Dietary choline restriction causes complex I dysfunction and increased H2O2 generation in liver mitochondria

These findings suggest an explanation for the rapid onset of oxidative stress and energy compromise in the choline deficiency model of hepatocellular carcinoma and indicate that dietary choline withdrawal may be a useful paradigm for the study of mitochondrial pathophysiology in carcinogenesis

K. Hensley


Scholarcy highlights

  • Dietary choline deficiency produces a non-genotoxic model of liver cancer in rats
  • Tandem mass spectrometric analysis performed on extracted mitochondrial lipids indicated that PC pools were substantially altered within 3 days after initiating CDAA, and this perturbation was maintained to 7 days, the longest time period studied
  • This study documents an unexpected effect of dietary choline deficiency on the composition and function of rat liver mitochondria
  • Liver lipid pools are known to be altered during choline restriction, and previous studies report decreases in the quantity of phosphatidylcholine in mitochondrial membranes, as well as an increase in some longer-chain
  • PC variants during choline restriction. We extend upon these previous studies by documenting a time course of PC
  • The time course of PC perturbation correlates with the development of a respiratory dysfunction in liver mitochondria
  • Such a lipid perturbation might affect complex II-linked respiration, which is altered in CDAA liver mitochondria, albeit to a lesser extent

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