Liver-specific mitochondrial respiratory chain complex I deficiency in fatal influenza encephalopathy

Brain Dev. 2012 Feb;34(2):115-7. doi: 10.1016/j.braindev.2011.03.002. Epub 2011 Mar 26.

Abstract

We report on a 4-year-old boy who died from influenza encephalopathy. The clinical course and microscopic findings of the autopsied liver were compatible with Reye's syndrome. We examined the mitochondrial respiratory chain function by blue native polyacrylamide gel electrophoresis (BN-PAGE), western blotting, and respiratory chain enzyme activity assays. The activity of liver respiratory chain complex (CO) I was markedly decreased (7.2% of the respective control activity); whereas, the other respiratory chain complex activities were substantially normal (CO II, 57.9%; CO III, 122.3%; CO IV, 161.0%). The activities of CO I-IV in fibroblasts were normal (CO I, 82.0%; CO II, 83.1%; CO III, 72.9%; CO IV, 97.3%). The patient was diagnosed with liver-specific complex I deficiency. This inborn disorder may have contributed to the fatal outcome. We propose that relying only on fibroblast respiratory chain complex activities may lead to the misdiagnosis of liver-specific complex I deficiency.

Publication types

  • Case Reports

MeSH terms

  • Child, Preschool
  • Electron Transport Complex I / deficiency
  • Electron Transport Complex I / metabolism
  • Electron Transport Complex IV / metabolism*
  • Encephalitis Viruses / pathogenicity*
  • Humans
  • Influenza, Human / complications*
  • Liver / enzymology*
  • Male
  • Mitochondrial Diseases* / complications
  • Mitochondrial Diseases* / metabolism
  • Mitochondrial Diseases* / pathology

Substances

  • Electron Transport Complex IV
  • Electron Transport Complex I

Supplementary concepts

  • Mitochondrial complex I deficiency