DNA damage and repair in Fuchs endothelial corneal dystrophy

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• 作者：Piotr Czarny (1)
  Ewelina Kasprzak (1)
  Mariusz Wielgorski (2)
  Monika Udziela (2)
  Beata Markiewicz (1)
  Janusz Blasiak (1)
  Jerzy Szaflik (2)
  Jacek P. Szaflik (2)
  
• 关键词：Fuchs endothelial corneal dystrophy ; FECD ; Oxidative stress ; DNA damage ; DNA repair
• 刊名：Molecular Biology Reports
• 出版年：2013
• 出版时间：April 2013
• 年：2013
• 卷：40
• 期：4
• 页码：2977-2983
• 全文大小：251KB
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• 作者单位：Piotr Czarny (1)
  Ewelina Kasprzak (1)
  Mariusz Wielgorski (2)
  Monika Udziela (2)
  Beata Markiewicz (1)
  Janusz Blasiak (1)
  Jerzy Szaflik (2)
  Jacek P. Szaflik (2)
  
  1. Department of Molecular Genetics, University of Lodz, Pomorska 141/143, 90-236, Lodz, Poland
  2. Department of Ophthalmology, Medical University of Warsaw and Samodzielny Publiczny Kliniczny Szpital Okulistyczny, Sierakowskiego 13, 03-710, Warsaw, Poland
  
• ISSN：1573-4978

文摘

Fuchs endothelial corneal dystrophy (FECD) is a slowly progressive eye disease leading to blindness, mostly affecting people above 40?years old. The only known method of curing FECD is corneal transplantation. The disease is characterized by the presence of extracellular deposits called “cornea guttata- apoptosis of corneal endothelial cells, dysfunction of Descement’s membrane and corneal edema. Oxidative stress is suggested to play a role in FECD pathogenesis. Reactive oxygen species produced during the stress may damage biomolecules, including DNA. In the present study we evaluated the extent of endogenous DNA damage, including oxidatively modified DNA bases, and damage induced by hydrogen peroxide as well as the kinetics of DNA repair in peripheral blood mononuclear cells of 50 patients with FECD and 43 age-matched controls without visual disturbances. To quantify DNA damage and repair we used the alkaline comet assay technique with the enzymes recognizing oxidative DNA damage, hOGG1 and EndoIII. We did not observe differences in the extent of endogenous and hydrogen peroxide-induced DNA damage between FECD patients and controls. However, we found a lower efficacy of DNA repair in FECD patients as compared with control individuals. The results obtained suggest that the lowering of the DNA repair capacity may be one of the mechanisms underlying the role of oxidative stress in the FECD pathology.