Melatonin prevents oxidative stress, inflammatory activity, and DNA damage in cirrhotic rats

In the blood serum of 70% individuals exposed to harmful factors of the working environment, a high level of oxidative stress and the DNA damage marker 8-Hydroxy-2’-Deoxyguanosine (8-OHdG) were detected.

Download Full-text

Faculty Opinions recommendation of Pathogen DNA as target for host-generated oxidative stress: role for repair of bacterial DNA damage in Helicobacter pylori colonization.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1012864.187953 ◽

2003 ◽

Author(s):

Ferric Fang

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Helicobacter Pylori ◽

Bacterial Dna ◽

Pathogen Dna

Download Full-text

Faculty Opinions recommendation of Metabolism-induced oxidative stress and DNA damage selectively trigger genome instability in polyploid fungal cells.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.736497622.793565072 ◽

2019 ◽

Author(s):

Neil Andrew Robert Gow ◽

Alessandra Dantas

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Genome Instability

Download Full-text

Antioxidative Effect of Rhus javanica Linne Extract Against Hydrogen Peroxide or Menadione Induced Oxidative Stress and DNA Damage in HepG2Cells

Preventive Nutrition and Food Science ◽

10.3746/jfn.2004.9.2.150 ◽

2004 ◽

Vol 9 (2) ◽

pp. 150-155 ◽

Cited By ~ 2

Author(s):

Chi-Sung Chun ◽

Ji-Hyun Kim ◽

Hyun-Ae Lim ◽

Ho-Yong Sohn ◽

Kun-Ho Son ◽

...

Keyword(s):

Oxidative Stress ◽

Hydrogen Peroxide ◽

Dna Damage ◽

Antioxidative Effect

Download Full-text

Oxidative Stress, Ocular Disease and Diabetes Retinopathy

Current Pharmaceutical Design ◽

10.2174/1381612825666190115121531 ◽

2019 ◽

Vol 24 (40) ◽

pp. 4726-4741 ◽

Cited By ~ 8

Author(s):

Orathai Tangvarasittichai ◽

Surapon Tangvarasittichai

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Cell Death ◽

Protein Modification ◽

Morphological Changes ◽

Corneal Dystrophy ◽

Age Related Macular Degeneration ◽

Ocular Diseases ◽

Retinal Light Damage ◽

Age Related

Background: Oxidative stress is caused by free radicals or oxidant productions, including lipid peroxidation, protein modification, DNA damage and apoptosis or cell death and results in cellular degeneration and neurodegeneration from damage to macromolecules. Results: Accumulation of the DNA damage (8HOdG) products and the end products of LPO (including aldehyde, diene, triene conjugates and Schiff’s bases) were noted in the research studies. Significantly higher levels of these products in comparison with the controls were observed. Oxidative stress induced changes to ocular cells and tissues. Typical changes include ECM accumulation, cell dysfunction, cell death, advanced senescence, disarrangement or rearrangement of the cytoskeleton and released inflammatory cytokines. It is involved in ocular diseases, including keratoconus, Fuchs endothelial corneal dystrophy, and granular corneal dystrophy type 2, cataract, age-related macular degeneration, primary open-angle glaucoma, retinal light damage, and retinopathy of prematurity. These ocular diseases are the cause of irreversible blindness worldwide. Conclusions: Oxidative stress, inflammation and autophagy are implicated in biochemical and morphological changes in these ocular tissues. The development of therapy is a major target for the management care of these ocular diseases.

Download Full-text

Non-canonical Functions of Telomerase Reverse Transcriptase: Emerging Roles and Biological Relevance

Current Topics in Medicinal Chemistry ◽

10.2174/1568026620666200131125110 ◽

2020 ◽

Vol 20 (6) ◽

pp. 498-507 ◽

Cited By ~ 4

Author(s):

Connor A.H. Thompson ◽

Judy M.Y. Wong

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Reverse Transcriptase ◽

Cancer Cells ◽

Telomere Length ◽

Telomere Maintenance ◽

Telomerase Reverse Transcriptase ◽

Alternative Mechanism ◽

Dependent Manner ◽

Mitochondrial Integrity

Increasing evidence from research on telomerase suggests that in addition to its catalytic telomere repeat synthesis activity, telomerase may have other biologically important functions. The canonical roles of telomerase are at the telomere ends where they elongate telomeres and maintain genomic stability and cellular lifespan. The catalytic protein component Telomerase Reverse Transcriptase (TERT) is preferentially expressed at high levels in cancer cells despite the existence of an alternative mechanism for telomere maintenance (alternative lengthening of telomeres or ALT). TERT is also expressed at higher levels than necessary for maintaining functional telomere length, suggesting other possible adaptive functions. Emerging non-canonical roles of TERT include regulation of non-telomeric DNA damage responses, promotion of cell growth and proliferation, acceleration of cell cycle kinetics, and control of mitochondrial integrity following oxidative stress. Non-canonical activities of TERT primarily show cellular protective effects, and nuclear TERT has been shown to protect against cell death following double-stranded DNA damage, independent of its role in telomere length maintenance. TERT has been suggested to act as a chromatin modulator and participate in the transcriptional regulation of gene expression. TERT has also been reported to regulate transcript levels through an RNA-dependent RNA Polymerase (RdRP) activity and produce siRNAs in a Dicer-dependent manner. At the mitochondria, TERT is suggested to protect against oxidative stress-induced mtDNA damage and promote mitochondrial integrity. These extra-telomeric functions of TERT may be advantageous in the context of increased proliferation and metabolic stress often found in rapidly-dividing cancer cells. Understanding the spectrum of non-canonical functions of telomerase may have important implications for the rational design of anti-cancer chemotherapeutic drugs.

Download Full-text

Hyperhomocysteinemia exacerbates ischemia-reperfusion injury-induced acute kidney injury by mediating oxidative stress, DNA damage, JNK pathway, and apoptosis

Open Life Sciences ◽

10.1515/biol-2021-0054 ◽

2021 ◽

Vol 16 (1) ◽

pp. 537-543

Author(s):

Mei Zhang ◽

Jing Yuan ◽

Rong Dong ◽

Jingjing Da ◽

Qian Li ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Cell Apoptosis ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Kidney Injury ◽

Tubular Cell ◽

Tubular Injury ◽

Jnk Pathway ◽

Pathway Activation

Abstract Background Hyperhomocysteinemia (HHcy) plays an important role in the progression of many kidney diseases; however, the relationship between HHcy and ischemia-reperfusion injury (IRI)-induced acute kidney injury (IRI-induced AKI) is far from clear. In this study, we try to investigate the effect and possible mechanisms of HHcy on IRI-induced AKI. Methods Twenty C57/BL6 mice were reared with a regular diet or high methionine diet for 2 weeks (to generate HHcy mice); after that, mice were subgrouped to receive sham operation or ischemia-reperfusion surgery. Twenty four hour after reperfusion, serum creatinine, blood urea nitrogen, and Malondialdehyde (MDA) were measured. H&E staining for tubular injury, western blot for γH2AX, JNK, p-JNK, and cleaved caspase 3, and TUNEL assay for tubular cell apoptosis were also performed. Results Our results showed that HHcy did not influence the renal function and histological structure, as well as the levels of MDA, γH2AX, JNK, p-JNK, and tubular cell apoptosis in control mice. However, in IRI-induced AKI mice, HHcy caused severer renal dysfunction and tubular injury, higher levels of oxidative stress, DNA damage, JNK pathway activation, and tubular cell apoptosis. Conclusion Our results demonstrated that HHcy could exacerbate IRI-induced AKI, which may be achieved through promoting oxidative stress, DNA damage, JNK pathway activation, and consequent apoptosis.

Download Full-text

Escherichia coli MutM Suppresses Illegitimate Recombination Induced by Oxidative Stress

Genetics ◽

10.1093/genetics/151.2.439 ◽

1999 ◽

Vol 151 (2) ◽

pp. 439-446 ◽

Cited By ~ 2

Author(s):

Masaaki Onda ◽

Katsuhiro Hanada ◽

Hirokazu Kawachi ◽

Hideo Ikeda

Keyword(s):

Oxidative Stress ◽

Escherichia Coli ◽

Hydrogen Peroxide ◽

Dna Damage ◽

Double Strand Breaks ◽

Illegitimate Recombination ◽

Recombination Analysis ◽

Wild Type ◽

Strand Breaks ◽

In The Wild

Abstract DNA damage by oxidative stress is one of the causes of mutagenesis. However, whether or not DNA damage induces illegitimate recombination has not been determined. To study the effect of oxidative stress on illegitimate recombination, we examined the frequency of λbio transducing phage in the presence of hydrogen peroxide and found that this reagent enhances illegitimate recombination. To clarify the types of illegitimate recombination, we examined the effect of mutations in mutM and related genes on the process. The frequency of λbio transducing phage was 5- to 12-fold higher in the mutM mutant than in the wild type, while the frequency in the mutY and mutT mutants was comparable to that of the wild type. Because 7,8-dihydro-8-oxoguanine (8-oxoG) and formamido pyrimidine (Fapy) lesions can be removed from DNA by MutM protein, these lesions are thought to induce illegitimate recombination. Analysis of recombination junctions showed that the recombination at Hotspot I accounts for 22 or 4% of total λbio transducing phages in the wild type or in the mutM mutant, respectively. The preferential increase of recombination at nonhotspot sites with hydrogen peroxide in the mutM mutant was discussed on the basis of a new model, in which 8-oxoG and/or Fapy residues may introduce double-strand breaks into DNA.

Download Full-text