RESUMEN
PURPOSE: The crystalline lens is a unique cellular organ that performs metabolic processes while maintaining transparency for optical functionality. Mitochondria play a role in providing cells with aerobic respiration necessary for these metabolic processes. Using menadione, a mitochondria-specific inhibitor of the quinone family, and bovine lenses in vitro, this study was undertaken to determine whether a relationship exists between mitochondrial function and optical function. METHODS: Bovine lenses were treated with 50 µM, 200 µM, 600 µM, and 1,000 µM menadione and lens optical function, assessed as optical quality, was observed over 9 days. Confocal micrographs of mitochondria in superficial secondary fiber cells were also analyzed in 50 µM, 200 µM, and 600 µM menadione-treated lenses over 48 h. RESULTS: A decrease in lens optical quality was observed in a dose-dependent manner within 24 h for the 200 µM- (p=0.0422), 600 µM- (p<0.0001), and 1,000 µM- (p<0.0001) treated lenses. No change in optical quality was observed for the 50 µM-treated lenses. Analysis of confocal micrographs indicated a trend of shorter mitochondria for 200 µM- and 600 µM-treated lenses with time and analysis of the distributions of mitochondrial lengths indicated a relative increase in the number of shorter mitochondria with higher doses of, and longer exposures to, menadione. CONCLUSIONS: The data show that menadione has a detrimental effect on mitochondrial integrity and this change is associated with degradation of optical quality, suggesting a possible link between mitochondrial function and optical function.
