Reactive oxygen species, oxidative stress, glaucoma and hyperbaric oxygen therapy

Abstract

This review examines the role of oxidative stress in damage to cells of the trabecular meshwork and associated impaired aqueous drainage as well as damage to retinal ganglion cells and associated visual field losses. Consideration is given to the interaction between vascular and mechanical explanations for pathological changes in glaucoma. For example, elevated intraocular pressure (IOP) forces may contribute to ischaemia but there is increasing evidence that altered blood flow in a wider sense is also involved. Both vascular and mechanical theories are involved through fluctuations in intraocular pressure and dysregulation of blood flow. Retinal function is very sensitive to changes in haemoglobin oxygen concentration and the associated variations in the production of reactive oxygen species. Reperfusion injury and production of reactive oxygen species occurs when IOP is elevated or blood pressure is low and beyond the capacity for blood flow autoregulation to maintain appropriate oxygen concentration. Activities such as those associated with postural changes, muscular effort, eye wiping and rubbing which cause IOP fluctuation, may have significant vascular, mechanical, reperfusion and oxidative stress consequences. Hyperbaric oxygen therapy exposes the eye to increased oxygen concentration and the risk of oxidative damage in susceptible individuals. However, oxygen concentration in aqueous humour, and the risk of damage to trabecular meshwork cells may be greater if hyperbaric oxygen is delivered by a hood which exposes the anterior ocular surface to higher than normal oxygen levels. Oronasal mask delivery of hyperbaric oxygen therapy appears to be indicated in these cases.

Autophagy and Age-Related Eye Diseases

“…It is an optic neuropathy involving in the progressive degeneration of retinal ganglion cells (RGCs). Oxidative stress serves as a crucial role in glaucoma development initially by injuring TM cells which modulate the exit of aqueous humor (AH) from the anterior chamber of the eye and are helpful for maintaining intraocular pressure (IOP) [65]. In the natural course of aging, the increase of ROS can decrease the number of trabecular-meshwork (TM) cells [66].…”

Annexins in Glaucoma

“…Mitochondrial dysfunction and oxidative stress are known mediators of RGC death in glaucoma [ 121 , 122 ]. Coenzyme Q10 (CoQ10) is an antioxidant with an important role in the normal functioning of the mitochondrial electron transport chain.…”

“…Coenzyme Q10 (CoQ10) is an antioxidant with an important role in the normal functioning of the mitochondrial electron transport chain. CoQ10 exhibits neuroprotection in neurological disorders, such as AD, PD and Huntington’s disease [ 122 ], as well as in experimental glaucoma [ 123 ]. DARC has been used recently to evaluate the topical administration of CoQ10 formed into micelles using the vehicle tocopherol polyethylene glycol succinate (TPGS) in an OHT rat model [ 102 ] (see Figure 4 ).…”

TRPA1 mediates damage of the retina induced by ischemia and reperfusion in mice

“…In a commonly used model of glaucoma, ischemia, and reperfusion (I/R) in rodent retina 7 is associated with increased reactive oxygen species (ROS) levels, tissue damage and cell death 3 . Increased oxidant levels have been proposed as the causal factor of glaucomatous retinal ganglion cell loss [8][9][10][11] , an explanation that is supported by data showing that administration of antioxidants protects retinal cells from injury following retinal I/R [12][13][14][15] . However, the specific pathways linking the oxidative stress burden to retinal damage remain unspecified.…”