Oxidative Damage to DNA: Do We Have a Reliable Biomarker?

Collins, Andrew; Dušinská, Maria; Gedik, Catherine M.; Štětina, Rudolf

doi:10.2307/3432805

Cited by 156 publications

(167 citation statements)

References 15 publications

(18 reference statements)

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“…In the future, studies of the level and specific nature of oxidative damage in unchallenged cells (as by Collins and colleagues [23,24]) would provide valuable knowledge about the variation among individuals, and contribute to development of hypotheses to test. As the environmental risk factors for these cancers are identified in case-control studies of the parent U.S. Radiologic…”

Section: Discussionmentioning

confidence: 99%

“…However, we did not randomly assay the lines nor did we assess "batch" effects. The closest proxy to "batch" was "cell scoring date", and we did not observe undue systematic variation over calendar time in the aggregate or by case or control groups.In the future, studies of the level and specific nature of oxidative damage in unchallenged cells (as by Collins and colleagues [23,24]) would provide valuable knowledge about the variation among individuals, and contribute to development of hypotheses to test. As the environmental risk factors for these cancers are identified in case-control studies of the parent U.S. Radiologic…”

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confidence: 99%

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DNA damage among thyroid cancer and multiple cancer cases, controls, and long-lived individuals

Sigurdson

Hauptmann

Alexander

et al. 2005

Mutation Research/Genetic Toxicology and Environmental Mutagene

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Variation in the detection, signaling, and repair of DNA damage contributes to human cancer risk. To assess capacity to modulate endogenous DNA damage among radiologic technologists who had been diagnosed with breast cancer and another malignancy (breast-other; n=42), early-onset breast cancer (early-onset, age ≤ 35; n=38), thyroid cancer (n=68), long-lived cancer-free individuals (hyper-normals; n=20) and cancer-free controls (n=49) we quantified DNA damage (single strand breaks and abasic sites) in untreated lymphoblastoid cell lines using the alkaline comet assay. Komet™ software provided comet tail length, % DNA in tail (tail DNA), comet distributed moment (CDM), and Olive tail moment (OTM) summarized as the geometric mean of 100 cells. Category cut-points (median and 75 th percentile) were determined from the distribution among controls. Tail length (for ≥ 75% vs. below the median, age adjusted) was most consistently associated with the highest odds ratios in the breast-other, early-onset, and thyroid cancer groups (with risk increased 10-, 5-or 19-fold, respectively, with wide confidence intervals) and decreased risk among the hyper-normal group. For the other three Comet measures, risk of breast-other was elevated approximately three-fold. Risk of early-onset breast cancer was mixed and risk of thyroid cancer ranged from null to a two-fold increase. The hyper-normal group showed decreased odds ratios for tail DNA and OTM, but not CDM. DNA damage, as estimated by all Comet measures, was relatively unaffected by survival time, reproductive factors, and prior radiation treatment. We detected a continuum of endogenous DNA damage that was highest among cancer cases, less in controls, and suggestively lowest in hyper-normal individuals. Measuring this DNA damage phenotype may contribute to the identification of susceptible sub-groups. Our observations require replication in a prospective study with a large number of pre-diagnostic samples. 3 IntroductionThere is considerable evidence that individual variation in the detection, signaling, toleration, and repair of DNA damage (from internal and external exposures and intrinsic instability of DNA) contributes to human cancer risk (reviewed in [1][2][3][4][5][6]). Several studies (with sample sizes in excess of 20 cases and 20 controls) have reported increased breast [7,8] and bladder [9] cancer risks associated with higher DNA damage measured by the comet assay [10]. In these studies elevated endogenous damage and post-mutagen challenge damage levels were associated with increased cancer risk. These results indicate that elevated endogenous damage is itself a risk factor, and are consistent with the notion that measures of endogenous damage are correlated with damage repair capability after an exogenous challenge.We characterized risk of solid cancer associated with ability to limit DNA damage from endogenous DNA metabolic processes among persons with selected malignancies, compared to controls by quantifying single strand DNA breaks (SSB) and abasic sites...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

DNA damage among thyroid cancer and multiple cancer cases, controls, and long-lived individuals

Sigurdson

Hauptmann

Alexander

et al. 2005

Mutation Research/Genetic Toxicology and Environmental Mutagene

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“…These results suggest that Aldh2 -/-mice may be more susceptible than Aldh2 +/+ mice to ethanol induced oxidative DNA damage. The tail moment in alkaline single-cell gel electrophoresis reflects base modifications 25) as well as DNA strand breaks, because the oxidized purine (8-OHdG and others) and pyrimidine bases can be converted into additional DNA single-strand breaks 26) . Higher content of 8-OHdG in cells is expected to lead to a higher formation of DNA strand breaks, although the steady-state level of damage can be modulated by DNA repair 27) .…”

Section: Discussionmentioning

confidence: 99%

Ethanol‐Induced Oxidative DNA Damage and CYP2E1 Expression in Liver Tissue of Aldh2 Knockout Mice

Kim

Eom

Ogawa

et al. 2007

Journal of Occupational Health

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“…The relative amount of DNA in the tail of the comet formed reflects the number of breaks in the DNA. The per cent of DNA in the tail was converted to the number of SSB/10 9 Da using the calibration of the method by X-ray irradiation (COLLINS et al 1996). The statistical significance of the difference between the treated and the control animals was tested by Mann-Whitney U test.…”

Section: Single Strand Breaks -Comet Assaymentioning

confidence: 99%

Antimutagenic effect of curcumin and its effect on the immune response in mice

Smerak¹,

Polívková²,

Sestakova³

et al. 2006

Czech J. Food Sci.

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A wide array of antioxidative and anti-inflammatory substances derived from edible plants have been reported to possess chemopreventive and chemoprotective activities. Among the most extensively investigated and well-defined dietary chemopreventives is curcumin. Using the Ames test and in vivo micronucleus test, chemiluminescence test, blastic transformation test, and comet assay, we examined the antimutagenic effects of the chemically identified chemoprotective substance curcumin (diferuloylmethane) in the pure form on mutagenicity induced by three reference mutagens: aflatoxin B<sub>1</sub> (AFB<sub>1</sub>), 2-amino-3-metylimidazo[4,5-f]quinoline (IQ), and N-nitroso-N-metylurea (MNU), and the effect of curcumin on the immunosuppression caused by these mutagens. Curcumin in the pure form showed a clear antimutagenic and immunomodulatory activities on mutagenicity and immunosuppression induced by reference mutagens.  

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Oxidative Damage to DNA: Do We Have a Reliable Biomarker?

Abstract: Oxidized bases in DNA can be measured directly by high-performance liquid chromatography (HPLC). 7, 465-469 (1996)

Cited by 156 publications

References 15 publications

DNA damage among thyroid cancer and multiple cancer cases, controls, and long-lived individuals

DNA damage among thyroid cancer and multiple cancer cases, controls, and long-lived individuals

Ethanol‐Induced Oxidative DNA Damage and CYP2E1 Expression in Liver Tissue of Aldh2 Knockout Mice

Antimutagenic effect of curcumin and its effect on the immune response in mice

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