Intravenous Sodium Iodate Administration Induces Macula-Specific RPE Damage and Rod-Dominant Apoptosis in the...

Area of Science:

• Ophthalmology
• Toxicology
• Primate Models

Background:

• Sodium iodate (SI) is a known inducer of retinal degeneration in rodent models.
• However, the specific macular pathology and differential cone/rod vulnerability following SI administration remain poorly understood.

Purpose of the Study:

• To characterize the macular pathology induced by SI in cynomolgus monkeys.
• To investigate the dose-dependent effects and cell-type-specific vulnerability in SI-induced retinal degeneration.

Main Methods:

• Intravenous SI injections were administered to adult and juvenile cynomolgus monkeys at varying doses.
• Retinal changes were assessed using fundus photography, fluorescein angiography (FA), optical coherence tomography (OCT), histology, and transmission electron microscopy (TEM).

Main Results:

• High-dose SI (37.5 mg/kg) induced prominent macular fluorescein leakage and retinal pigment epithelium (RPE) elevation, accompanied by RPE migration.
• While peripheral rod apoptosis was observed, macular cone cell death was limited even at high doses.
• Lower doses showed outer segment damage and RPE melanolipofuscin accumulation without RPE barrier disruption.

Conclusions:

• Systemic SI administration can induce macular degeneration with RPE barrier disruption in young adult monkeys.
• These findings support a macula-specific vulnerability and differential cell-type susceptibility in SI-induced retinal degeneration.