The crystalline lens is a unique cellular organ that performs metabolic processes while maintaining optical functionality. Mitochondria play a vital role in providing the cell with the energy necessary for these metabolic processes and have recently been shown to be more metabolically active than previously thought.
To test the hypothesis that mitochondrial function directly influences the optical function of the lens, bovine lenses were treated with 50 μM, 200 μM, 600 μM and 1000 μM menadione, a mitochondrial specific toxin that renders the mitochondria inactive, and the Back Vertex Distance (BVD) variability was observed over 216 hours. Confocal micrographs of secondary fibre cells’ mitochondria were also analyzed for 50 μM, 200 μM, and 600 μM menadione treatment over 48 hours. Increase in BVD variability (± s.e.m.) was observed within 24 hours from 0.28 ± 0.021 to 1.83 ± 0.75 for the 600 μM treated lenses. Confocal micrograph analysis showed a trend toward a decrease in the average length of mitochondria from 7.9 ± 0.8 to 3.7 ± 0.9 over for 200 μM treated lenses and from 5.9 ± 1.0 to 3.6 ± 0.6 for the 600 μM treated lenses over 48 hours.
These data show that indeed menadione has a detrimental effect on mitochondria as a function of both time and concentration and this change in mitochondria precedes changes in BVD variability directly linking mitochondrial function to optical function.
| Identifer | oai:union.ndltd.org:WATERLOO/oai:uwspace.uwaterloo.ca:10012/4184 |
| Date | January 2008 |
| Creators | Olsen, Kenneth Wayne |
| Source Sets | University of Waterloo Electronic Theses Repository |
| Language | English |
| Detected Language | English |
| Type | Thesis or Dissertation |
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