Level of primary DNA damage in the early stage of metabolic syndrome

Mirta Milić, Maja Kišan, Dinko Rogulj, Maja Radman, Marijana Vučić Lovrenčić, Paško Konjevoda, Ana Marija Domijan

Research output: Contribution to journalArticlepeer-review

Abstract

Metabolic syndrome (MetS) is a multi-component disease, characterised by abdominal obesity, hypertension, hyperglycaemia and dyslipidaemia. Since the number of MetS patients has significantly increased over the past two decades and because MetS may lead to development of cardiovascular diseases, diabetes type-2, and cancer, it has become important to extend the knowledge on the pathogenesis of MetS and to establish its possible early biomarkers. Studies on MetS and DNA damage are few and are inconclusive. The aim of this study was to elucidate the involvement of DNA damage in the development of MetS and to establish if DNA damage can serve as early biomarker of MetS. A total of 121 subjects participated in the study: 56 healthy controls and 65 MetS patients who were diagnosed with MetS for the first time. The amount of primary DNA damage in peripheral leukocytes of the subjects was assessed with three types of comet assay: the alkaline, the hOGG1-modified, and the neutral comet assay. In addition, the extent of oxidative DNA damage was monitored in urine by assessing 8-oxo-dG. The parameters of the three types of comet assay did not differ between the control and the MetS group. Interestingly, urinary 8-oxo-dG level in the control group was higher than in the MetS group. Our results imply that DNA damage is not involved in the early stage of MetS and, therefore, DNA damage cannot serve as an early marker of MetS.

Original languageEnglish
Pages (from-to)1-5
Number of pages5
JournalMutation Research - Genetic Toxicology and Environmental Mutagenesis
Volume758
Issue number1-2
DOIs
Publication statusPublished - Dec 12 2013

Keywords

  • Alkaline comet assay
  • HOGG1-modified comet assay
  • Neutral comet assay
  • Oxidative stress
  • Urinary 8-oxo-dG

ASJC Scopus subject areas

  • Health, Toxicology and Mutagenesis
  • Genetics

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