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Corneal edema induced by bis (tributyltin) oxide
M Yoshizuka1, N Haramaki, M Yokoyama
1Department of Anatomy, University of Occupational and Environmental Health, School of Medicine, Kitakyushu, Japan.
Archives of Toxicology
|January 1, 1991
Summary
Bis (tributyltin) oxide (TBTO) causes corneal edema by accumulating in and damaging mitochondria of corneal endothelial cells. This toxic effect disrupts endothelial cell function, leading to swelling in the cornea.
Area of Science:
- Toxicology
- Ocular Pathology
- Cell Biology
Background:
- Bis (tributyltin) oxide (TBTO) is an organotin compound with known toxicity.
- Corneal edema is a condition characterized by swelling of the cornea.
Purpose of the Study:
- To investigate the mechanism of corneal edema induced by TBTO.
- To identify the cellular accumulation sites of tin (Sn) following TBTO administration.
Main Methods:
- Electron microscopy was used to examine corneal tissue structure.
- X-ray microanalysis was employed to determine the localization of tin within corneal cells.
- Male Wistar rats were injected intramuscularly with TBTO, and corneas were analyzed at various time points.
Main Results:
- Mitochondrial swelling in corneal endothelial cells was observed as early as 4 hours post-injection.
- Corneal edema manifested in the endothelial layer and stroma by 6 hours.
- X-ray microanalysis confirmed tin accumulation within the swollen mitochondria of endothelial cells.
- Advanced edematous swelling of corneal tissue was noted at 12 hours.
Conclusions:
- Parenterally administered TBTO accumulates in the mitochondria of corneal endothelial cells.
- TBTO's direct toxic effects on mitochondria likely impair endothelial cell pump function.
- This mitochondrial damage and subsequent functional impairment induce corneal edema.