scholarly journals Evidence for different mechanisms of action behind the mutagenic effects of 4-NOPD and OPD: the role of DNA damage, oxidative stress and an imbalanced nucleotide pool

Mutagenesis ◽  
2013 ◽  
Vol 28 (6) ◽  
pp. 637-644 ◽  
Author(s):  
R. Asgard ◽  
S. Haghdoost ◽  
S. O. Golkar ◽  
B. Hellman ◽  
S. Czene
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Mechanisms Of Action ◽  
Mutagenic Effects

scholarly journals The Role of Oxidative Stress in NAFLD–NASH–HCC Transition—Focus on NADPH Oxidases

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 687
Author(s):  
Daniela Gabbia ◽  
Luana Cannella ◽  
Sara De De Martin
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Current Knowledge ◽  
Mechanisms Of Action ◽  
Nadph Oxidases ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

A peculiar role for oxidative stress in non-alcoholic fatty liver disease (NAFLD) and its transition to the inflammatory complication non-alcoholic steatohepatitis (NASH), as well as in its threatening evolution to hepatocellular carcinoma (HCC), is supported by numerous experimental and clinical studies. NADPH oxidases (NOXs) are enzymes producing reactive oxygen species (ROS), whose abundance in liver cells is closely related to inflammation and immune responses. Here, we reviewed recent findings regarding this topic, focusing on the role of NOXs in the different stages of fatty liver disease and describing the current knowledge about their mechanisms of action. We conclude that, although there is a consensus that NOX-produced ROS are toxic in non-neoplastic conditions due to their role in the inflammatory vicious cycle sustaining the transition of NAFLD to NASH, their effect is controversial in the neoplastic transition towards HCC. In this regard, there are indications of a differential effect of NOX isoforms, since NOX1 and NOX2 play a detrimental role, whereas increased NOX4 expression appears to be correlated with better HCC prognosis in some studies. Further studies are needed to fully unravel the mechanisms of action of NOXs and their relationships with the signaling pathways modulating steatosis and liver cancer development.

scholarly journals Role of histone deacetylase 2 in epigenetics and cellular senescence: implications in lung inflammaging and COPD

2012 ◽  
Vol 303 (7) ◽  
pp. L557-L566 ◽  
Author(s):  
Hongwei Yao ◽  
Irfan Rahman
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Histone Deacetylase ◽  
Dna Damage Response ◽  
Cellular Senescence ◽  
Premature Aging ◽  
Epigenetic Mechanism ◽  
Histone Deacetylase 2 ◽  
Damage Response

Histone deacetylase 2 (HDAC2) is a class I histone deacetylase that regulates various cellular processes, such as cell cycle, senescence, proliferation, differentiation, development, apoptosis, and glucocorticoid function in inhibiting inflammatory response. HDAC2 has been shown to protect against DNA damage response and cellular senescence/premature aging via an epigenetic mechanism in response to oxidative stress. These phenomena are observed in patients with chronic obstructive pulmonary disease (COPD). HDAC2 is posttranslationally modified by oxidative/carbonyl stress imposed by cigarette smoke and oxidants, leading to its reduction via an ubiquitination-proteasome dependent degradation in lungs of patients with COPD. In this perspective, we have discussed the role of HDAC2 posttranslational modifications and its role in regulation of inflammation, histone/DNA epigenetic modifications, DNA damage response, and cellular senescence, particularly in inflammaging, and during the development of COPD. We have also discussed the potential directions for future translational research avenues in modulating lung inflammaging and cellular senescence based on epigenetic chromatin modifications in diseases associated with increased oxidative stress.

The role of melatonin in oxidative stress, DNA damage, apoptosis and angiogenesis in fetal eye under preeclampsia and melatonin deficiency stress

2019 ◽  
Author(s):  
Zeynep Banu Doganlar ◽  
Hande Güçlü ◽  
Özlem Öztopuz ◽  
Hakan Türkön ◽  
Ayten Dogan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage

Protective role of chrysin on doxorubicin‐induced oxidative stress and DNA damage in rat testes

Andrologia ◽  
2020 ◽  
Vol 52 (9) ◽  
Author(s):  
Saadet Belhan ◽  
Mustafa Özkaraca ◽  
Uğur Özdek ◽  
Ahmet Ufuk Kömüroğlu
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Protective Role

scholarly journals The role of oxidative stress in citreoviridin‐induced DNA damage in human liver‐derived HepG2 cells

2013 ◽  
Vol 30 (5) ◽  
pp. 530-537 ◽  
Author(s):  
Yuntao Bai ◽  
Li‐Ping Jiang ◽  
Xiao‐Fang Liu ◽  
Dong Wang ◽  
Guang Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Hepg2 Cells ◽  
Human Liver

scholarly journals Mitochondrial, lysosomal and DNA damages induced by acrylamide attenuate by ellagic acid in human lymphocyte

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0247776
Author(s):  
Ahmad Salimi ◽  
Elahe Baghal ◽  
Hassan Ghobadi ◽  
Niloufar Hashemidanesh ◽  
Farzad Khodaparast ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Dna Damage ◽  
Ellagic Acid ◽  
Human Lymphocytes ◽  
Health Concern ◽  
Cytochrome P450 Enzyme ◽  
Dna Damages ◽  
Ros Formation

Acrylamide (AA), is an important contaminant formed during food processing under high temperature. Due to its potential neurotoxicity, reproductive toxicity, hepatotoxicity, immunotoxicity, genotoxicity and carcinogenicity effects, this food contaminant has been recognized as a human health concern. Previous studies showed that acrylamide-induced toxicity is associated with active metabolite of acrylamide by cytochrome P450 enzyme, oxidative stress, mitochondrial dysfunction and DNA damage. In the current study, we investigated the role of oxidative stress in acrylamide’s genotoxicity and therapeutic potential role of ellagic acid (EA) in human lymphocytes. Human lymphocytes were simultaneously treated with different concentrations of EA (10, 25 and 50 μM) and acrylamide (50 μM) for 4 h at 37°C. After 4 hours of incubation, the toxicity parameters such cytotoxicity, ROS formation, oxidized/reduced glutathione (GSH/GSSG) content, malondialdehyde (MDA) level, lysosomal membrane integrity, mitochondria membrane potential (ΔΨm) collapse and 8-hydroxy-2’-deoxyguanosine (8-OHdG) were analyzed using biochemical and flow cytometry evaluations. It has been found that acrylamide (50 μM) significantly increased cytotoxicity, ROS formation, GSH oxidation, lipid peroxidation, MMP collapse, lysosomal and DNA damage in human lymphocytes. On the other hand, cotreatment with EA (25 and 50 μM) inhibited AA-induced oxidative stress which subsequently led to decreasing of the cytotoxicity, GSH oxidation, lipid peroxidation, MMP collapse, lysosomal and DNA damage. Together, these results suggest that probably the co-exposure of EA with foods containing acrylamide could decrease mitochondrial, lysosomal and DNA damages, and oxidative stress induced by acrylamide in human body.

scholarly journals Ataxia Telangiectasia Mutated Protein Kinase: A Potential Master Puppeteer of Oxidative Stress-Induced Metabolic Recycling

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Marguerite Blignaut ◽  
Sarah Harries ◽  
Amanda Lochner ◽  
Barbara Huisamen
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Protein Kinase ◽  
Ataxia Telangiectasia ◽  
Regulatory Protein ◽  
Protein Aggregates ◽  
Ataxia Telangiectasia Mutated ◽  
Damage Repair ◽  
Ataxia Telangiectasia Mutated Protein

Ataxia Telangiectasia Mutated protein kinase (ATM) has recently come to the fore as a regulatory protein fulfilling many roles in the fine balancing act of metabolic homeostasis. Best known for its role as a transducer of DNA damage repair, the activity of ATM in the cytosol is enjoying increasing attention, where it plays a central role in general cellular recycling (macroautophagy) as well as the targeted clearance (selective autophagy) of damaged mitochondria and peroxisomes in response to oxidative stress, independently of the DNA damage response. The importance of ATM activation by oxidative stress has also recently been highlighted in the clearance of protein aggregates, where the expression of a functional ATM construct that cannot be activated by oxidative stress resulted in widespread accumulation of protein aggregates. This review will discuss the role of ATM in general autophagy, mitophagy, and pexophagy as well as aggrephagy and crosstalk between oxidative stress as an activator of ATM and its potential role as a master regulator of these processes.

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