Menadione degrades the optical quality and mitochondrial integrity of bovine crystalline lenses.

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. 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. 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. 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.