Involvement of nitric oxide and other molecules with redox potential in primary open angle glaucoma
Nitric oxide (NO) and other molecules with redox potential are involved in cell signalling, including endothelial-dependent relaxation and the maintenance of vascular homeostasis. We investigated the availability of NO and the formation of reactive oxygen species (ROS) in the aqueous humour and its...
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Published in: | Archivos de la Sociedad Española de Oftalmología Vol. 83; no. 6; p. 365 |
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Main Authors: | , , , , , , |
Format: | Journal Article |
Language: | Spanish |
Published: |
Spain
01-06-2008
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Subjects: | |
Online Access: | Get full text |
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Summary: | Nitric oxide (NO) and other molecules with redox potential are involved in cell signalling, including endothelial-dependent relaxation and the maintenance of vascular homeostasis. We investigated the availability of NO and the formation of reactive oxygen species (ROS) in the aqueous humour and its relationship to the pathogenic mechanisms of primary open-angle glaucoma (POAG).
We analysed biochemically aqueous humour samples from patients having anterior segment surgery that were divided into two separate groups: 1) patients having a Watson's trabeculectomy because of worsening of the glaucoma evolution (GG; n=60), and 2) a comparative group of individuals having phacoemulsification for non-complicated cataracts (CG; n=60). Enzymatic-colorimetric methods were used to analyse the NO concentration, the lipid peroxidation by-product malondialdehyde (MDA) and the total antioxidant status (TAS). Statistical analysis was carried out in the two groups by means of the SPSS 15.0 programme.
A significant increase in both the NO concentration (p<0.05) and MDA levels (p<0.05), and a significant decrease of the TAS (p<0.05) were detected in the GG versus the CG samples.
Changes in NO availability and the concomitance of oxidative stress in the aqueous humour of the POAG patients may be useful markers for identifying those at risk of glaucoma progression and visual loss. |
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ISSN: | 0365-6691 |