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

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