Miyata ◽  
Shunya Takizawa ◽  
Charles van Ypersele de Strihou
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanisms ◽  
Tissue Injury ◽  
Hypoxia Inducible Factor ◽  
Oxygen Metabolism ◽  
Related Factor ◽  
Novel Therapy ◽  
Prolyl Hydroxylases ◽  
Hypoxic Tolerance ◽  
And Oxidative Stress

A variety of human disorders, e.g., ischemic heart disease, stroke, kidney disease, eventually share the deleterious consequences of a common, hypoxic and oxidative stress pathway. In this review, we utilize recent information on the cellular defense mechanisms against hypoxia and oxidative stress with the hope to propose new therapeutic tools. The hypoxia-inducible factor (HIF) is a key player as it activates a broad range of genes protecting cells against hypoxia. Its level is determined by its degradation rate by intracellular oxygen sensors prolyl hydroxylases (PHDs). There are three different PHD isoforms (PHD1–3). Small molecule PHD inhibitors improve hypoxic injury in experimental animals but, unfortunately, may induce adverse effects associated with PHD2 inhibition, e.g., angiogenesis. As yet, no inhibitor specific for a distinct PHD isoform is currently available. Still, the specific disruption of the PHD1 gene is known to induce hypoxic tolerance, without angiogenesis and erythrocytosis, by reprogramming basal oxygen metabolism with an attendant decreased oxidative stress in hypoxic mitochondria. A specific PHD1 inhibitor might therefore offer a novel therapy against hypoxia. The nuclear factor-erythroid 2 p45-related factor 2 (Nrf2) regulates the basal and inducible expression of numerous antioxidant stress genes. Disruption of its gene exacerbates oxidative tissue injury. Nrf2 activity is modulated by Kelch-like ECH-associated protein 1 (Keap1), an intracellular sensor for oxidative stress. Inhibitors of Keap 1 may prove therapeutic against oxidative tissue injury.

scholarly journals Mangiferin exerts neuroprotective activity against lead-induced toxicity and oxidative stress via Nrf2 pathway

2020 ◽  
Vol 12 (1) ◽  
pp. 36-46 ◽  
Author(s):  
Hao-wen Li ◽  
Tai-jin Lan ◽  
Chen-xia Yun ◽  
Ke-di Yang ◽  
Zheng-cai Du ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuroprotective Activity ◽  
Nrf2 Pathway ◽  
And Oxidative Stress

scholarly journals Effects of toner-handling work on respiratory function, chest X-ray findings, and biomarkers of inflammation, allergy, and oxidative stress: a 10-year prospective Japanese cohort study

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Niina Terunuma ◽  
Kazunori Ikegami ◽  
Hiroko Kitamura ◽  
Hajime Ando ◽  
Shizuka Kurosaki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cohort Study ◽  
Adverse Effects ◽  
Respiratory Function ◽  
Exposure Group ◽  
High Concentration ◽  
X Ray ◽  
Low Concentration ◽  
Chest X Ray ◽  
And Oxidative Stress

Abstract Background Exposure to toner, a substance used in photocopiers and printers, has been associated with siderosilicosis and other adverse effects. However, these findings are limited, and there is insufficient evidence on the long-term effects of toner exposure. Using longitudinal analysis, this study aimed to examine the effects of work involving toner exposure on the respiratory system over time. Methods We conducted a prospective cohort study in a Japanese toner and copier manufacturing enterprise between 2003 and 2013. The cohort included a total of 1468 workers, which comprised 887 toner-handling workers and 581 non-toner-handling workers. We subdivided the toner-handling workers into two groups according to the toner exposure concentration, based on the baseline survey in 2003. We compared the chest X-ray results, respiratory function indicators, and serum and urinary biomarkers of inflammation, allergy, and oxidative stress among the three groups: high-concentration toner exposure group, low-concentration toner exposure group, and non-toner-handling group. To consider the effects of individual differences on the longitudinal data, we used a linear mixed model. Results Similar chest X-ray results, the biomarkers, and most of the respiratory function indicators were found in the non-toner-handling and toner-handling groups. There were no significant yearly changes in the percentage of vital capacity (%VC) in the high-concentration toner exposure group, while there was a significant yearly increase in %VC in the low-concentration toner exposure group and non-toner-handling group. The yearly change in each group was as follows: high-concentration toner exposure group, − 0.11% (95% confidence interval [CI], − 0.29 to 0.08; P = 0.250); low-concentration toner exposure group, 0.13% (95% CI, 0.09–0.17; P < 0.001); and non-toner-handling group, 0.15% (95% CI, 0.01–0.20; P < 0.001). Conclusions In our 10-year prospective study, toner-handling work was not associated with the deterioration of respiratory function and an increase in biomarker values for inflammation, allergy, and oxidative stress. This finding suggests that toner-handling work is irrelevant to the onset of respiratory disease and has minimal adverse effects on the respiratory system under a well-managed work environment.

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