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Residual bodies in the retinal pigment epithelium induced by intravitreal netilmicin
C A Tabatabay1, D J D'Amico, L A Hanninen
1Howe Laboratory of Ophthalmology, Harvard Medical School, Boston, Massachusetts.
Abstract:
Intravitreal injection of aminoglycoside antibiotics is known to induce morphological changes in the retinal pigment epithelium (RPE) resembling a lipidosis. The RPE of netilmicin-treated rabbits displays a dose-related increase in autofluorescence compared to untreated controls. Netilmicin produces an accumulation of membrane-limited osmiophilic lamellated inclusions in the pigment epithelial cell. These inclusions measure from 1 to 3 microns in diameter, and have acid hydrolase activity demonstrated by cytidine monophosphate cytochemistry. These findings suggest that netilmicin-induced inclusions are residual bodies and that the accumulation of these residual bodies is responsible for the observed cellular lipidosis.
Insights
Intravitreal injection of netilmicin causes lipidosis in the retinal pigment epithelium (RPE). This antibiotic induces residual body accumulation, leading to cellular changes and increased autofluorescence in RPE cells.
Area of Science:
- Ophthalmology
- Cell Biology
- Pharmacology
Background:
- Intravitreal aminoglycoside antibiotics can cause retinal pigment epithelium (RPE) morphological changes.
- These changes often resemble lipidosis, characterized by cellular lipid accumulation.
Purpose of the Study:
- To investigate the effects of netilmicin, an aminoglycoside antibiotic, on the RPE.
- To elucidate the mechanism behind netilmicin-induced RPE lipidosis.
Main Methods:
- Rabbits received intravitreal injections of netilmicin.
- Retinal pigment epithelium (RPE) morphology and autofluorescence were analyzed.
- Cytochemical staining (cytidine monophosphate) was used to assess enzyme activity within cellular inclusions.
Main Results:
- Netilmicin-treated RPE showed a dose-related increase in autofluorescence compared to controls.
- Accumulation of membrane-limited, osmiophilic, lamellated inclusions (1-3 microns) was observed in RPE cells.
- These inclusions exhibited acid hydrolase activity, indicating they are residual bodies.
Conclusions:
- Netilmicin induces the formation of residual bodies within RPE cells.
- The accumulation of these netilmicin-induced residual bodies is responsible for the observed RPE lipidosis.
- This study clarifies the cellular mechanisms underlying aminoglycoside-induced RPE toxicity.