摘要

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 mu M, 200 mu M, 600 mu M, and 1,000 mu M 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 mu M, 200 mu M, and 600 mu M 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 mu M- p=0.0422), 600 mu M- (p<0.0001), and 1,000 mu M- (p<0.0001) treated lenses. No change in optical quality was observed for the 50 mu M-treated lenses. Analysis of confocal micrographs indicated a trend of shorter mitochondria for 200 mu M- and 600 mu M-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.