2004
DOI: 10.1016/s0002-9394(03)00788-8
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Oxidative stress markers in aqueous humor of glaucoma patients

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Cited by 334 publications
(280 citation statements)
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References 30 publications
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“…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].…”
Section: Introductionmentioning
confidence: 99%
“…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].…”
Section: Introductionmentioning
confidence: 99%
“…Since the total volume of aqueous humor in the anterior chamber is around 150-200 mL [41], and even decreases with age [42], it is hardly possible to obtain more than 100-150 mL of the sample from one subject [43,44].…”
Section: Aqueous Humormentioning
confidence: 99%
“…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.…”
Section: Introductionmentioning
confidence: 99%
“…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.…”
Section: Introductionmentioning
confidence: 99%