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Tronov, V. A.; Konstantinov, Edward; Petrakou, Eftichia; Tsilimigaki, Smaragdi; Piperakis, Stylianos M.

doi:10.1023/a:1020859405262

Cited by 15 publications

(2 citation statements)

References 32 publications

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“…PARP-1 inhibition by nicotinamide has been shown to switch the mode of cell death from necrosis to apoptosis in ex vivo human lymphocytes treated with hydrogen peroxide [124]. In addition, it has been widely reported that in the cells exposed to oxidative stress, both ATP and NAD + levels serve as crucial molecular switches between apoptosis and necrosis [125–133].…”

Section: Nicotinamide Parp-1 and Cellular Responses To Dna Damagementioning

confidence: 99%

Role of Nicotinamide in DNA Damage, Mutagenesis, and DNA Repair

Surjana

Halliday

Damian

2010

Journal of Nucleic Acids

180

174

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Nicotinamide is a water-soluble amide form of niacin (nicotinic acid or vitamin B3). Both niacin and nicotinamide are widely available in plant and animal foods, and niacin can also be endogenously synthesized in the liver from dietary tryptophan. Nicotinamide is also commercially available in vitamin supplements and in a range of cosmetic, hair, and skin preparations. Nicotinamide is the primary precursor of nicotinamide adenine dinucleotide (NAD+), an essential coenzyme in ATP production and the sole substrate of the nuclear enzyme poly-ADP-ribose polymerase-1 (PARP-1). Numerous in vitro and in vivo studies have clearly shown that PARP-1 and NAD+ status influence cellular responses to genotoxicity which can lead to mutagenesis and cancer formation. This paper will examine the role of nicotinamide in the protection from carcinogenesis, DNA repair, and maintenance of genomic stability.

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Section: Nicotinamide Parp-1 and Cellular Responses To Dna Damagementioning

confidence: 99%

Role of Nicotinamide in DNA Damage, Mutagenesis, and DNA Repair

Surjana

Halliday

Damian

2010

Journal of Nucleic Acids

180

174

View full text Add to dashboard Cite

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“…One of the ROS which causes DNA damage is H 2 O 2 . H 2 O 2 induces double strand breaks (DSBs), which are followed by DNA repair [1], [2]. The H 2 O 2 -induced DNA repair measured in peripheral blood mononuclear cells (PBMC) has been previously used in our laboratory [1], [3], [4].…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress-Induced DNA Damage and Repair in Human Peripheral Blood Mononuclear Cells: Protective Role of Hemoglobin

et al. 2013

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BackgroundDNA repair is a cellular defence mechanism responding to DNA damage caused in large part by oxidative stress. There is a controversy with regard to the effect of red blood cells on DNA damage and cellular response.AimTo investigate the effect of red blood cells on H2O2-induced DNA damage and repair in human peripheral blood mononuclear cells.MethodsDNA breaks were induced in peripheral blood mononuclear cells by H2O2 in the absence or presence of red blood cells, red blood cells hemolysate or hemoglobin. DNA repair was measured by 3H-thymidine uptake, % double-stranded DNA was measured by fluorometric assay of DNA unwinding. DNA damage was measured by the comet assay and by the detection of histone H2AX phosphorylation.ResultsRed blood cells and red blood cells hemolysate reduced DNA repair in a dose-dependent manner. Red blood cells hemolysate reduced % double-stranded DNA, DNA damage and phosphorylation of histone H2AX. Hemoglobin had the same effect as red blood cells hemolysate on % double-stranded DNA.ConclusionRed blood cells, via red blood cells hemolysate and hemoglobin, reduced the effect of oxidative stress on peripheral blood mononuclear cell DNA damage and phosphorylation of histone H2AX. Consequently, recruitment of DNA repair proteins diminished with reduction of DNA repair. This suggests that anemia predisposes to increased oxidative stress induced DNA damage, while a higher hemoglobin level provides protection against oxidative-stress-induced DNA damage.

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DNA damage and repair capacity in lymphocytes from obstructive sleep apnea patients

Kontogianni

Messini-Nikolaki

Christou

et al. 2007

Environ and Mol Mutagen

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Obstructive sleep apnea (OSA) syndrome is a respiratory disease that is linked to heart attacks and high blood pressure. In the present study, we used the Comet assay to compare basal DNA damage and DNA damage induction by hydrogen peroxide, ethanol, and g-irradiation in lymphocytes from 35 OSA patients and 35 controls. We also measured the apoptosis and necrosis produced by these agents and the ability of the lymphocytes to repair the induced DNA damage. It was found that lymphocytes isolated from OSA patients had higher basal levels of DNA damage and were more sensitive to the effects of the DNA-damaging agents than lymphocytes from controls. OSA patients also had a reduced capacity to repair the DNA damage induced by the three agents, but apoptosis and necrosis were similar in OSA patients and the controls. Environ. Mol. Mutagen. 48:722-727, 2007. V V C 2007 Wiley-Liss, Inc.

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Cited by 15 publications

References 32 publications

Role of Nicotinamide in DNA Damage, Mutagenesis, and DNA Repair

Role of Nicotinamide in DNA Damage, Mutagenesis, and DNA Repair

Oxidative Stress-Induced DNA Damage and Repair in Human Peripheral Blood Mononuclear Cells: Protective Role of Hemoglobin

DNA damage and repair capacity in lymphocytes from obstructive sleep apnea patients

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