The authors propose that light entering the eye interacts with retinal ganglion cell (RGC) axon mitochondria to generate reactive oxygen intermediates (ROI) and that when these neurons are in an energetically low state, their capacity to remove these damaging molecules is exceeded and their survival is compromised. They suggest that in the initial stages of glaucoma, RGCs exist at a low energy level because of a reduced blood flow at the optic nerve head and that in the mitochondrial optic neuropathies (MONs), this results from a primary, genetic defect in aerobic metabolism. In these states RGCs function at a reduced energy level and incident light on the retina becomes a risk factor. Preliminary laboratory studies support this proposition. Firstly, the authors have shown that light is detrimental to isolated mitochondria in an intensity dependent manner. Secondly, light triggers apoptosis of cultured, transformed RGCs and this effect is exacerbated when the cells are nutritionally deprived. Detailed studies are under way to strengthen the proposed theory. On the basis of this proposal, the authors suggest that patients with optic neuropathies such as glaucoma or at risk of developing a MON may benefit from the use of spectral filters and reducing the intensity of light entering the eye.
- ADOA, autosomal dominant optic atrophy
- HTG, high tension glaucoma
- IOP, intraocular pressure
- LHON, Leber’s hereditary optic neuropathy
- MON, mitochondrial optic neuropathy
- NTG, normal tension glaucoma
- POAG, primary open angle glaucoma
- RGC, retinal ganglion cell
- ROI, reactive oxygen intermediates
- RPE, retinal pigment epithelium
- TUNEL, TdT-dUTP linked nick end labelling technique
- mitochondrial optic neuropathies
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