Normal respiratory chain function in patients with low-tension glaucoma
E. J. Brierley, P. G. Griffiths, K. Weber, M. A. Johnson and D. M. Turnbull
Division of Clinical Neuroscience, University of Newcastle upon Tyne, England.
OBJECTIVE: To test the hypothesis that low-tension glaucoma has a
pathogenesis similar to Leber's hereditary optic neuropathy and results
from a defect in the mitochondrial respiratory chain. METHODS:
Mitochondrial fractions were prepared from skeletal muscle samples
collected from eight subjects with low-tension glaucoma. Their oxidative
metabolism was compared with that of age- and sex-matched controls.
Skeletal muscle DNA prepared from the subjects with glaucoma was also
screened for the 3,460, 11,778, and 14,484 mitochondrial DNA mutations that
are associated with Leber's hereditary optic neuropathy. RESULTS: No
subject with low-tension glaucoma had a defect in respiratory chain
activity or one of three mitochondrial DNA mutations that are commonly
associated with Leber's hereditary optic neuropathy. CONCLUSION: Although
these results do not exclude the possibility that low-tension glaucoma is
caused by an organ-specific defect of mitochondrial function, we have
excluded a systemic defect of the mitochondrial respiratory chain.