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Association between Diabetes Mellitus and Leucocytic DNA Damage

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  • Yim Tong Szeto
  • Ho Yan Yeung

Abstract

It has been suggested that diabetes is the disease associated with increased oxidative stress and might reflect with increased cellular DNA damage. To investigate the association between hyperglycaemic state and NDA damage of human white blood cells. The basal and UV-induced leucocytic DNA damages of 80 individuals, including 41 diabetic, 19 pre-diabetic patients and 20 normal subjects, were measured by comet assay. The HbA1c and fasting glucose levels were correlated to the DNA damage to detect the potential association. The leucocytic DNA damage was visualized under light microscope with Giemsa stain. The degree of DNA lesion was quantified by visual scoring. The diabetic patients showed the highest basal and UV induced DNA damage, while lowest scores were seen in healthy subjects. The DNA damages among diabetic, pre-diabetic patient and healthy subjects were significantly different from each other. There were significant positive correlations between the basal and UV-induced leucocytic DNA damages with HbA1c as well as fasting glucose levels. DNA damage as a marker of oxidative stress was seen in diabetic and pre-diabetic patients. The damage was positively correlated to the hyperglycaemic state of patient.

Suggested Citation

  • Yim Tong Szeto & Ho Yan Yeung, 2021. "Association between Diabetes Mellitus and Leucocytic DNA Damage," European Journal of Biology and Biotechnology, European Open Science, vol. 2(3), pages 7-10, May.
  • Handle: RePEc:epw:ejbio0:v:2:y:2021:i:3:id:17151
    DOI: 10.24018/ejbio.2021.2.3.151
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    1. Esra' Shishtar & John L Sievenpiper & Vladimir Djedovic & Adrian I Cozma & Vanessa Ha & Viranda H Jayalath & David J A Jenkins & Sonia Blanco Meija & Russell J de Souza & Elena Jovanovski & Vladimir V, 2014. "The Effect of Ginseng (The Genus Panax) on Glycemic Control: A Systematic Review and Meta-Analysis of Randomized Controlled Clinical Trials," PLOS ONE, Public Library of Science, vol. 9(9), pages 1-11, September.
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