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. (c) 2007 Elsevier B.V. All rights reserved.
LDL resistance to oxidation: Effects of lipid phenotype, autologous HDL and alanine
BALDI, SIMONA;FERRANNINI, ELEUTERIO;NATALI, ANDREA
2007-01-01
Abstract
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. (c) 2007 Elsevier B.V. All rights reserved.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
