Abstract
Purpose: :
A major reason for ganglion cells dying in primary open angle glaucoma (POAG) may be due to oxidative stress. It has been suggested, for example, that ischemia to the optic nerve results in an elevation of nitric oxide to eventually cause oxidative/nitrosative stress and lipid peroxidation to retinal ganglion cells. The present study was therefore designed to determine the oxidative status in the aqueous humour and serum of POAG patients.
Methods: :
Total antioxidative activity (mmol trolox equivalent/l, mean ± SD), a marker of free radical formation, was investigated stage–dependently in aqueous humour and serum samples of 50 POAG patients and 50 controls undergoing cataract surgery using the Trolox equivalent oxidative activity assay (TEAC II test). Patients included in this study had no known other eye diseases, ocular surgery which included laser treatment other than the category selected for or antioxidative therapy prior to cataract surgery. TEAC II, a photometric test measures colour desaturation of blue green 2,2'–acino–bis(3–ethylbenzothiazoline–6–sulfonic acid)–radical kation (ABTS.+), which is reduced to colour free 2,2'–acino–bis(3–ethylbenzothiazoline–6–sulfonic acid)–kation (ABTS+) by antioxidants.
Results: :
A preliminary evaluation in 11 POAG patients and 34 controls shows a significant (p< 0.002) increase of total antioxidative activity in the aqueous humour of POAG eyes in the initial phase (2,33 ± 0,46) and no significant (p > 0.922) change in the late phase (1.62 ± 0.69) of this disease when compared to controls (1.64 ± 0.42). Serum total antioxidative activity was unchanged in all groups. A full data analysis of 50 POAG patients and 50 controls will be presented.
Conclusions: :
Total antioxidative activity is increased in the aqueous humour but not the serum of initial POAG which may reflect a local mechanism to compensate for increased oxidative stress in this progressive optic neuropathy exhausted at a later stage. The results suggest that treatment of POAG patients with agents like antioxidants to increase antioxidative activity may help to stabilize progression of visual field loss in these patients.
Keywords: antioxidants • neuroprotection • protective mechanisms