Inhibition of lipid peroxidation by heme-nonapeptide derived from cytochrome c

Biochim Biophys Acta. 1985 Jul 9;835(2):411-4. doi: 10.1016/0005-2760(85)90299-1.

Abstract

Heme-nonapeptide, derived from cytochrome c, inhibited both the NADPH- and NADH-dependent lipid peroxidation of brain microsomes but, in the case of liver microsomes, this inhibitory effect manifested itself in the presence of SKF-525A (a specific blocker of cytochrome P-450) only. Heme-nonapeptide prevented the transient accumulation of lipid peroxides in microsomes during lipid peroxidation. The oxygen consumption of microsomes in the presence of NADPH or NADH was stimulated by heme-nonapeptide. From these results we concluded that, in vitro, there are two independent mechanisms of lipid peroxidation in liver microsomes. It is suggested that, in vivo, the heme-peptide-sensitive mechanism, observed in brain microsomes, is more important.

MeSH terms

  • Animals
  • Brain / metabolism*
  • Cytochrome c Group / metabolism*
  • Cytochrome c Group / pharmacology
  • Cytochromes c*
  • Heme / metabolism*
  • Heme / pharmacology
  • Kinetics
  • Lipid Peroxides / metabolism*
  • Microsomes / metabolism*
  • Microsomes, Liver / metabolism*
  • NAD / metabolism
  • NADP / metabolism
  • Oxygen Consumption
  • Peptide Fragments / metabolism*
  • Peptide Fragments / pharmacology
  • Rats
  • Rats, Inbred Strains

Substances

  • Cytochrome c Group
  • Lipid Peroxides
  • Peptide Fragments
  • heme nonapeptide
  • NAD
  • Heme
  • NADP
  • Cytochromes c