title: Folic acid supplementation delays atherosclerotic lesion development in apoE-deficient mice.
abstract: Folic acid is a vitamin that when used as a dietary supplementation can improve endothelial function. To assess the effect of folic acid on the development of atherosclerosis, male apolipoprotein E-deficient mice fed a standard chow diet received either water (control group) or an aqueous solution of folic acid that provided a dose of 75 microg/kg/day, for ten weeks. At the time of sacrifice, blood was drawn and the heart removed. The study measured plasma homocysteine, lipids, lipoproteins, low-density lipoprotein (LDL) oxidation, isoprostane, paraoxonase, and apolipoproteins, and aortic atherosclerotic areas. In folic acid-treated animals, total cholesterol, mainly carried in very low-density and low-density lipoproteins, increased significantly, and homocysteine, HDL cholesterol, paraoxonase, and triglyceride levels did not change significantly. Plasma isoprostane and apolipoprotein (apo) B levels decreased. The resistance of LDL to oxidization and plasma apoA-I and apoA-IV levels increased with a concomitant decrease in the area of atherosclerotic lesions. The administration of folic acid decreased atherosclerotic lesions independently of plasma homocysteine and cholesterol levels, but was associated with plasma levels of apolipoproteins A-I, A-IV and B, and decreased oxidative stress.
authors.affiliation: Departamento de Bioquímica y Biología Molecular y Celular, Facultad de Veterinaria, Universidad de Zaragoza, Zaragoza, Spain.
authors.forename: Ricardo
authors.initials: R
authors.lastname: Carnicer
authors.forename: María A
authors.initials: MA
authors.lastname: Navarro
authors.forename: José M
authors.initials: JM
authors.lastname: Arbonés-Mainar
authors.forename: Sergio
authors.initials: S
authors.lastname: Acín
authors.forename: Mario A
authors.initials: MA
authors.lastname: Guzmán
authors.forename: Joaquín C
authors.initials: JC
authors.lastname: Surra
authors.forename: Carmen
authors.initials: C
authors.lastname: Arnal
authors.forename: Marcelo
authors.initials: M
authors.lastname: de Las Heras
authors.forename: Francisco
authors.initials: F
authors.lastname: Blanco-Vaca
authors.forename: Jesús
authors.initials: J
authors.lastname: Osada
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D001053:Apolipoproteins / Q000235:genetics / Q000378:metabolism; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics; D050197:Atherosclerosis / Q000378:metabolism / Q000517:prevention & control*; D019587:Dietary Supplements; D005492:Folic Acid / Q000008:administration & dosage*; D006710:Homocysteine / Q000097:blood; D008055:Lipids / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D018384:Oxidative Stress / Q000187:drug effects; D014803:Vitamin B Complex / Q000008:administration & dosage*
chemical_list: D001053:Apolipoproteins; D001057:Apolipoproteins E; D008055:Lipids; D006710:Homocysteine; D014803:Vitamin B Complex; D005492:Folic Acid