Literature DB >> 11680798

Exercise intolerance resulting from a muscle-restricted mutation in the mitochondrial tRNA(Leu (CUN)) gene.

C Vives-Bauza1, J Gamez, M Roig, P Briones, C Cervera, A Solano, J Montoya, A L Andreu.   

Abstract

BACKGROUND: Some patients presenting with isolated lifelong exercise intolerance and ragged-red fibres, harbour skeletal-muscle restricted mutations in their mitochondrial DNA. AIM: To identify the molecular defect in a patient presenting with lifelong exercise intolerance, ragged-red fibres and deficiencies of complexes III and IV in skeletal muscle.
METHODS: The muscle biopsy was studied for activities of the respiratory chain, histochemical stains, and sequencing the tRNA genes of mitochondrial DNA.
RESULTS: The patient had a heteroplasmic mutation in the tRNA(Leu (CUN)) gene of mitochondrial DNA (G12334A). Clinical and morphological data as well as restriction fragment length polymorphism (RFLP) and single-fibre polymerase chain reaction (PCR) analyses strongly indicate that this molecular defect is the primary cause of the myopathy.
CONCLUSION: Mutations in any mitochondrial gene should be considered in the differential diagnosis of patients with lifelong exercise intolerance, even when the neurological examination is normal.

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Year:  2001        PMID: 11680798     DOI: 10.3109/07853890109002099

Source DB:  PubMed          Journal:  Ann Med        ISSN: 0785-3890            Impact factor:   4.709


  2 in total

Review 1.  Genomics and genetics in the biology of adaptation to exercise.

Authors:  Claude Bouchard; Tuomo Rankinen; James A Timmons
Journal:  Compr Physiol       Date:  2011-07       Impact factor: 9.090

2.  Slowly progressive encephalopathy with hearing loss due to a mutation in the mtDNA tRNA(Leu(CUN)) gene.

Authors:  Jorida Coku; Sara Shanske; Mahsa Mehrazin; Kurenai Tanji; Ali Naini; Valentina Emmanuele; Marc Patterson; Michio Hirano; Salvatore DiMauro
Journal:  J Neurol Sci       Date:  2009-12-22       Impact factor: 3.181

  2 in total

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