Characterization of complex III deficiency and liver dysfunction in GRACILE syndrome caused by a BCS1L mutation

Mitochondrion. 2010 Aug;10(5):497-509. doi: 10.1016/j.mito.2010.05.009. Epub 2010 May 23.

Abstract

A homozygous mutation in the complex III chaperone BCS1L causes GRACILE syndrome (intrauterine growth restriction, aminoaciduria, cholestasis, hepatic iron overload, lactacidosis). In control and patient fibroblasts we localized BCS1L in inner mitochondrial membranes. In patient liver, kidney, and heart BCS1L and Rieske protein levels, as well as the amount and activity of complex III, were decreased. Major histopathology was found in kidney and liver with cirrhosis and iron deposition, but of iron-related proteins only ferritin levels were high. In placenta from a GRACILE fetus, the ferrooxidases ceruloplasmin and hephaestin were upregulated suggesting association between iron overload and placental dysfunction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • ATPases Associated with Diverse Cellular Activities
  • Ceruloplasmin / metabolism
  • Congenital Abnormalities / pathology*
  • Electron Transport Complex III / deficiency
  • Electron Transport Complex III / metabolism*
  • Female
  • Ferritins / metabolism
  • Histocytochemistry
  • Humans
  • Infant
  • Infant, Newborn
  • Iron / metabolism
  • Kidney / pathology
  • Liver / pathology
  • Liver Diseases*
  • Membrane Proteins / metabolism
  • Myocardium / pathology
  • Placenta / pathology
  • Pregnancy
  • Up-Regulation

Substances

  • BCS1L protein, human
  • HEPH protein, human
  • Membrane Proteins
  • Ferritins
  • Iron
  • Ceruloplasmin
  • ATPases Associated with Diverse Cellular Activities
  • Electron Transport Complex III