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Elizabeth J. Brierley, MRCP; Philip G. Griffiths, FRCOphth; Katharina Weber; Margaret A. Johnson, PhD; Douglass M. Turnbull, MD, PhD, FRCP

Arch Ophthalmol. 1996;114(2):142-146.

Abstract
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 3460, 11 778, and 14484 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.

Author Affiliations
From the Divisions of Clinical Neuroscience (Drs Brierley and Turnbull and Ms Weber), Ophthalmology (Mr Griffiths), and Neurobiology (Dr Johnson), University of Newcastle upon Tyne (England).

Footnotes
The authors have no commercial or propriety interest in the products or equipment discussed in this article.

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