ArticlePloS one2013
Oxidative stress-induced DNA damage and repair in human peripheral blood mononuclear cells: protective role of hemoglobin.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 30 citations in OpenAlex.
- Effects of hepatic lipid ratio on lipid metabolism indices and hepatic gene expression in late-phase laying hens.Poultry science · 2026Article
- Hemoglobin as a pseudoperoxidase and drug target for oxidative stress-related diseases.Signal transduction and targeted therapy · 2025Article
- Evaluation of DNA repair capacity in parents of pediatric patients diagnosed with autism spectrum disorder using the comet assay procedure.IBRO neuroscience reports · 2023Article
- The transcriptome pattern of liver, spleen and hypothalamus provides insights into genetic and biological changes in roosters in response to castration.Frontiers in genetics · 2022Article
- Genomic alterations and abnormal expression of APE2 in multiple cancers.Scientific reports · 2020Article
- Association between human T cell leukemia virus type-1 (HTLV-1) infection and advanced periodontitis in relation to atherosclerosis among elderly Japanese: a cross-sectional study.Environmental health and preventive medicine · 2019Article
- Association between human T cell leukemia virus 1 (HTLV-1) infection and advanced periodontitis in relation to hematopoietic activity among elderly participants: a cross-sectional study.Environmental health and preventive medicine · 2019Article
- Induction of oxidative stress, apoptosis and DNA damage by koumine in Tetrahymena thermophila.PloS one · 2019Article
- Mechanisms of DNA damage, repair, and mutagenesis.Environmental and molecular mutagenesis · 2017Review
- Upregulation and Mitochondrial Sequestration of Hemoglobin Occur in Circulating Leukocytes during Critical Illness, Conferring a Cytoprotective Phenotype.Molecular medicine (Cambridge, Mass.) · 2015Article
- GFR in Patients with β-Thalassemia Major.Clinical journal of the American Society of Nephrology : CJASN · 2015Article
- Serum Uric Acid, Alanine Aminotransferase, Hemoglobin and Red Blood Cell Count Levels in Pseudoexfoliation Syndrome.Journal of ophthalmology · 2015Article
- Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress.Cellular and molecular life sciences : CMLS · 2014Review
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 (3)H-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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