title: Susceptibility of LDL to oxidation in vitro and antioxidant capacity in familial combined hyperlipidemia: comparison of patients with different lipid phenotypes.
abstract: BACKGROUND
  There is increasing evidence that oxidation of low-density lipoprotein (LDL) plays an important role in atherogenesis.
  
  
  OBJECTIVE
  To explore the LDL oxidizability and its determinants in familial combined hyperlipidemia (FCHL) patients with different phenotypes.
  
  
  METHODS
  The study included 59 FCHL family members with different lipid phenotypes, 39 non-affected relatives, and 30 spouses as healthy controls.
  
  
  RESULTS
  The lag time for LDL oxidation was significantly shorter in FCHL patients with different lipid phenotypes as compared to healthy controls. There were no significant differences in the propagation rate and conjugated diene formation and alpha-tocopherol content in LDL between the FCHL groups and healthy controls. Plasma concentrations of alpha-tocopherol in all FCHL patients and uric acid in FCHL patients with IIB and IV phenotypes were significantly higher than in healthy controls. Plasma total peroxyl radical trapping capacity measured (TRAPmea) and TRAPcalc tended to be higher in affected FCHL groups, but the difference was significant only for IIB phenotype. The peak LDL particle size in the combined group of FCHL patients was significantly smaller than in healthy controls. The lag time for LDL oxidation correlated significantly with LDL size both in the group of FCHL family members (r = 0.477, P<0.001) and in the healthy controls (r = 0.482, P<0.01).
  
  
  CONCLUSIONS
  LDL from FCHL patients irrespectively of lipid phenotypes is more susceptible to oxidation in vitro than LDL from healthy controls. This increased susceptibility of LDL to oxidation in vitro seems to be attributed to the abundance of small dense LDL particles and not to the defect of antioxidant capacity in FCHL
authors.affiliation: Department of Medicine, Helsinki University Central Hospital, Finland.
authors.forename: Ming-Lin
authors.initials: ML
authors.lastname: Liu
authors.forename: Kati
authors.initials: K
authors.lastname: Ylitalo
authors.forename: Juha
authors.initials: J
authors.lastname: Vakkilainen
authors.forename: Ilpo
authors.initials: I
authors.lastname: Nuotio
authors.forename: Miia
authors.initials: M
authors.lastname: Valkonen
authors.forename: Sanni
authors.initials: S
authors.lastname: Lahdenperä
authors.forename: Jorma
authors.initials: J
authors.lastname: Viikari
authors.forename: Marja-Riitta
authors.initials: MR
authors.lastname: Taskinen
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D000975:Antioxidants / Q000032:analysis*; D001161:Arteriosclerosis / Q000235:genetics* / Q000503:physiopathology; D016022:Case-Control Studies; D015331:Cohort Studies; D005260:Female; D006801:Humans; D006950:Hyperlipidemia, Familial Combined / Q000235:genetics* / Q000378:metabolism*; D015227:Lipid Peroxidation / Q000502:physiology*; D008077:Lipoproteins, LDL / Q000235:genetics / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D010316:Particle Size; D010641:Phenotype; D011336:Probability; D012016:Reference Values
chemical_list: D000975:Antioxidants; D008077:Lipoproteins, LDL