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Determination of DNA damage induced by oxidative stress in hyperlipidemic patients
Affiliation:1. American University of Beirut-Medical Center, Beirut, Lebanon;2. Calcium Metabolism and Osteoporosis Program, WHO Collaborating Center for Metabolic Bone Disorders at the American University of Beirut-Medical Center, Beirut, Lebanon;1. Department of Family Medicine, College of Medicine, Qassim University, Buraidah, Kingdom of Saudi Arabia;2. Department of Medical Biochemistry, College of Medicine, Qassim University, Buraidah, Kingdom of Saudi Arabia;1. Universidade Estadual Paulista (UNESP), Centro de Aquicultura da Unesp, Via de Acesso Prof. Paulo Donato Castelane, 14.884-900 Jaboticabal, São Paulo, Brazil;2. Universidade Estadual Paulista (UNESP), Via de Acesso Prof. Paulo Donato Castelane, 14.884-900 Jaboticabal, São Paulo, Brazil;3. Centro Nacional de Pesquisa e Conservação de Peixes Continentais (CEPTA/ICMBio). Rodovia Euberto Pereira de Godoy, km 6,5, 13630-000 Pirassununga, São Paulo, Brazil;4. Universidade de Rio Verde - FESURV, Campus Universitário, s/n., 75901-970 Rio Verde, Goiás, Brazil
Abstract: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.
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