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Updated: May 22, 2026
Intravitreous Injection for Establishing Ocular Diseases Model
Published on: October 1, 2007
[Modification of the nitric oxide concentration regulates the development of the apoptosis in the eye retina]
Abstract:
Using model elaborated it was shown that the retinal ischemia initiated the development of the apoptosis in the inner layers of the retina. Administration of NOS inhibitor prevented the development of the apoptosis in the retina. To ascertain if nitric oxide could induce the retinal apoptosis by itself the nontoxic donor of nitric oxide (dinitrosyl iron complex) was injected intravitreally. Administration of DNIC in low concentrations induced the development of the apoptosis in the same retinal layers as in ischemia. The injection of dinitrosyl iron complex at the higher concentration resulted in the decrease of the apoptosis level. Administration of dinitrosyl iron complex with excess of glutathione didn't lead to the development of the retinal apoptosis. The obtained data demonstrates the neurotoxic properties of the excess of nitric oxide in the retina.
Insights
Retinal ischemia triggers apoptosis in inner retinal layers. Nitric oxide, when administered, also induced apoptosis, but excess nitric oxide with glutathione prevented it, indicating neurotoxic effects of excess nitric oxide.
Area of Science:
- Ophthalmology
- Neuroscience
- Biochemistry
Context:
- Retinal ischemia is a significant cause of vision loss.
- Nitric oxide (NO) plays a complex role in retinal physiology and pathology.
- Understanding NO's role in apoptosis is crucial for developing neuroprotective strategies.
Purpose:
- To investigate the role of nitric oxide in retinal apoptosis.
- To determine if nitric oxide can induce apoptosis independently of ischemia.
- To explore the concentration-dependent effects of nitric oxide donors on retinal cells.
Summary:
- Retinal ischemia was shown to initiate apoptosis in the inner retinal layers.
- Administration of a nitric oxide synthase (NOS) inhibitor prevented ischemia-induced apoptosis.
- Intravitreal injection of a nitric oxide donor, dinitrosyl iron complex (DNIC), induced apoptosis in a concentration-dependent manner.
- Low DNIC concentrations mimicked ischemia-induced apoptosis, while higher concentrations reduced it.
- Co-administration of DNIC with excess glutathione abolished apoptosis, suggesting a protective role of antioxidants against NO-induced toxicity.
Impact:
- This study demonstrates the neurotoxic potential of excess nitric oxide in the retina.
- The findings highlight the dual role of nitric oxide in retinal injury and protection.
- Provides insights into therapeutic interventions targeting nitric oxide pathways in retinal diseases.
