347
Views
15
CrossRef citations to date
0
Altmetric
Original Article

The Changes of 8-OHdG, hOGG1, APE1 and Pol β in Lenses of Patients with Age-Related Cataract

, , , , , & show all
Pages 378-385 | Received 23 Feb 2014, Accepted 01 May 2014, Published online: 09 Jun 2014
 

Abstract

Purpose: To evaluate the changes of oxidative DNA damage (in the form of 8-OHdG) and three key DNA base-excision repair (BER) proteins, human 8-oxoguanine DNA glycosylase 1 (hOGG1), apurinic/apyrimidinic endonuclease 1 (APE1) and DNA polymerase β (Pol β), in lens epithelium cells (LECs), cortex and nucleus of lenses with age-related cataract (ARC) and age-matched controls.

Methods: A total of 90 patients with ARC and 21 control subjects were enrolled. The samples included the anterior lens capsules (mainly composed of LECs) and various portions of lens. An ELISA assay was used to assess the 8-OHdG levels of genomic DNA extracted. Immunofluorescence and Western blot were used to analyze the localization and quantification of three BER proteins, respectively.

Results: The 8-OHdG levels in lenses with ARC were higher than those of controls, and were not different among ARC subtypes. The 8-OHdG levels were the highest in the nucleus, followed by the LECs and cortex. The repair proteins were predominantly detected in the cellular nuclei of the LECs and superficial cortical cells. In the LECs, the protein levels of the three BER enzymes were higher in ARC than in controls. In the cortex, a downward trend of the levels of three BER enzymes was found with the increasing opaque degrees. In the nucleus, no enzymes were detected.

Conclusions: Our findings indicate that the oxidative DNA damage increases in lenses with ARC, and the three BER enzymes compensatively increase in the LECs, while decreasing in the opaque cortex. The results suggest that the oxidative DNA damage may be related ARC and the alteration of DNA repair enzyme levels in ARC is associated with the location and opaque degrees of lens.

Acknowledgements

We appreciate the great contribution of Affiliated Hospital of Nantong University.

Declaration of interest

The authors declare no conflicts of interest related to this work.

This study was supported by the National Natural Science Foundation of China (No. 81070718 and No. 81270987).

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.