γ-Tocopherol-rich supplementation additively improves vascular endothelial function during smoking cessation.
Oxidative stress and inflammation persist years after smoking cessation thereby limiting the restoration of vascular endothelial function (VEF). Although short-term smoking cessation improves VEF, no studies have examined co-therapy of antioxidants in combination with smoking cessation to improve VEF. We hypothesized that improvements in γ-tocopherol (γ-T) status during smoking cessation would improve VEF beyond that from smoking cessation alone by decreasing oxidative stress and proinflammatory responses. A randomized, double-blind, placebo-controlled study was conducted in otherwise healthy smokers (22 ± 1 years; mean ± SEM) who quit smoking for 7 days with placebo (n=14) or γ-T-rich supplementation (n=16; 500 mg γ-T/day). Brachial artery flow-mediated dilation (FMD), cotinine, and biomarkers of antioxidant status, oxidative stress, and inflammation were measured before and after 7 days of smoking cessation. Smoking cessation regardless of supplementation similarly decreased plasma cotinine, whereas γ-T-rich supplementation increased plasma γ-T by seven times and its urinary metabolite γ-carboxyethyl hydroxychroman by nine times (P<0.05). Smoking cessation with γ-T-rich supplementation increased FMD responses by 1.3% (P<0.05) beyond smoking cessation alone (4.1 ± 0.6% vs 2.8 ± 0.3%; mean ± SEM). Although plasma malondialdehyde decreased similarly in both groups (P<0.05), plasma oxidized LDL and urinary F2-isoprostanes were unaffected by smoking cessation or γ-T-rich supplementation. Plasma TNF-α and myeloperoxidase decreased (P<0.05) only in those receiving γ-T-rich supplements and these were inversely related to FMD (P<0.05; R=-0.46 and -0.37, respectively). These findings demonstrate that short-term γ-T-rich supplementation in combination with smoking cessation improved VEF beyond that from smoking cessation alone in young smokers, probably by decreasing the proinflammatory mediators TNF-α and myeloperoxidase.
Human Nutrition Program, Department of Human Sciences, The Ohio State University, Columbus, OH 43210, USA.
Eunice
E
Mah
Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269, USA.
Ruisong
R
Pei
Human Nutrition Program, Department of Human Sciences, The Ohio State University, Columbus, OH 43210, USA.
Yi
Y
Guo
Department of Nutritional Sciences, University of Connecticut, Storrs, CT 06269, USA.
Kevin D
KD
Ballard
The Orthopedic Specialty Hospital, Murray, UT 84107, USA.
Tyler
T
Barker
The Orthopedic Specialty Hospital, Murray, UT 84107, USA.
Victoria E
VE
Rogers
Department of Cardiology, Henry Low Heart Center, Hartford Hospital, Hartford, CT 06102, USA.
Beth A
BA
Parker
Linus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA.
Alan W
AW
Taylor
Linus Pauling Institute, Oregon State University, Corvallis, OR 97331, USA.
Maret G
MG
Traber
Department of Kinesiology, University of Connecticut, Storrs, CT 06269, USA.
Jeff S
JS
Volek
Human Nutrition Program, Department of Human Sciences, The Ohio State University, Columbus, OH 43210, USA. Electronic address: Bruno.27@osu.edu.
Richard S
RS
Bruno
D000328:Adult; D000975:Antioxidants / Q000008:administration & dosage / Q000378:metabolism; D015415:Biomarkers / Q000097:blood; D001916:Brachial Artery / Q000502:physiology; D002339:Carotid Arteries / Q000502:physiology; D002839:Chromans / Q000652:urine; D003367:Cotinine / Q000097:blood; D019587:Dietary Supplements; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000502:physiology*; D028441:F2-Isoprostanes / Q000652:urine; D005260:Female; D006801:Humans; D007249:Inflammation / Q000188:drug therapy*; D018836:Inflammation Mediators / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D018384:Oxidative Stress / Q000187:drug effects*; D009195:Peroxidase / Q000097:blood; D010919:Placebos; D012907:Smoking / Q000097:blood; D016540:Smoking Cessation; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D055815:Young Adult; D024502:alpha-Tocopherol / Q000008:administration & dosage / Q000097:blood / Q000378:metabolism*
D000975:Antioxidants; D015415:Biomarkers; D002839:Chromans; D028441:F2-Isoprostanes; D018836:Inflammation Mediators; D008077:Lipoproteins, LDL; D010919:Placebos; D014409:Tumor Necrosis Factor-alpha; C483420:carboxyethyl-hydroxychroman; C099252:oxidized low density lipoprotein; D008315:Malondialdehyde; D009195:Peroxidase; D024502:alpha-Tocopherol; D003367:Cotinine
2,3 dinor-8-iso-PGF(2α); 2,3-dinor-5,6-dihydro-8-iso-PGF(2α); 2,3-dinor-F1; 2,3-dinor-F2; C-reactive protein; CRP; CVD; FMD; Flow-mediated dilation; Free radicals; IFN-γ; Inflammation; MCP-1; MPO; Oxidative stress; RNS; ROS; Smoking cessation; VEF; Vascular function; Vitamin E; cIMT; cardiovascular disease; carotid intima media thickness; flow-mediated dilation; interferon-γ; monocyte chemoattractant protein-1; myeloperoxidase; reactive nitrogen species; reactive oxygen species; sICAM-1; soluble intracellular adhesion molecule-1; vascular endothelial function; γ-CEHC; γ-T; γ-T-rich mixture of tocopherols; γ-TmT; γ-carboxyethyl hydroxychroman; γ-tocopherol