Melatonin protects LDL from oxidation but does not prevent the apolipoprotein derivatization

Biochem Biophys Res Commun. 1996 May 15;222(2):256-60. doi: 10.1006/bbrc.1996.0731.

Abstract

Protective effect of melatonin against Cu++ induced peroxidative modification of low density lipoprotein (LDL) was studied in vitro. Melatonin was used for this purpose because of its known scavenging capacity against hydroxyl and peroxyl radicals. It was demonstrated by the diene formation kinetic analysis that melatonin protected polyunsaturated fatty acids of LDL lipids against peroxidation. Lag time duration was prolonged, peak time was delayed, whereas rate of diene formation was decreased in melatonin treated LDL; however, parameters related to apolipoprotein (apo-B) showed that the protein was derivatized. Fluorescence, relative electrophoretic mobility, lysine residues analysis data, as well as the uptake by macrophages all showed properties similar to those of oxidised LDL. Present data suggest that by-products of melatonin oxidation might react with lysine residues of apo-B, transforming LDL in its atherogenic form.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apolipoproteins B / drug effects*
  • Apolipoproteins B / metabolism
  • Biological Transport
  • Copper / pharmacology
  • Humans
  • Kinetics
  • Lipid Peroxidation / drug effects*
  • Lipoproteins, LDL / drug effects*
  • Lipoproteins, LDL / isolation & purification
  • Lipoproteins, LDL / metabolism
  • Macrophages, Peritoneal / metabolism*
  • Male
  • Melatonin / pharmacology*
  • Mice
  • Mice, Inbred BALB C
  • Oxidation-Reduction

Substances

  • Apolipoproteins B
  • Lipoproteins, LDL
  • Copper
  • Melatonin