title: Low high-density lipoprotein cholesterol is not responsible for decreased paraoxonase activity in chronic renal failure.
abstract: OBJECTIVE
  Human paraoxonase-1 (PON1) is responsible for the antioxidant effect of high-density lipoprotein (HDL) by inhibiting low-density lipoprotein oxidation. Previous studies discovered dyslipidemia (DL) and decreased PON1 activity in chronic renal failure (CRF). We aimed to determine PON and arylesterase activity, phenotypic distribution of the PON1 enzyme, and lipid profile in low and normal HDL cholesterol (HDL-C) patients with CRF, and renal transplant (TX), compared to primary DL.
  
  
  METHODS
  116 CRF (low or normal HDL-C), 52 TX (low or normal HDL-C), and 62 DL patients (low or normal HDL-C) were included. PON and arylesterase activities were measured spectrophotometrically. Phenotype was determined using the dual substrate method.
  
  
  RESULTS
  Aryl/HDL-C was significantly higher in low HDL-C patients. Patients with CRF had significantly lower arylesterase activity compared to DL, independent of HDL-C. PON activity and PON/HDL-C did not differ significantly in CRF compared to TX and DL. Phenotypic distribution was similar in patient groups. Low HDL-C CRF patients had significantly lower cholesterol and triglyceride than DL.
  
  
  CONCLUSIONS
  Decreased arylesterase activity, correlating with PON1 enzyme protein quantity, is not explicable by decreased HDL-C in CRF. Low HDL-C CRF patients' increased cardiovascular morbidity is not attributable to changes in PON1 activity, or phenotypic distribution.
authors.affiliation: First Department of Medicine, University of Debrecen Medical and Health Science Center, Debrecen, Hungary.
authors.forename: Éva
authors.initials: É
authors.lastname: Varga
authors.forename: Ildikó
authors.initials: I
authors.lastname: Seres
authors.forename: Mariann
authors.initials: M
authors.lastname: Harangi
authors.forename: István
authors.initials: I
authors.lastname: Kárpáti
authors.forename: Péter
authors.initials: P
authors.lastname: Koncsos
authors.forename: Ferenc
authors.initials: F
authors.lastname: Sztanek
authors.forename: György
authors.initials: G
authors.lastname: Paragh
mesh_terms: D000328:Adult; D000368:Aged; D043303:Aryldialkylphosphatase / Q000037:antagonists & inhibitors* / Q000097:blood* / Q000502:physiology; D015415:Biomarkers / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood* / Q000502:physiology; D004789:Enzyme Activation / Q000502:physiology; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000201:enzymology / Q000453:epidemiology; D008297:Male; D008875:Middle Aged
chemical_list: D015415:Biomarkers; D008076:Cholesterol, HDL; D043303:Aryldialkylphosphatase