Oxidative DNA Damage Induced by a Metabolite of Carcinogenic o-Anisidine: Enhancement of DNA Damage and Alteration in Its Sequence Specificity by Superoxide Dismutase

2001 ◽  
Vol 389 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Yasuhiro Ohkuma ◽  
Shosuke Kawanishi
Keyword(s):  
Dna Damage ◽  
Superoxide Dismutase ◽  
Oxidative Dna Damage ◽  
Its Sequence ◽  
Sequence Specificity

scholarly journals A highly conserved endonuclease activity present in Escherichia coli, bovine, and human cells recognizes oxidative DNA damage at sites of pyrimidines.

1987 ◽  
Vol 7 (1) ◽  
pp. 26-32 ◽  
Author(s):  
P W Doetsch ◽  
W D Henner ◽  
R P Cunningham ◽  
J H Toney ◽  
D E Helland
Keyword(s):  
Escherichia Coli ◽  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Uv Light ◽  
Human Fibroblasts ◽  
Human Cells ◽  
Sequence Specificity ◽  
Endonuclease Activity ◽  
E Coli ◽  
Endonuclease Iii

We have compared the sites of nucleotide incision on DNA damaged by oxidizing agents when cleavage is mediated by either Escherichia coli endonuclease III or an endonuclease present in bovine and human cells. E. coli endonuclease III, the bovine endonuclease isolated from calf thymus, and the human endonuclease partially purified from HeLa and CEM-C1 lymphoblastoid cells incised DNA damaged with osmium tetroxide, ionizing radiation, or high doses of UV light at sites of pyrimidines. For each damaging agent studied, regardless of whether the E. coli, bovine, or human endonuclease was used, the same sequence specificity of cleavage was observed. We detected this endonuclease activity in a variety of human fibroblasts derived from normal individuals as well as individuals with the DNA repair deficiency diseases ataxia telangiectasia and xeroderma pigmentosum. The highly conserved nature of such a DNA damage-specific endonuclease suggests that a common pathway exists in bacteria, humans, and other mammals for the reversal of certain types of oxidative DNA damage.

scholarly journals DNA Damage in Lymphocytes in Hypertensive Subjects in Bangladesh

2013 ◽  
Vol 5 (3) ◽  
pp. 535-543
Author(s):  
M. Saiedullah ◽  
S. Hayat ◽  
M. R. Zamir ◽  
M. Arif ◽  
Z. H. Howlader ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Dna Damage ◽  
Superoxide Dismutase ◽  
Oxidative Dna Damage ◽  
Protein Carbonyl ◽  
Protein Carbonyl Content ◽  
Ribonucleic Acids ◽  
Stress Oxidative ◽  
Bangladeshi Population

Oxidative stress due to imbalance between the production of reactive oxygen species and their dismutation is claimed to be higher in hypertensive subjects than normotensive subjects. In hypertensive subjects oxidative stress may damage deoxy-ribonucleic acids (DNA). In this study plasma superoxide dismutase (SOD) activities, protein carbonyl contents (PCCs) and extent of DNA damage in lymphocytes were measured in specimens obtained from 86 subjects to compare oxidative stress and oxidative DNA damage between normotensive and hypertensive subjects and to assess their relationship with the degree of blood pressure. Results were expressed as mean±SD. Two-tailed unpaired t test and Pearson’s correlation test were done to compare or to determine the relationship between groups or variables. SOD activities were 2.85±0.12 unit/mg protein and 3.84±0.45 unit/mg protein (p<0.05) in hypertensive and normotensive groups respectively. PCCs were 4.77±0.36 nmol/mg protein and 3.75±0.23 nmol/mg protein in hypertensive and normotensive groups respectively. Olive tail moments (OTM) were 124.7±11.69 units and 108.9±9.27 units in hypertensive and normotensive groups respectively. The correlation coefficient of OTM was 0.3924 (p<0.05) for diastolic blood pressure and 0.3618 (p<0.05) for systolic blood pressure. Oxidative stress and DNA damage was higher in hypertensives than normotensives and DNA damage correlated positively with blood pressure. Keywords: Superoxide dismutase, Protein carbonyl content, Oxidative stress, Oxidative DNA damage, Hypertension, Bangladeshi population. © 2013 JSR Publications. ISSN: 2070-0237 (Print); 2070-0245 (Online). All rights reserved. doi: http://dx.doi.org/10.3329/jsr.v5i3.15022 J. Sci. Res. 5 (3), 535-543 (2013)  

scholarly journals Cu,Zn-superoxide dismutase deficiency in mice leads to organ-specific increase in oxidatively damaged DNA and NF-κB1 protein activity.

2010 ◽  
Vol 57 (4) ◽  
Author(s):  
Agnieszka Siomek ◽  
Kamil Brzoska ◽  
Barbara Sochanowicz ◽  
Daniel Gackowski ◽  
Rafal Rozalski ◽  
...  
Keyword(s):  
Dna Damage ◽  
Superoxide Dismutase ◽  
Dna Binding ◽  
Urinary Excretion ◽  
Oxidative Dna Damage ◽  
Binding Activity ◽  
Wild Type ◽  
Dna Binding Activity ◽  
Organ Specific ◽  
Damaged Dna

Earlier experimental studies have demonstrated that: i) Cu,Zn-superoxide dismutase deficiency leads to oxidative stress and carcinogenesis; ii) dysregulation of NF-κB pathway can mediate a wide variety of diseases, including cancer. Therefore, we decided, for the first time, to examine the level of oxidative DNA damage and the DNA binding activity of NF-κB proteins in SOD1 knockout, heterozygous and wild-type mice. Two kinds of biomarkers of oxidatively damaged DNA: urinary excretion of 8-oxodG and 8-oxoGua, and the level of oxidatively damaged DNA were analysed using HPLC-GC-MS and HPLC-EC. The DNA binding activity of p50 and p65 proteins in a nuclear extracts was assessed using NF-κB p50/p65 EZ-TFA transcription factor assay. These parameters were determined in the brain, liver, kidney and urine of SOD1 knockout, heterozygous and wild-type mice. The level of 8-oxodG in DNA was higher in the liver and kidney of knockout mice than in wild type. No differences were found in urinary excretion of 8-oxoGua and 8-oxodG between wild type and the SOD1-deficient animals. The activity of the p50 protein was higher in the kidneys, but surprisingly not in the livers of SOD1-deficient mice, whereas p65 activity did not show any variability. Our results indicate that in Cu,Zn-SOD-deficient animals the level of oxidative DNA damage and NF-κB1 activity are elevated in certain organs only, which may provide some explanation for organ-specific ROS-induced carcinogenesis.

Effect of Allium flavum L. and Allium melanantherum Panč. Extracts on Oxidative DNA Damage and Antioxidative Enzymes Superoxide Dismutase and Catalase

2015 ◽  
Vol 71 (1) ◽  
pp. 28-34 ◽  
Author(s):  
Dragana Mitić-Ćulafić ◽  
Biljana Nikolić ◽  
Nataša Simin ◽  
Nebojša Jasnić ◽  
Dragana Četojević-Simin ◽  
...  
Keyword(s):  
Dna Damage ◽  
Superoxide Dismutase ◽  
Antioxidative Enzymes ◽  
Oxidative Dna Damage

A highly conserved endonuclease activity present in Escherichia coli, bovine, and human cells recognizes oxidative DNA damage at sites of pyrimidines

1987 ◽  
Vol 7 (1) ◽  
pp. 26-32
Author(s):  
P W Doetsch ◽  
W D Henner ◽  
R P Cunningham ◽  
J H Toney ◽  
D E Helland
Keyword(s):  
Escherichia Coli ◽  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Uv Light ◽  
Human Fibroblasts ◽  
Human Cells ◽  
Sequence Specificity ◽  
Endonuclease Activity ◽  
E Coli ◽  
Endonuclease Iii

We have compared the sites of nucleotide incision on DNA damaged by oxidizing agents when cleavage is mediated by either Escherichia coli endonuclease III or an endonuclease present in bovine and human cells. E. coli endonuclease III, the bovine endonuclease isolated from calf thymus, and the human endonuclease partially purified from HeLa and CEM-C1 lymphoblastoid cells incised DNA damaged with osmium tetroxide, ionizing radiation, or high doses of UV light at sites of pyrimidines. For each damaging agent studied, regardless of whether the E. coli, bovine, or human endonuclease was used, the same sequence specificity of cleavage was observed. We detected this endonuclease activity in a variety of human fibroblasts derived from normal individuals as well as individuals with the DNA repair deficiency diseases ataxia telangiectasia and xeroderma pigmentosum. The highly conserved nature of such a DNA damage-specific endonuclease suggests that a common pathway exists in bacteria, humans, and other mammals for the reversal of certain types of oxidative DNA damage.

Acrylamide Exposure and Oxidative DNA Damage, Lipid Peroxidation and Fasting Plasma Glucose Alteration: Association and Mediation Analyses in Chinese Urban Adults

2020 ◽  
Author(s):  
Bin Wang ◽  
Weihong Qiu ◽  
Shijie Yang ◽  
Limin Cao ◽  
Chunmei Zhu ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Dna Damage ◽  
Plasma Glucose ◽  
Fasting Plasma Glucose ◽  
Oxidative Dna Damage ◽  
Adult Population ◽  
Prostaglandin F2α ◽  
Mediation Analyses ◽  
Mediating Role ◽  
Fasting Plasma

<a><b>OBJECTIVE: </b></a>Acrylamide exposure from daily-consumed food has raised global concern.<b> </b>We aimed to assess the exposure-response relationships of internal acrylamide exposure with oxidative DNA damage, lipid peroxidation and fasting plasma glucose (FPG) alteration, and investigate the mediating role of oxidative DNA damage and lipid peroxidation in the association of internal acrylamide exposure with FPG. <p><b>RESEARCH DESIGN AND METHODS:</b> FPG and urinary biomarkers of oxidative DNA damage (8-hydroxy-deoxy-guanosine, 8-OHdG), lipid peroxidation (8-iso-prostaglandin-F2α, 8-iso-PGF2α) and acrylamide exposure (N-acetyl-S-(2-carbamoylethyl)-L-cysteine, AAMA; N-acetyl-S-(2-carbamoyl-2-hydroxyethyl)-L-cysteine, GAMA) were measured for 3,270 general adults from the Wuhan-Zhuhai cohort. The associations of urinary acrylamide metabolites with 8-OHdG, 8-iso-PGF2α and FPG were assessed by linear mixed models. The mediating roles of 8-OHdG and 8-iso-PGF2α were evaluated by mediation analysis.</p> <p><b>RESULTS:</b> We found significant linear positive dose-response relationships of urinary acrylamide metabolites with 8-OHdG, 8-iso-PGF2α and FPG (except GAMA with FPG), and 8-iso-PGF2α with FPG. Each 1-unit increase in log-transformed level of AAMA, ΣUAAM (AAMA+GAMA) or 8-iso-PGF2α was associated with a 0.17-, 0.15- or 0.23-mmol/L increase in FPG, respectively (<i>P </i>or/and<i> P trend</i><0.05). Each 1% increase in AAMA, GAMA or ΣUAAM was associated with a 0.19%, 0.27% or 0.22% increase in 8-OHdG, respectively, and a 0.40%, 0.48% or 0.44% increase in 8-iso-PGF2α, respectively (<i>P </i>and<i> P trend</i><0.05). Increased 8-iso-PGF2α rather than 8-OHdG significantly mediated 64.29% and 76.92% of the AAMA and ΣUAAM associated-FPG increases, respectively.</p> <p><b>CONCLUSIONS:</b> Exposure of general adult population to acrylamide was associated with FPG elevation, oxidative DNA damage and lipid peroxidation, which in turn partly mediated acrylamide-associated FPG elevation.<b></b></p>

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