scholarly journals Epigenetic therapy attenuates oxidative stress in BMSCs during ageing

2021 ◽  
Author(s):  
Xiaoxia Su ◽  
Haoyu Zhang ◽  
Fengzhen Lei ◽  
Rui Wang ◽  
Tingting Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epigenetic Therapy

Epigenetic Therapy as a Potential Approach for Targeting Oxidative Stress–Induced Non-Small-Cell Lung Cancer

2021 ◽  
pp. 1-16
Author(s):  
Ridhima Wadhwa ◽  
Keshav Raj Paudel ◽  
Shakti Shukla ◽  
Madhur Shastri ◽  
Gaurav Gupta ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Epigenetic Therapy ◽  
Small Cell Lung ◽  
Potential Approach

scholarly journals Oxidative stress induced lung cancer and COPD: opportunities for epigenetic therapy

2009 ◽  
Vol 13 (9a) ◽  
pp. 2800-2821 ◽  
Author(s):  
Matthew W. Lawless ◽  
Kenneth J. O’Byrne ◽  
Steven G. Gray
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Epigenetic Therapy

scholarly journals Oxidative Stress and DNA Methylation in Prostate Cancer

2010 ◽  
Vol 2010 ◽  
pp. 1-14 ◽  
Author(s):  
Krishna Vanaja Donkena ◽  
Charles Y. F. Young ◽  
Donald J. Tindall
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Prostate Cancer ◽  
Dna Methylation ◽  
Cancer Patients ◽  
Epigenetic Modification ◽  
Regulation Of Gene Expression ◽  
Antioxidant Properties ◽  
Lifestyle Changes ◽  
Epigenetic Therapy

The protective effects of fruits, vegetables, and other foods on prostate cancer may be due to their antioxidant properties. An imbalance in the oxidative stress/antioxidant status is observed in prostate cancer patients. Genome oxidative damage in prostate cancer patients is associated with higher lipid peroxidation and lower antioxidant levels. Oxygen radicals are associated with different steps of carcinogenesis, including structural DNA damage, epigenetic changes, and protein and lipid alterations. Epigenetics affects genetic regulation, cellular differentiation, embryology, aging, cancer, and other diseases. DNA methylation is perhaps the most extensively studied epigenetic modification, which plays an important role in the regulation of gene expression and chromatin architecture, in association with histone modification and other chromatin-associated proteins. This review will provide a broad overview of the interplay of oxidative stress and DNA methylation, DNA methylation changes in regulation of gene expression, lifestyle changes for prostate cancer prevention, DNA methylation as biomarkers for prostate cancer, methods for detection of methylation, and clinical application of DNA methylation inhibitors for epigenetic therapy.

Epigenetic Therapy as a Potential Approach for Targeting Oxidative Stress–Induced Non-Small-Cell Lung Cancer

2021 ◽  
pp. 1-16
Author(s):  
Ridhima Wadhwa ◽  
Keshav Raj Paudel ◽  
Shakti Shukla ◽  
Madhur Shastri ◽  
Gaurav Gupta ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Epigenetic Therapy ◽  
Small Cell Lung ◽  
Potential Approach

Lycopene alleviates sulfamethoxazole-induced hepatotoxicity in grass carp (Ctenopharyngodon idellus) via suppression of oxidative stress, inflammation and apoptosis

2020 ◽  
Vol 11 (10) ◽  
pp. 8547-8559
Author(s):  
Hongjing Zhao ◽  
Yu Wang ◽  
Mengyao Mu ◽  
Menghao Guo ◽  
Hongxian Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Secondary Metabolites ◽  
Human Health ◽  
Grass Carp ◽  
Aquatic Environment ◽  
Ctenopharyngodon Idellus

Antibiotics are used worldwide to treat diseases in humans and other animals; most of them and their secondary metabolites are discharged into the aquatic environment, posing a serious threat to human health.

Copper-dependent ATP7B up-regulation drives the resistance of TMEM16A-overexpressing head-and-neck cancer models to platinum toxicity

2019 ◽  
Vol 476 (24) ◽  
pp. 3705-3719 ◽  
Author(s):  
Avani Vyas ◽  
Umamaheswar Duvvuri ◽  
Kirill Kiselyov
Keyword(s):  
Oxidative Stress ◽  
Head And Neck ◽  
Transcriptional Activation ◽  
Platinum Resistance ◽  
Mrna Levels ◽  
Strong Positive Correlation ◽  
Platinum Compounds ◽  
Copper Chelation ◽  
Novel Approach ◽  
Cancer Models

Platinum-containing drugs such as cisplatin and carboplatin are routinely used for the treatment of many solid tumors including squamous cell carcinoma of the head and neck (SCCHN). However, SCCHN resistance to platinum compounds is well documented. The resistance to platinum has been linked to the activity of divalent transporter ATP7B, which pumps platinum from the cytoplasm into lysosomes, decreasing its concentration in the cytoplasm. Several cancer models show increased expression of ATP7B; however, the reason for such an increase is not known. Here we show a strong positive correlation between mRNA levels of TMEM16A and ATP7B in human SCCHN tumors. TMEM16A overexpression and depletion in SCCHN cell lines caused parallel changes in the ATP7B mRNA levels. The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS). Pretreatment with either chelator significantly increased cisplatin's sensitivity, particularly in the context of TMEM16A overexpression. We propose that increased oxidative stress in TMEM16A-overexpressing cells liberates the chelated copper in the cytoplasm, leading to the transcriptional activation of ATP7B expression. This, in turn, decreases the efficacy of platinum compounds by promoting their vesicular sequestration. We think that such a new explanation of the mechanism of SCCHN tumors’ platinum resistance identifies novel approach to treating these tumors.

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

Pancreatic stones shockwave lithotripsy induces oxidative stress. A study of lipoperoxidation products in pure pancreatic juice

2001 ◽  
Vol 120 (5) ◽  
pp. A217-A217
Author(s):  
C SPADA ◽  
S SANTINI ◽  
F FOSCHIA ◽  
M PANDOLFI ◽  
V PERRI ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pancreatic Juice ◽  
Shockwave Lithotripsy ◽  
Pure Pancreatic Juice ◽  
Pancreatic Stones

Dilinoleoylphosphatidylcholine (DLPC) protects against alcohol-induced oxidative stress in rats

2001 ◽  
Vol 120 (5) ◽  
pp. A116-A116
Author(s):  
S ALEYNIK ◽  
M ALEYNIK ◽  
C LIEBER
Keyword(s):  
Oxidative Stress
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