scholarly journals Cigarette Smoke Promotes Interleukin-8 Production in Alveolar Macrophages Through the Reactive Oxygen Species/Stromal Interaction Molecule 1/Ca2+ Axis

2021 ◽  
Vol 12 ◽  
Author(s):  
Xianying Zhu ◽  
Yuan Zhan ◽  
Yiya Gu ◽  
Qian Huang ◽  
Ting Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cigarette Smoke ◽  
Alveolar Macrophages ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Stromal Interaction Molecule 1 ◽  
Copd Patients

Chronic obstructive pulmonary disease (COPD), primarily attributed to cigarette smoke (CS), is characterized by multiple pathophysiological changes, including oxidative stress and inflammation. Stromal interaction molecule 1 (STIM1) is a Ca2+ sensor that regulates Ca2+ entry in different types of cells. The present study aimed to explore the relationship between CS-induced oxidative stress and inflammation, as well as the functional role of STIM1 thereinto. Our results showed that the reactive oxygen species (ROS)/STIM1/Ca2+ axis played a critical role in CS-induced secretion of interleukin (IL)-8 in human alveolar macrophages. Specifically, smokers with COPD (SC) showed higher levels of ROS in the lung tissues compared with healthy non-smokers (HN). STIM1 was upregulated in the lung tissues of COPD patients. The expression of STIM1 was positively associated with ROS levels and negatively correlated with pulmonary function. The expression of STIM1 was also increased in the bronchoalveolar lavage fluid (BALF) macrophages of COPD patients and PMA-differentiated THP-1 macrophages stimulated by cigarette smoke extract (CSE). Additionally, CSE-induced upregulation of STIM1 in PMA-differentiated THP-1 macrophages was inhibited by pretreatment with N-acetylcysteine (NAC), a ROS scavenger. Transfection with small interfering RNA (siRNA) targeting STIM1 and pretreatment with NAC alleviated CSE-induced increase in intracellular Ca2+ levels and IL-8 expression. Furthermore, pretreatment with SKF-96365 and 2-APB, the inhibitors of Ca2+ influx, suppressed CSE-induced secretion of IL-8. In conclusion, our study demonstrates that CSE-induced ROS production may increase the expression of STIM1 in macrophages, which further promotes the release of IL-8 by regulating Ca2+ entry. These data suggest that STIM1 may play a crucial role in CSE-induced ROS production and inflammation, and participate in the pathogenesis of COPD.

scholarly journals The Characterization of TA-289, a Novel Antifungal from Fusarium sp.

2021 ◽  
Author(s):  
◽  
Natelle C H Quek
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Cell Death ◽  
Reactive Oxygen ◽  
Chemical Diversity ◽  
Mitochondrial Morphology ◽  
Ros Production ◽  
Oxygen Species ◽  
Wild Type

<p>Natural products offer vast structural and chemical diversity highly sought after in drug discovery research. Saccharomyces cerevisiae makes an ideal model eukaryotic organism for drug mode-of-action studies owing to ease of growth, sophistication of genetic tools and overall homology to higher eukaryotes. Equisetin and a closely related novel natural product, TA-289, are cytotoxic to fermenting yeast, but seemingly less so when yeast actively respire. Cell cycle analyses by flow cytometry revealed a cell cycle block at S-G2/M phase caused by TA-289; previously described oxidative stress-inducing compounds causing cell cycle delay led to further investigation in the involvement of equisetin and TA-289 in mitochondrial-mediated generation of reactive oxygen species. Chemical genomic profiling involving genome-wide scans of yeast deletion mutant strains for TA-289 sensitivity revealed sensitization of genes involved in the mitochondria, DNA damage repair and oxidative stress responses, consistent with a possible mechanism-of-action at the mitochondrion. Flow cytometric detection of reactive oxygen species (ROS) generation caused by TA-289 suggests that the compound may induce cell death via ROS production. The generation of a mutant strain resistant to TA-289 also displayed resistance to a known oxidant, H2O2, at concentrations that were cytotoxic to wild-type cells. The resistant mutant displayed a higher basal level of ROS production compared to the wild-type parent, indicating that the resistance mutation led to an up-regulation of antioxidant capacity which provides cell survival in the presence of TA-289. Yeast mitochondrial morphology was visualized by confocal light microscopy, where it was observed that cells treated with TA-289 displayed abnormal mitochondria phenotypes, further indicating that the compound is acting primarily at the mitochondrion. Similar effects observed with equisetin treatment suggest that both compounds share the same mechanism, eliciting cell death via ROS production in the mitochondrial respiratory chain.</p>

scholarly journals Comparative Reactive Oxygen Species (ROS) Content among Various Flavored Disposable Vape Bars, including Cool (Iced) Flavored Bars

Toxics ◽  
2021 ◽  
Vol 9 (10) ◽  
pp. 235
Author(s):  
Shaiesh Yogeswaran ◽  
Thivanka Muthumalage ◽  
Irfan Rahman
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Health Effects ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Aerosol Generator ◽  
Pulmonary Cells ◽  
Single Puff ◽  
Insight Into

Studies have shown that aerosols generated from flavored e-cigarettes contain Reactive Oxygen Species (ROS), promoting oxidative stress-induced damage within pulmonary cells. Our lab investigated the ROS content of e-cigarette vapor generated from disposable flavored e-cigarettes (vape bars) with and without nicotine. Specifically, we analyzed vape bars belonging to multiple flavor categories (Tobacco, Minty Fruit, Fruity, Minty/Cool (Iced), Desserts, and Drinks/Beverages) manufactured by various vendors and of different nicotine concentrations (0–6.8%). Aerosols from these vape bars were generated via a single puff aerosol generator; these aerosols were then individually bubbled through a fluorogenic solution to semi-quantify ROS generated by these bars in H2O2 equivalents. We compared the ROS levels generated by each vape bar as an indirect determinant of their potential to induce oxidative stress. Our results showed that ROS concentration (μM) within aerosols produced from these vape bars varied significantly among different flavored vape bars and identically flavored vape bars with varying nicotine concentrations. Furthermore, our results suggest that flavoring chemicals and nicotine play a differential role in generating ROS production in vape bar aerosols. Our study provides insight into the differential health effects of flavored vape bars, in particular cool (iced) flavors, and the need for their regulation.

scholarly journals Oxidative stress mediates the apoptosis and epigenetic modification of the Bcl-2 promoter via DNMT1 in a cigarette smoke-induced emphysema model

2020 ◽  
Author(s):  
Huihui Zeng ◽  
Tiao Li ◽  
Xue He ◽  
Shan Cai ◽  
Hong Luo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Protein Expression ◽  
Promoter Methylation ◽  
Dna Methyltransferase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Antioxidant Treatment ◽  
Copd Patients ◽  
Dnmt1 Expression

Abstract Background: Emphysema is a crucial pathological characteristic of chronic obstructive pulmonary disease (COPD). Oxidative stress, apoptosis and epigenetic mechanisms contribute to the pathogenesis of emphysema. However, an attempt to accurately identify whether these mechanisms interact with each other and how they are triggered has never been conducted. Method: The total reactive oxygen species (ROS) level, pulmonary apoptosis and B-cell lymphoma/ leukemia-2 (Bcl-2) expression, an apoptosis regulator, were detected in samples from COPD patients. Bisulfite sequencing PCR (BSP) was conducted to observe the alterations in the methylation of the Bcl-2 promoter in specimens. The dysregulation of DNA methyltransferase enzyme 1 (DNMT1), a vital DNA methyltransferase enzyme, in the lungs of patients was confirmed through western blotting. To find out interactions between oxidative stress and DNA methylation in emphysema, mouse models were built with antioxidant treatment and DNMT1 silencing, and were examined with the pulmonary apoptosis, Bcl-2 and DNMT1 expression, and epigenetic alterations of Bcl-2. Results: Higher reactive oxygen species (ROS) levels and pulmonary apoptosis were observed in COPD patients than in healthy controls. Downregulated Bcl-2 expression with increased promoter methylation and DNMT1 protein expression was found in COPD patients. Antioxidant treatment reduced the level of ROS and dysregulation of DNMT1 expression and emphysematous progression in the smoking models. Following DNMT1 blockage, smoking models showed improved lung function, pulmonary apoptosis, emphysematous progression, and increased Bcl-2 protein expression with less promoter methylation than emphysema mice.Conclusion: Cigarette-induced oxidative stress mediates pulmonary apoptosis and hypermethylation of the Bcl-2 promoter in emphysema models through DNMT1.

scholarly journals Modulators of Oxidative Stress: Chemical and Pharmacological Aspects

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 657 ◽  
Author(s):  
Luciano Saso ◽  
Hande Gürer-Orhan ◽  
Višnja Stepanić
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Antioxidant Proteins

Oxidative stress is represented as an imbalance between reactive oxygen species (ROS) production and the response of antioxidant proteins [...]

scholarly journals Survival Signaling by C-RAF: Mitochondrial Reactive Oxygen Species and Ca2+ Are Critical Targets

2008 ◽  
Vol 28 (7) ◽  
pp. 2304-2313 ◽  
Author(s):  
Andrey V. Kuznetsov ◽  
Julija Smigelskaite ◽  
Christine Doblander ◽  
Manickam Janakiraman ◽  
Martin Hermann ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Mitochondrial Ros ◽  
Survival Signaling ◽  
First Time

ABSTRACT Survival signaling by RAF occurs through largely unknown mechanisms. Here we provide evidence for the first time that RAF controls cell survival by maintaining permissive levels of mitochondrial reactive oxygen species (ROS) and Ca2+. Interleukin-3 (IL-3) withdrawal from 32D cells resulted in ROS production, which was suppressed by activated C-RAF. Oncogenic C-RAF decreased the percentage of apoptotic cells following treatment with staurosporine or the oxidative stress-inducing agent tert-butyl hydroperoxide. However, it was also the case that in parental 32D cells growing in the presence of IL-3, inhibition of RAF signaling resulted in elevated mitochondrial ROS and Ca2+ levels. Cell death is preceded by a ROS-dependent increase in mitochondrial Ca2+, which was absent from cells expressing transforming C-RAF. Prevention of mitochondrial Ca2+ overload after IL-3 deprivation increased cell viability. MEK was essential for the mitochondrial effects of RAF. In summary, our data show that survival control by C-RAF involves controlling ROS production, which otherwise perturbs mitochondrial Ca2+ homeostasis.

scholarly journals Reactive Oxygen Species in Neurodegenerative Diseases: Implications in Pathogenesis and Treatment Strategies

2021 ◽  
Author(s):  
Johnson Olaleye Oladele ◽  
Adenike T. Oladiji ◽  
Oluwaseun Titilope Oladele ◽  
Oyedotun M. Oyeleke
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Neurodegenerative Diseases ◽  
Neurodegenerative Disorders ◽  
Protein Misfolding ◽  
Critical Role ◽  
Treatment Strategies ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
The Brain

Neurodegenerative diseases are debilitating disorders which compromise motor or cognitive functions and are rapidly becoming a global communal disorder with over 46.8 million people suffering dementia worldwide. Aetiological studies have showed that people who are exposed to agricultural, occupational and environmental toxic chemicals that can interfere and degenerate dopaminergic neurons are prone to developing neurodegenerative diseases such as Parkinson Disease. The complex pathogenesis of the neurodegenerative diseases remains largely unknown; however, mounting evidence suggests that oxidative stress, neuroinflammation, protein misfolding, and apoptosis are the hallmarks of the diseases. Reactive oxygen species (ROS) are chemically reactive molecules that have been implicated in the pathogenesis of neurodegenerative diseases. ROS play a critical role as high levels of oxidative stress are commonly observed in the brain of patients with neurodegenerative disorders. This chapter focus on the sources of ROS in the brain, its involvement in the pathogenesis of neurodegenerative diseases and possible ways to mitigate its damaging effects in the affected brain.

scholarly journals Extracellular Reactive Oxygen Species (ROS) Production in Fresh Donkey Sperm Exposed to Reductive Stress, Oxidative Stress and NETosis

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1367
Author(s):  
Iván Yánez-Ortiz ◽  
Jaime Catalán ◽  
Yentel Mateo-Otero ◽  
Marta Dordas-Perpinyà ◽  
Sabrina Gacem ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Selection Process ◽  
Reactive Oxygen ◽  
Polymorphonuclear Neutrophils ◽  
Ros Production ◽  
Oxygen Species ◽  
Oxidative Stresses ◽  
Stress Oxidative

Jenny shows a large endometrial reaction after semen influx to the uterus with a large amount of polymorphonuclear neutrophils (PMN) migrating into the uterine lumen. PMN act as a sperm selection mechanism through phagocytosis and NETosis (DNA extrudes and, together with proteins, trap spermatozoa). While a reduced percentage of spermatozoa are phagocytosed by PMN, most are found to be attached to neutrophil extracellular traps (NETs). This selection process together with sperm metabolism produces a large amount of reactive oxygen species (ROS) that influence the reproductive success. The present study aimed to determine the extracellular ROS production in both sperm and PMN. With this purpose, (1) donkey sperm were exposed to reductive and oxidative stresses, through adding different concentrations of reduced glutathione (GSH) and hydrogen peroxide (H2O2), respectively; and (2) PMN were subjected to NETosis in the presence of the whole semen, sperm, seminal plasma (SP) or other activators such as formyl-methionyl-leucyl-phenylalanine (FMLP). Extracellular ROS production (measured as H2O2 levels) was determined with the Amplex® Red Hydrogen Peroxide/Peroxidase Assay Kit. Donkey sperm showed more resilience to oxidative stress than to the reductive one, and GSH treatments led to greater H2O2 extracellular production. Moreover, not only did SP appear to be the main inducer of NETosis in PMN, but it was also able to maintain the extracellular H2O2 levels produced by sperm and NETosis.

scholarly journals Oxidative stress mediates the apoptosis and epigenetic modification of the Bcl-2 promoter via DNMT1 in a cigarette smoke-induced emphysema model

2020 ◽  
Author(s):  
Huihui Zeng ◽  
Tiao Li ◽  
Xue He ◽  
Shan Cai ◽  
Hong Luo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Protein Expression ◽  
Promoter Methylation ◽  
Dna Methyltransferase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Antioxidant Treatment ◽  
Copd Patients ◽  
Dnmt1 Expression

Abstract Background: Emphysema is a crucial pathological characteristic of chronic obstructive pulmonary disease (COPD). Oxidative stress, apoptosis and epigenetic mechanisms contribute to the pathogenesis of emphysema. However, an attempt to accurately identify whether these mechanisms interact with each other and how they are triggered has never been conducted.Method: The total reactive oxygen species (ROS) level, pulmonary apoptosis and B-cell lymphoma/ leukemia-2 (Bcl-2) expression, an apoptosis regulator, were detected in samples from COPD patients. Bisulfite sequencing PCR (BSP) was conducted to observe the alterations in the methylation of the Bcl-2 promoter in specimens. The dysregulation of DNA methyltransferase enzyme 1 (DNMT1), a vital DNA methyltransferase enzyme, in the lungs of patients was confirmed through western blotting. To find out interactions between oxidative stress and DNA methylation in emphysema, mouse models were built with antioxidant treatment and DNMT1 silencing, and were examined with the pulmonary apoptosis, Bcl-2 and DNMT1 expression, and epigenetic alterations of Bcl-2.Results: Higher reactive oxygen species (ROS) levels and pulmonary apoptosis were observed in COPD patients than in healthy controls. Downregulated Bcl-2 expression with increased promoter methylation and DNMT1 protein expression was found in COPD patients. Antioxidant treatment reduced the level of ROS and dysregulation of DNMT1 expression and emphysematous progression in the smoking models. Following DNMT1 blockage, smoking models showed improved lung function, pulmonary apoptosis, emphysematous progression, and increased Bcl-2 protein expression with less promoter methylation than emphysema mice.Conclusion: Cigarette-induced oxidative stress mediates pulmonary apoptosis and hypermethylation of the Bcl-2 promoter in emphysema models through DNMT1.

scholarly journals Reactive Oxygen Species (ROS), Oxidative Stress and its role In HIV Infection

2020 ◽  
Vol 11 (3) ◽  
pp. 4560-4568
Author(s):  
Sunita S Patil ◽  
Vaishali S Patil ◽  
Arvind Gulbake
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Hiv Infection ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Hiv Patients ◽  
Signalling Molecules ◽  
The Impact

Throughout several regular cell cycles, reactive oxygen species (ROS) play a critical role. When ROS values are high, and when the defence mechanism (antioxidants) cannot neutralise, they harm and modify the part of biological molecules. They also act as signalling molecules which generate a spectrum of disease.In this study, we reviewed existing oxidants, oxidative stress, and their relationship with infection by human immunodeficiency virus in patients, and the effects of oxidative stress in patients with HIV.Our prospect is to do a clinical study on HIV patients and estimate oxidative parameters like nitric oxide, total antioxidant level and correlate them with CD4 count and viral load which may be helpful during monitoring and giving efficient ART to the HIV patients. And also the importance of ROS in infection has been established through clinical and in vitro studies. Here we review the role of oxidative stress in HIV pathogenesis, the impact of ROS on immune responses in HIV patients, and ROS-mediated regulation of HIV infection. Future studies on the interplay between ROS and HIV infection may offer a new strategy for prevention and treatment.

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