LDL resistance to oxidation: effects of lipid phenotype, autologous HDL and alanine

Clin Chim Acta. 2007 Apr;379(1-2):95-100. doi: 10.1016/j.cca.2006.12.019. Epub 2007 Jan 5.


Background: Although LDL resistance to copper-induced oxidation is a time-honoured method, how it is modulated by the physiologic variability of lipid phenotype and what influences the protective action of homologous HDL and exogenous alanine is still unclear.

Methods: In 159 subjects without severe dyslipidemias, LDL resistance to copper-induced oxidation (lag phase) was measured under standardised conditions, with alanine and with autologous HDL.

Results: Lag phase was normally distributed and averaged 68+/-10 min (range: 40-105 min). Both VLDL-triglycerides (37+/-5, 52+/-7, 59+/-7, 53+/-5 mg/dl, p<0.05) and LDL-triglycerides (27+/-2, 27+/-1, 30+/-2, 35+/-3 mg/dl, p<0.01) increased across quartiles of lag phase. The relative LDL enrichment in triglycerides (triglycerides percent or triglycerides/cholesterol ratio) was strongly related to lag phase (r=0.29 and r=0.31, p<0.0005 for both) independently of age, gender, BMI, and presence of diabetes or hypertension. The protective effect of HDL was variable (+42+/-18 min) and largely dependent on the capacity of HDL to resist oxidation (r=0.69, p<0.0001). Alanine induced a rather constant lag phase prolongation (+32+/-7 min) that was weakly related only to baseline lag phase (r=0.17, p<0.05).

Conclusions: Relative triglyceride abundance protects LDL from ex-vivo oxidation, HDL particles protect LDL mainly through substrate dilution and alanine probably through a direct anti-oxidant effect.

MeSH terms

  • Adult
  • Alanine / chemistry*
  • Copper / chemistry
  • Female
  • Humans
  • Lipoproteins, HDL / chemistry*
  • Lipoproteins, LDL / analysis
  • Lipoproteins, LDL / chemistry*
  • Male
  • Middle Aged
  • Oxidation-Reduction
  • Triglycerides / analysis*


  • Lipoproteins, HDL
  • Lipoproteins, LDL
  • Triglycerides
  • low density lipoprotein triglyceride
  • Copper
  • Alanine