Determination of DNA damage induced by oxidative stress in hyperlipidemic patients

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In the present paper, we report data on the genotoxic properties of hydrogen peroxide in polymorphonuclear neutrophils (PMNLs) separated from normolipidemic and type II/a hyperlipidemic patients. In all, 15 hyperlipidemic patients (11 female, 4 male, mean age 54.6±10.25 years) were involved in the study, and 7 normolipidemic patients (5 female, 2 male, mean age 53.4±8.07 years) served as controls. Using the comet assay, there was a significant difference in the degree of DNA damage between the two groups. The visual score characteristic of the degree of DNA damage was 350.97±31.31 in the hyperlipidemic group, while it was 289.5±29.49 in the control group (P < 0.001). In the hyperlipidemic patients, a positive correlation was found between the degree of DNA damage and the basic oxidation of PMNLs (r = 0.517), and the superoxide anion production of the cells stimulated with phorbolmiristate acetate (PMA) (r = 0.326) and formyl-Met-Leu-Phe (FMLP) (r = 0.525) as well. There was a negative correlation between DNA damage and HDL-associated antioxidant paraoxonase (PON) activity (r = -0.469), and the PON/HDL ratio (r = -0.631). No correlation was found between the degree of DNA damage and the plasma concentration of nitric oxide (NO) (r = 0.098) and thiobarbituric acid-reactive substances (TBARS) (r = 0.061) in hyperlipidemic patients. Our results show that in hyperlipidemic patients there is an increase in lymphocyte DNA damage caused by oxidative stress when compared to normolipidemic individuals as demonstrated by comet assay. Decreased antioxidant capacity in hyperlipidemic patients may play a significant role in this process.

Original languageEnglish
Pages (from-to)17-25
Number of pages9
JournalMutation Research - Genetic Toxicology and Environmental Mutagenesis
Issue number1-2
Publication statusPublished - Jan 15 2001


  • Comet assay
  • DNA damage
  • Hyperlipidemia
  • Oxidative stress
  • Paraoxonase

ASJC Scopus subject areas

  • Genetics
  • Health, Toxicology and Mutagenesis

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