Nitric Oxide: A Potential Mediator of Retinal Ganglion Cell Damage in Glaucoma

In the glaucomatous optic nerve head, excessive nitric oxide (NO) may be responsible, at least in part, for degeneration of axons of retinal ganglion cells. We have demonstrated the apparent up-regulation and induction of certain isoforms of nitric oxide synthase (NOS), the enzyme that synthesizes N...

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Bibliographic Details
Published in:Survey of Ophthalmology 1999-06, Vol.43, p.S129-S135
Main Author: Neufeld, Arthur H
Format: Article
Language:English
Subjects:
Animals
Apoptosis - drug effects
Astrocytes - drug effects
Astrocytes - metabolism
Astrocytes - pathology
Enzyme Inhibitors - therapeutic use
glaucoma
Glaucoma - drug therapy
Glaucoma - metabolism
Glaucoma - pathology
Humans
Intraocular Pressure
Neuroprotective Agents - therapeutic use
Nitric Oxide - metabolism
nitric oxide synthase
Nitric Oxide Synthase - antagonists & inhibitors
Nitric Oxide Synthase - metabolism
Optic Disk - metabolism
Optic Disk - pathology
optic nerve
rat
Retinal Ganglion Cells - drug effects
Retinal Ganglion Cells - metabolism
Retinal Ganglion Cells - pathology
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Summary:In the glaucomatous optic nerve head, excessive nitric oxide (NO) may be responsible, at least in part, for degeneration of axons of retinal ganglion cells. We have demonstrated the apparent up-regulation and induction of certain isoforms of nitric oxide synthase (NOS), the enzyme that synthesizes NO, in astrocytes in the prelaminar and lamina cribrosa regions of optic nerve heads of patients with glaucoma. Evidence of NO toxicity, histochemical staining for nitrotyrosine, is present in these damaged optic nerve heads. In rats with experimentally induced, moderately elevated intraocular pressure, the isoforms of NOS were also identified.
ISSN:0039-6257
1879-3304
DOI:10.1016/S0039-6257(99)00010-7