title: HDL composition and HDL antioxidant capacity in patients on regular haemodialysis.
abstract: Recent evidence suggests that HDL can directly inhibit LDL oxidation, a key early stage in atherogenesis. Patients with chronic renal failure are at increased cardiovascular risk, have reduced HDL levels and altered HDL composition. We have therefore investigated whether compositional changes in HDL lead to decreased HDL antioxidant capacity in these patients. In comparison to control subject HDL, patient HDL contained less total cholesterol, cholesterol esters, phospholipids and alpha-tocopherol. LDL, HDL and LDL + HDL were standardised for protein and oxidised in the presence of Cu2+. The rate of propagation during HDL oxidation was reduced in the patient group (3.28+/-0.65 x 10(-5) vs. 4.60+/-0.97 x 10(-5) abs. U/min, P < 0.01). Lipid peroxide generation in patient HDL was decreased: 6.56+4.4 versus 13.42+/-7.0 nmol malondialdehyde (MDA)/mg HDL protein after 90 min and 14.45+/-3.8 versus 20.11+/-7.8 nmol MDA/mg HDL protein after 180 min. This is attributable to reduced HDL polyunsaturated fatty acid content in patients (0.53+/-0.12 vs. 0.72+/-0.16 mmol/g HDL, P < 0.01). The inhibitory effect of HDL on LDL oxidation was similar: 71 and 33% for patient HDL compared to 68 and 31% for control HDL, after 90 and 180 min, respectively. Compositional changes of HDL in patients on haemodialysis did not affect the antioxidant capacity of HDL after standardisation for HDL protein. However, reduced HDL levels in vivo may result in reduced HDL antioxidant capacity in these patients.
authors: School of Clinical Medicine, The Queen's University of Belfast, UK.
authors: O
authors: O
authors: Hasselwander
authors: J
authors: J
authors: McEneny
authors: D
authors: D
authors: McMaster
authors: D G
authors: DG
authors: Fogarty
authors: D P
authors: DP
authors: Nicholls
authors: A P
authors: AP
authors: Maxwell
authors: I S
authors: IS
authors: Young
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D000975:Antioxidants / Q000032:analysis*; D001161:Arteriosclerosis / Q000378:metabolism; D043303:Aryldialkylphosphatase; D002338:Carotenoids / Q000032:analysis; D002784:Cholesterol / Q000032:analysis; D002788:Cholesterol Esters / Q000032:analysis; D008076:Cholesterol, HDL / Q000737:chemistry* / Q000378:metabolism; D008078:Cholesterol, LDL / Q000378:metabolism; D004950:Esterases / Q000032:analysis; D005227:Fatty Acids / Q000032:analysis; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000628:therapy; D015227:Lipid Peroxidation; D000077276:Lycopene; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D010741:Phospholipases A / Q000032:analysis; D010743:Phospholipids / Q000032:analysis; D010972:Platelet Activating Factor; D006435:Renal Dialysis; D012307:Risk Factors; D014810:Vitamin E / Q000032:analysis; D019207:beta Carotene / Q000032:analysis
chemical_list: D000975:Antioxidants; D002788:Cholesterol Esters; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005227:Fatty Acids; D010743:Phospholipids; D010972:Platelet Activating Factor; D019207:beta Carotene; D014810:Vitamin E; D002338:Carotenoids; D002784:Cholesterol; D004950:Esterases; D010741:Phospholipases A; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D043303:Aryldialkylphosphatase; D000077276:Lycopene