[Open angle glaucoma: epidemiology, pathogenesis and prevention]

There is growing evidence that reactive oxygen species (ROS) play a key role in the pathogenesis of primary open angle glaucoma (POAG). The occurrence of oxidative DNA damage in trabecular meshwork (TM) has been demonstrated by measuring the increase of 8-hydroxy-2'-deoxyguanosine, the most abundant DNA oxidative alteration, which is significantly increased in glaucoma-bearing subjects as compared with unaffected controls. Several lines of evidence support the hypothesis that ROS play a fundamental pathogenic role, including the following: (a) outflow resistance in the anterior chamber increases in the presence of high levels of hydrogen peroxide; (b) TM possesses abundant antioxidant activities; (c) significant increases in superoxide dismutase and glutathione peroxidase activities were detected in the aqueous humour of glaucoma patients; (d) hydrogen peroxide compromises TM integrity. The existence of a significant correlation between oxidative DNA damage and intraocular pressure in glaucoma patients has been reported. POAG patients appear to have a genetic predisposition rendering them susceptible to ROS-induced damage because of a more frequent deletion, as compared to controls, of the gene encoding for glutathione-S-transferase M1, a pivotal anti-oxidant activity. Furthermore, oxidative stress, occurring not only in TM but also in retinal cells, appears to be involved in the neuronal cell death that characterizes POAG. These considerations could bear relevance for POAG prevention and suggest that genetic analyses and the use of drugs or dietary measures attenuating the effects of ROS, if validated in future studies, could be useful tools contributing to the control of this disease.