Hydrogen peroxide induced genomic instability in nucleotide excision repair-deficient lymphoblastoid cells

Gopalakrishnan, Kalpana; Low, Grace Kah Mun; Ting, Aloysius Poh Leong; Srikanth, Prarthana; Slijepčević, Predrag; Hande, M. Prakash

doi:10.1186/2041-9414-1-16

Cited by 25 publications

(19 citation statements)

References 53 publications

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“…Recently, Martino and colleagues (2011) found that intracellular hydrogen peroxide production in cancer cells and artery endothelial cells was suppressed in the HMF [36]. Reactive oxygen species, especially hydrogen peroxide, has been reported to induce genomic instability in mammalian cells [37], [38]. Thus, further investigation into the changes in genetic material and intracellular reactive oxygen species levels during HMF exposure would be of value.…”

Section: Discussionmentioning

confidence: 99%

Magnetic Shielding Accelerates the Proliferation of Human Neuroblastoma Cell by Promoting G1-Phase Progression

Zhang

Liu

et al. 2013

PLoS ONE

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Organisms have been exposed to the geomagnetic field (GMF) throughout evolutionary history. Exposure to the hypomagnetic field (HMF) by deep magnetic shielding has recently been suggested to have a negative effect on the structure and function of the central nervous system, particularly during early development. Although changes in cell growth and differentiation have been observed in the HMF, the effects of the HMF on cell cycle progression still remain unclear. Here we show that continuous HMF exposure significantly increases the proliferation of human neuroblastoma (SH-SY5Y) cells. The acceleration of proliferation results from a forward shift of the cell cycle in G1-phase. The G2/M-phase progression is not affected in the HMF. Our data is the first to demonstrate that the HMF can stimulate the proliferation of SH-SY5Y cells by promoting cell cycle progression in the G1-phase. This provides a novel way to study the mechanism of cells in response to changes of environmental magnetic field including the GMF.

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Section: Discussionmentioning

confidence: 99%

Magnetic Shielding Accelerates the Proliferation of Human Neuroblastoma Cell by Promoting G1-Phase Progression

Zhang

Liu

et al. 2013

PLoS ONE

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“…Consistent with the above hypothesis, XPB- and XPD-deficient lymphoblastoid cells are hypersensitive to H 2 O 2 and display higher H 2 O 2 -induced DNA damage compared to wild type cells [94]. XPA-deficient cells also display defects in response to oxidative DNA damaging agents, including an increase in H 2 O 2 genotoxicity, a lower threshold for H 2 O 2 -induced cell cycle arrest, and reduced repair of H 2 O 2 generated DNA lesions [95].…”

Section: Oxidative Dna Damage In Human Diseasementioning

confidence: 65%

Pathways for repairing and tolerating the spectrum of oxidative DNA lesions

2012

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Reactive oxygen species (ROS) arise from both endogenous and exogenous sources. These reactive molecules possess the ability to damage both the DNA nucleobases and the sugar phosphate backbone, leading to a wide spectrum of lesions, including non-bulky (8-oxoguanine and formamidopyrimidine) and bulky (cyclopurine and etheno adducts) base modifications, abasic sites, non-conventional single-strand breaks, protein-DNA adducts, and intra/interstrand DNA crosslinks. Unrepaired oxidative DNA damage can result in bypass mutagenesis during genome copying or gene expression, or blockage of the essential cellular processes of DNA replication or transcription. Such outcomes underlie numerous pathologies, including, but not limited to, carcinogenesis and neurodegeneration, as well as the aging process. Cells have adapted and evolved defense systems against the deleterious effects of ROS, and specifically devote a number of cellular DNA repair and tolerance pathways to combat oxidative DNA damage. Defects in these protective pathways trigger hereditary human diseases that exhibit increased cancer incidence, developmental defects, neurological abnormalities, and/or premature aging. We review herein classic and atypical oxidative DNA lesions, outcomes of encountering these damages during DNA replication and transcription, and the consequences of losing the ability to repair the different forms of oxidative DNA damage. We particularly focus on the hereditary human diseases Xeroderma Pigmentosum, Cockayne Syndrome and Fanconi Anemia, which may involve defects in the efficient repair of oxidative modifications to chromosomal DNA.

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“…Loss of XPB or XPD increases telomere attrition and enhances DNA damage at telomeres under oxidative stress, suggesting that XPB and XPD may have an important role in maintaining telomere integrity [54, 55]. Another key NER component, XPC, has been implicated in telomere maintenance as well, particularly upon UV exposure.…”

Section: Ner At Telomeresmentioning

confidence: 99%

DNA excision repair at telomeres

2015

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DNA damage is caused by either endogenous cellular metabolic processes such as hydrolysis, oxidation, alkylation, and DNA base mismatches, or exogenous sources including ultraviolet (UV) light, ionizing radiation, and chemical agents. Damaged DNA that is not properly repaired can lead to genomic instability, driving tumorigenesis. To protect genomic stability, mammalian cells have evolved highly conserved DNA repair mechanisms to remove and repair DNA lesions. Telomeres are composed of long tandem TTAGGG repeats located at the ends of chromosomes. Maintenance of functional telomeres is critical for preventing genome instability. The telomeric sequence possesses unique features that predispose telomeres to a variety of DNA damage induced by environmental genotoxins. This review briefly describes the relevance of excision repair pathways in telomere maintenance, with the focus on base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR). By summarizing current knowledge on excision repair of telomere damage and outlining many unanswered questions, it is our hope to stimulate further interest in a better understanding of excision repair processes at telomeres and in how these processes contribute to telomere maintenance.

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Hydrogen peroxide induced genomic instability in nucleotide excision repair-deficient lymphoblastoid cells

Cited by 25 publications

References 53 publications

Magnetic Shielding Accelerates the Proliferation of Human Neuroblastoma Cell by Promoting G1-Phase Progression

Magnetic Shielding Accelerates the Proliferation of Human Neuroblastoma Cell by Promoting G1-Phase Progression

Pathways for repairing and tolerating the spectrum of oxidative DNA lesions

DNA excision repair at telomeres

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