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Brain, Vol. 115, No. 4, 991-1000, 1992
© 1992 Guarantors of Brain

research-article

TREATMENT OF EXPERIMENTAL NADH UBIQUINONE REDUCTASE DEFICIENCY WITH MENADIONE

J. M. COOPER1, D. J. HAYES2, R. A. J. CHALLISS3, J. A. MORGAN-HUGHES4 and J. B. CLARK5

1Departments of Neuroscience and Protein and Molecular Biology, Royal Free Hospital School of Medicine London 2Biochemical Sciences, Wellcome Research Laboratories Beckenham 3Department of Pharmacology and Therapeutics, University of Leicester Leicester 4Clinical Neurology London, UK 5Neurochemistry, Institute of Neurology London, UK

Correspondence to: Correspondence to Dr J. M. Cooper, Department of Neuroscience, Royal Free Hospital School of Medicine, Rowland Hill Street, London NW3 2PF, UK

Chronic administration of diphenylene iodonium (DPI) to rats has been shown to model the characteristics of mitochondrial myopathy. Using this model the efficacy of menadione therapy has been assessed. Menadione treatment of rats injected with DPI was associated with improved weight gain and increased survival rate This was accompanied by an improvement in muscle function as judged by analysis of isometric twitch tension of the gastrocnemius muscle (1 Hz for 20 min). The decline in phosphocreatine (PCr) levels in the gastrocnemius muscle during stimulation and delayed recovery in PCr after stimulation were similar in the menadione treated and untreated models Menadione treatment of the DPI model resulted in a resting intramuscular pH significantly lower than control or untreated DPI rats, but a similar decline in intramuscular pH to the DPI rats during stimulation. The changes in metabolite levels were broadly similar in both the menadione treated and untreated DPI models following stimulation, although the changes, except for increased lactate concentration, were generally less marked in the menadione-treated DPI model

Received January 24, 1992. Revised April 2, 1992. Accepted May 1, 1992.


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