title: Antioxidant supplementation decreases lipid peroxidation biomarker F(2)-isoprostanes in plasma of smokers.
abstract: Free radicals in cigarette smoke (CS) cause oxidative damage to proteins, DNA, and lipids, contributing to the pathobiology of atherosclerosis, heart disease, and cancer. In vitro studies have shown that antioxidants quench free radicals and ameliorate certain aspects of biomolecular damage caused by CS. It is hypothesized that a combination of antioxidants is more effective than a single antioxidant, due to their interactions. To investigate whether supplemental antioxidants reduce CS-related lipid peroxidation in vivo and whether they are more effective in combination, we conducted an intervention study in smokers. In a randomized double-blind placebo-controlled trial, we investigated whether vitamin C or an antioxidant mixture containing vitamin C, alpha-lipoic acid, and vitamin E decreases plasma F(2)-isoprostane levels, an index of oxidant stress, in smokers. Plasma of 126 smokers (mean age, 46 years; age range, 20-78 years) was analyzed for F(2)-isoprostanes at baseline and after intervention with antioxidants and placebo. In smokers with a body mass index (BMI) above the median, 2 months of daily supplementation with 500 mg of vitamin C decreased plasma F(2)-isoprostane levels by 28.8 pmol/liter when compared with the placebo group (P = 0.001); levels in the mixture group were 7.45 pmol/liter lower after treatment, but this difference was not statistically significant (P = 0.14). There was no treatment effect in smokers with a low BMI. BMI was significantly positively associated with plasma F(2)-isoprostane levels (trend P = 0.001). Antioxidants decrease smoking-related lipid peroxidation markers of oxidative stress in humans with high BMI. Our results do not indicate that an antioxidant combination is more effective than vitamin C alone. The intake of antioxidants may help prevent smoking-related diseases. Smoking cessation should still be considered the most effective way to prevent smoking-related diseases.
authors.affiliation: Department of Nutritional Sciences, School of Public Health, University of California, 140 Warren Hall, Berkeley, CA 94720-7360, USA. mdietric@uclink4.berkeley.edu
authors.forename: Marion
authors.initials: M
authors.lastname: Dietrich
authors.forename: Gladys
authors.initials: G
authors.lastname: Block
authors.forename: Mark
authors.initials: M
authors.lastname: Hudes
authors.forename: Jason D
authors.initials: JD
authors.lastname: Morrow
authors.forename: Edward P
authors.initials: EP
authors.lastname: Norkus
authors.forename: Maret G
authors.initials: MG
authors.lastname: Traber
authors.forename: Carroll E
authors.initials: CE
authors.lastname: Cross
authors.forename: Lester
authors.initials: L
authors.lastname: Packer
mesh_terms: D000328:Adult; D000368:Aged; D000975:Antioxidants / Q000008:administration & dosage*; D001205:Ascorbic Acid / Q000008:administration & dosage*; D015415:Biomarkers / Q000032:analysis; D019587:Dietary Supplements; D004311:Double-Blind Method; D028441:F2-Isoprostanes / Q000032:analysis*; D005260:Female; D006801:Humans; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011336:Probability; D012016:Reference Values; D012907:Smoking / Q000097:blood*; D000074606:Smoking Prevention
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D028441:F2-Isoprostanes; D001205:Ascorbic Acid