Glaucoma is an optic neuropathy in which the optic nerve axons are damaged, resulting in death of retinal ganglion cells (RGCs). The primary region of damage is thought to be the optic nerve head (ONH), with the lateral geniculate nucleus (LGN) and optic radiations to the visual cortex being secondarily affected. Neurotrophin deprivation resulting from optic nerve injury is thought to cause RGCs to die by apoptosis by inhibition of cell survival pathways. However, disruption of retrograde axonal transport is not the only mechanism associated with optic nerve damage and RGC death, and thus, an additional mechanism of injury is likely to be involved in glaucomatous optic neuropathy.
We propose 2 mechanisms of uveitis-glaucoma-hyphema (UGH) syndrome in 2 patients with intracapsular or in-the-bag single-piece acrylic intraocular lenses (IOLs). In the first case, pseudophacodonesis secondary to zonular laxity from pseudoexfoliation syndrome caused chafing of the posterior iris by the square-edged haptic. In the second case, focal capsular fibrosis around the square-edged haptics combined with anteriorly rotated ciliary processes in plateau iris configuration caused points of chafing. Extensive capsular fibrosis of the haptic in both cases precluded IOL exchange. In the first case, a capsular tension ring redistributed zonular tension and reduced symptoms. In the second case, endoscopic cyclophotocoagulation relieved areas of chafing and resolved symptoms. In-the-bag square-edged haptics of single-piece acrylic IOLs are a potential source of iridociliary chafing in certain situations. The mechanisms observed here should be considered to promptly diagnose and treat UGH.
Retinal ganglion cells (RGCs) are central neurons that undergo apoptosis after axonal injury. As the relationship between mitochondrial and oxidative signaling of apoptosis in neuronal systems is unclear, we sought to achieve a better understanding of the interplay of these two pathways by investigating the effect of direct oxidative stress on mitochondrial membrane potential in cultured RGCs, as measured with the dual-emission probe JC-1. Treatment with hydrogen peroxide caused RGC mitochondrial depolarization. Several pharmacological treatments were used to define the mechanism. Whereas cycloheximide, tris(2-carboxyethyl)phosphine, and cyclosporin A were unable to prevent the depolarization, bongkrekic acid significantly reduced the severity of the depolarization. This suggests that the hydrogen peroxide-induced depolarization may act through mitochondrial permeability transition pore opening independent of thiol oxidation, and may be preventable under certain conditions.
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