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Editors Selection IGR 7-1
Basic research: Oxidative stress
Comment by Arthur Weber on:
11870 Oxidative injury by peroxynitrite in neural and vascular tissue of the lateral geniculate nucleus in experimental glaucoma, Luthra A; Gupta N; Kaufman PL et al., Experimental Eye Research, 2005; 80: 43-49
Glaucoma is an optic neuropathy often associated with higher than 'normal' intraocular pressure (IOP), progressive changes in the appearance of the optic disc and retinal nerve fiber layer, and visual field defects. The disease process is thought to originate at the level of the lamina cribrosa within the optic nerve head, where exiting nerve fibers are subjected to mechanical, vascular, and/or biochemical injury as a result of increased IOP. While considerable emphasis has been placed on understanding the degenerative effects that elevation of IOP and optic nerve injury have on the structure and function of the retina, much less attention has been directed toward understanding the degenerative changes that occur at other levels of the central visual pathway. More recently, Luthra et al. (86) have taken the lead in a renewed effort to clarify the cellular events that occur within the dorsal lateral geniculate nucleus (LGN), a primary target of retinal ganglion cell axons, and an important site for the integration and relay of visual information between the eye and visual cortex. In the present study, using immunohistochemical staining techniques and quantitative light microscopy, Luthra et al. report elevated levels of nitrotyrosine (NT) associated with the neuropil and vasculature of the glaucomatous primate LGN. Nitrotyrosine is considered an indicator of peroxynitrite, a product of the interaction of nitric oxide and superoxide, and a potent oxidant and mediator of cell/tissue injury. Thus, the results of this study provide the first evidence that oxidative stress may be a major factor contributing to the cellular changes that occur within glaucomatous LGN. The association of NT with the LGN vasculature also could provide an explanation for the non-specific degenerative effects described previously following a variety of insults to the retinogeniculate pathway. While defining the cellular and molecular events that lead up to the increase in peroxynitrite levels remains, the present study provides a foundation for future work aimed at the development of novel treatment strategies. Equally important, however, it again highlights our need to think beyond the retina when considering the implementation of such strategies in glaucoma.
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