Antioxidant status in the aqueous humour of patients with glaucoma associated with exfoliation syndrome

Abstract

Purpose To establish the antioxidant status of the aqueous humour in glaucoma associated with exfoliation syndrome (XFG) and to compare it to primary open-angle glaucoma (POAG) and cataract patients. Methods Patients were diagnosed with POAG, XFG, or cataract (n ¼ 25 for each group). Total reactive antioxidant potential (TRAP) was measured by chemiluminescence. Ascorbic acid levels and the activities of catalase, glutathione peroxidase (GPx), and superoxide dismutase (SOD) were measured spectrophotometrically.Results TRAP value was lower in XFG (28 ± 2 lM Trolox) than in POAG (55 ± 8 lM Trolox; Po0.001). TRAP values in both glaucomas were lower than the cataract value (124±5 lM Trolox; Po0.001). A decrease in ascorbic acid was measured in XFG (230±20 lM) compared with POAG (415±17 lM; Po0.001). Ascorbic acid in both glaucomas was lower than in cataract (720 ± 30 lM; Po0.001). A significant increase in GPx was found in XFG (30 ± 2 U/ml) compared with POAG (16 ± 3 U/ml). GPx activity in both glaucomas was increased when compared with cataracts (6±2 U/ml; Po0.001). A significant increase of 67% in SOD activity was observed in the glaucoma group vs cataract group (27 ± 3 U/ml; Po0.001), but no changes were found between both glaucomas. Conclusions The antioxidant status of the aqueous humour may play a role in the pathophysiology of both glaucomas.

Influence of cataract maturity on aqueous humor lipid peroxidation markers and antioxidant enzymes

“…22 However, oxidants can strongly enhance the transcriptional activity of the lens SOD genes, 23 probably contributing to average SOD activity of 24.5 ± 7.1 U/ml in SC, as seen in this and some previous studies. 4,7 The SOD activity was decreasing with age (Table 1; Figure 1c) and, although this was in contradiction with the results by Sawada et al, 5 it is in line with the evidence of decreased SOD in cataractous lens epithelial cells and trabecular meshwork of elderly. 24,25 Enzymatic conversion of superoxide anion radicals to less reactive H 2 O 2 by SOD is an important step that prevents oxidative damage.…”

“…1,2 Unlike ocular tissues, AH contains only small quantities of proteins and antioxidant enzymes, and its antioxidant defense thus relies on unusually high levels of low-molecular weight antioxidants, mostly ascorbic acid, present at the level of B1 mM, even in SC. 7 There is, however, no reliable data about peroxide levels in AH under either physiological or pathological conditions, presumably because such amounts of ascorbic acid strongly interfere with most biochemical methods commonly used for the estimation of H 2 O 2 . 8 An alternative method is to measure different LPO adducts that, due to essentially dynamic nature of the LPO process, may offer a temporal insight into oxidant/ antioxidant balance.…”

“…11 Concentration of oxidants is in AH regulated by a variety of low-molecular as well as enzymatic antioxidants, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidases (GPx). 4,5,7,12 Although AH is in direct contact with lens surface, little is known about changes in LPO markers and antioxidants caused by the progression of SC. Considering that oxidative stress markers in SC are often compared with other eye diseases, and that AH pathway may be used for targeting ocular antioxidant defense, we aimed this study at assessing the impact of SC maturity on AH LPO markers and antioxidants.…”

“…It is now well established that excess levels of ocular oxidants can cause damage to the lens and other tissues, which are implicated in normal ageing process and in pathogenesis of several eye diseases, such as pseudoexfoliation syndrome, diabetic retinopathy, glaucoma, and senile cataract (SC). [1][2][3][4][5][6][7] The toxicity of oxidants depends on their ability to induce cross-linking, aggregation, fragmentation, and insolubilization of structural proteins, inactivation of enzymes, and lipid peroxidation (LPO) of the membrane-bound polyunsaturated fatty acids (PUFA), leading to impaired cell function, apoptosis, and necrosis. 1,2 Unlike ocular tissues, AH contains only small quantities of proteins and antioxidant enzymes, and its antioxidant defense thus relies on unusually high levels of low-molecular weight antioxidants, mostly ascorbic acid, present at the level of B1 mM, even in SC.…”

Mitochondrial haplogroup U is associated with a reduced risk to develop exfoliation glaucoma in the German population

“…The latter is relevant to neuronal damage in the glaucomatous retina and optic nerve head since it triggers mitochondrial dysfunction and leads to retinal ganglion cell (RGC) death in a cell culture model [7]. The pathogenic role of reactive oxygen species in glaucoma is supported by various experimental findings, such as an increase of the oxidative stress markers superoxide dismutase, catalase, and glutathione peroxidase in the aqueous humor of patients with primary open angle glaucoma and exfoliation glaucoma [8,9]. A significant correlation between oxidative DNA damage in the trabecular meshwork and intraocular pressure (IOP) increase and visual field defects was observed in glaucomatous patients [10].…”