Effect of administration of galactosamine hydrochloride on rat liver mitochondria

Indian J Biochem Biophys. 1997 Jun;34(3):296-301.

Abstract

The effect of galactosamine on liver mitochondrial functions was studied in vivo in rats at 12hr, 24hr and 36hr after the administration of the drug. State 3 respiration decreased significantly with both NAD+ linked and FAD linked substrates. Respiratory control ratio, an index of membrane integrity and P/O ratio which is a measure of phosphorylation efficiency decreased significantly. There was a significant decrease in the activities of NADH dehydrogenase, succinate dehydrogenase and cytochrome oxidase. A significant decrease was also seen on membrane potential, cytochrome aa3, cytochrome b, cytochrome c and on phospholipids of mitochondria. The observed mitochondrial dysfunctions were related to increased lipid peroxidation, which could cause loss of membrane integrity and a decreased rate of phosphorylation. It is proposed that increased lipid peroxidation was responsible for the inhibition on both oxidation and phosphorylation in mitochondria in galactosamine treated rats.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Respiration / drug effects
  • Cytochromes / analysis
  • Electron Transport / drug effects
  • Electron Transport Complex IV / metabolism
  • Galactosamine / pharmacology*
  • Lipid Peroxides / analysis
  • Lipids / analysis
  • Mitochondria, Liver / drug effects*
  • Mitochondria, Liver / metabolism
  • NADH Dehydrogenase / metabolism
  • Phosphorylation
  • Rats
  • Succinate Dehydrogenase / metabolism

Substances

  • Cytochromes
  • Lipid Peroxides
  • Lipids
  • Galactosamine
  • Succinate Dehydrogenase
  • NADH Dehydrogenase
  • Electron Transport Complex IV