Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Apoptosis / drug effects
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Astrocytes / drug effects
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Astrocytes / metabolism
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Astrocytes / pathology
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Enzyme Inhibitors / therapeutic use
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Glaucoma / drug therapy
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Glaucoma / metabolism*
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Glaucoma / pathology
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Humans
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Intraocular Pressure
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Neuroprotective Agents / therapeutic use
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Nitric Oxide / metabolism*
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Nitric Oxide Synthase / antagonists & inhibitors
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Nitric Oxide Synthase / metabolism
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Optic Disk / metabolism
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Optic Disk / pathology
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Retinal Ganglion Cells / drug effects
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Retinal Ganglion Cells / metabolism
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Retinal Ganglion Cells / pathology*
Substances
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Enzyme Inhibitors
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Neuroprotective Agents
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Nitric Oxide
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Nitric Oxide Synthase