title: Reduction in plasma total homocysteine through increasing folate intake in healthy individuals is not associated with changes in measures of antioxidant activity or oxidant damage.
abstract: BACKGROUND
  Various mechanisms have been proposed to explain the association between plasma total homocysteine (tHcy) and risk of cardiovascular disease, including oxidative activity of homocysteine.
  
  
  OBJECTIVE
  To explore the putative role of reactive oxygen species in the association between plasma tHcy and risk of cardiovascular disease in healthy individuals.
  
  
  METHODS
  A double-blind, placebo-controlled crossover intervention to increase folate intake through diet (increased consumption of folate-rich foods) and supplement (400 micro g folic acid) was carried out in 126 healthy men and women. Measurements were made of antioxidant activity in red blood cells and plasma, and products of oxidant damage in plasma.
  
  
  RESULTS
  Diet and supplement-based interventions led to an increase in measures of folate status and a reduction in plasma tHcy. This was not associated with any significant change in measures of antioxidant activity (plasma and red blood cell glutathione peroxidase activity and red blood cell superoxide dismutase activity) or oxidant damage (plasma malondialdehyde), although an improvement in plasma total antioxidant capacity just failed to reach significance.
  
  
  CONCLUSIONS
  In healthy individuals lowering plasma tHcy does not have any functional implications regarding oxidative damage.
authors.affiliation: The Centre for Human Nutrition, University of Sheffield, The Northern General Hospital, UK.
authors.forename: S J
authors.initials: SJ
authors.lastname: Moat
authors.forename: M H
authors.initials: MH
authors.lastname: Hill
authors.forename: I F W
authors.initials: IF
authors.lastname: McDowell
authors.forename: C H
authors.initials: CH
authors.lastname: Pullin
authors.forename: P A L
authors.initials: PA
authors.lastname: Ashfield-Watt
authors.forename: Z E
authors.initials: ZE
authors.lastname: Clark
authors.forename: J M
authors.initials: JM
authors.lastname: Whiting
authors.forename: R G
authors.initials: RG
authors.lastname: Newcombe
authors.forename: M J
authors.initials: MJ
authors.lastname: Lewis
authors.forename: H J
authors.initials: HJ
authors.lastname: Powers
mesh_terms: D000328:Adult; D000368:Aged; D000975:Antioxidants / Q000378:metabolism*; D002318:Cardiovascular Diseases / Q000097:blood* / Q000453:epidemiology / Q000378:metabolism; D018592:Cross-Over Studies; D019587:Dietary Supplements; D004311:Double-Blind Method; D005260:Female; D005492:Folic Acid / Q000008:administration & dosage* / Q000097:blood / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006710:Homocysteine / Q000097:blood* / Q000378:metabolism; D006801:Humans; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008875:Middle Aged; D009752:Nutritional Status; D010084:Oxidation-Reduction; D017382:Reactive Oxygen Species; D012307:Risk Factors; D016037:Single-Blind Method; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D006710:Homocysteine; D008315:Malondialdehyde; D005492:Folic Acid; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase