Measurement of DNA damage with the comet assay in high-prevalence diseases: current status and future directions

Author:

Møller Peter1ORCID,Stopper Helga2,Collins Andrew R3

Affiliation:

1. Department of Public Health, Section of Environmental Health, University of Copenhagen, Copenhagen H, Denmark

2. Institute of Pharmacology and Toxicology, University of Wuerzburg, Wuerzburg, Germany

3. Department of Nutrition, Institute for Basic Medical Sciences, University of Oslo, Oslo, Norway

Abstract

Abstract The comet assay is widely used in studies on genotoxicity testing, human biomonitoring and clinical studies. The simple version of the assay detects a mixture of DNA strand breaks and alkali-labile sites; these lesions are typically described as DNA strand breaks to distinguish them from oxidatively damaged DNA that are measured with the enzyme-modified comet assay. This review assesses the association between high-prevalence diseases in high-income countries and DNA damage measured with the comet assay in humans. The majority of case–control studies have assessed genotoxicity in white blood cells. Patients with coronary artery disease, diabetes, kidney disease, chronic obstructive pulmonary disease and Alzheimer’s disease have on average 2-fold higher levels of DNA strand breaks compared with healthy controls. Patients with coronary artery disease, diabetes, kidney disease and chronic obstructive pulmonary disease also have 2- to 3-fold higher levels of oxidatively damaged DNA in white blood cells than controls, although there is not a clear difference in DNA damage levels between the different diseases. Case–control studies have shown elevated levels of DNA strand breaks in patients with breast cancer, whereas there are only few studies on colorectal and lung cancers. At present, it is not possible to assess if these neoplastic diseases are associated with a different level of DNA damage compared with non-neoplastic diseases.

Funder

COST Action

Publisher

Oxford University Press (OUP)

Subject

Health, Toxicology and Mutagenesis,Genetics (clinical),Toxicology,Genetics

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