title: Vitamin C and E intake is associated with increased paraoxonase activity.
abstract: OBJECTIVE
  Paraoxonase (PON1), an esterase physically associated with high density lipoprotein, has been shown to inhibit atherogenic low density lipoprotein and high density lipoprotein oxidation. PON1 activity appears to be primarily under genetic control with some environmental modification and is a predictor of vascular disease. Vitamins C and E, dietary antioxidants, scavenge free-oxygen radical products that may depress PON1 activity. Therefore, we evaluated the relationship between dietary vitamin C and E intake and PON1 activity.
  
  
  RESULTS
  The vitamin C and E intakes of male white subjects (n=189) were estimated by using a standardized food frequency survey. With covariates, vitamin C or E intakes were found to be significant positive predictors of PON1 activity for the hydrolysis of paraoxon and diazoxon with the use of linear regression. Smoking and use of statins were independent predictors of PON1 activity.
  
  
  CONCLUSIONS
  PON1 activity, which is primarily genotype dependent, varies with antioxidant vitamins, cigarette smoking, and statin drug use. Because PON1 activity is a better predictor of vascular disease than is the currently described genetic variation in PON1, further studies of the environmental influences on PON1 activity and additional PON1 genetic variants are warranted.
authors.affiliation: Department of Medicine, Division of Medical Genetics, University of Washington 98195, USA. pair@u.washington.edu
authors.forename: Gail P
authors.initials: GP
authors.lastname: Jarvik
authors.forename: Nancey Trevanian
authors.initials: NT
authors.lastname: Tsai
authors.forename: Laura A
authors.initials: LA
authors.lastname: McKinstry
authors.forename: Roohi
authors.initials: R
authors.lastname: Wani
authors.forename: Victoria H
authors.initials: VH
authors.lastname: Brophy
authors.forename: Rebecca J
authors.initials: RJ
authors.lastname: Richter
authors.forename: Gerard D
authors.initials: GD
authors.lastname: Schellenberg
authors.forename: Patrick J
authors.initials: PJ
authors.lastname: Heagerty
authors.forename: Thomas S
authors.initials: TS
authors.lastname: Hatsukami
authors.forename: Clement E
authors.initials: CE
authors.lastname: Furlong
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001161:Arteriosclerosis / Q000378:metabolism / Q000517:prevention & control; D043303:Aryldialkylphosphatase; D001205:Ascorbic Acid / Q000008:administration & dosage*; D008076:Cholesterol, HDL / Q000378:metabolism; D008078:Cholesterol, LDL / Q000378:metabolism; D004032:Diet; D004950:Esterases / Q000235:genetics / Q000378:metabolism*; D005838:Genotype; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D015227:Lipid Peroxidation; D008297:Male; D008875:Middle Aged; D012907:Smoking / Q000009:adverse effects; D014810:Vitamin E / Q000008:administration & dosage*
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D000960:Hypolipidemic Agents; D014810:Vitamin E; D004950:Esterases; D043303:Aryldialkylphosphatase; C468406:PON1 protein, human; D001205:Ascorbic Acid