Erythrocyte vitamin E and plasma ascorbate concentrations in relation to erythrocyte peroxidation in smokers and nonsmokers

dose response to vitamin E supplementation

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63 Citations (Scopus)

Abstract

Many human degenerative diseases involve free radical processes that nutritional antioxidants may ameliorate or prevent, but the optimum intake of such nutrients has yet to be established. Requirement will depend in part on the level of exposure to exogenous and endogenous reactive oxygen species. Smokers incur a sustained degree of oxidant stress from both of these sources, increasing their requirements for vitamins E and C. Male smokers (n = 50) from a Scottish population with habitually low vitamin E and vitamin C intakes consistently had lower plasma ascorbate concentrations (P < 0.02) and greater susceptibility to hydrogen peroxide-stimulated erythrocyte peroxidation in vitro (P < 0.001) than did nonsmokers (n = 50) from the same population. Erythrocyte vitamin E concentrations increased in a dose-dependent manner during 20 wk of supplementation with 70, 140, 560, and 1050 mg D-alpha-tocopherol. In smokers each dose was associated with a significant decrease in susceptibility of erythrocytes to peroxidation (P < 0.001). However, red cells of nonsmokers receiving the 1050-mg supplement had an increased susceptibility to peroxidation. Moreover, prolonged supplementation with D-alpha-tocopherol in nonsmokers induced a decline in plasma ascorbate concentration (P < 0.02) in association with an increasing erythrocyte vitamin E uptake (P < 0.001), and in nonsmokers receiving 1050 mg, the susceptibility to peroxidation also increased (P < 0.001). Thus, vitamin E may have prooxidant activity in nonsmokers at high and prolonged intakes.

Original languageEnglish
Pages (from-to)496-502
Number of pages7
JournalThe American Journal of Clinical Nutrition
Volume65
Issue number2
Publication statusPublished - Feb 1997

Keywords

  • vitamin E supplementation
  • lipid peroxidation
  • ascorbate
  • smoking
  • prooxidant
  • low-density-lipoprotein
  • lipid-peroxidation
  • cigarette-smoking
  • oxidative damage
  • alpha-tocopherol
  • free-radicals
  • antioxidant
  • acid
  • accumulation

Cite this

@article{87b85831c909425292356797d5c0a663,
title = "Erythrocyte vitamin E and plasma ascorbate concentrations in relation to erythrocyte peroxidation in smokers and nonsmokers: dose response to vitamin E supplementation",
abstract = "Many human degenerative diseases involve free radical processes that nutritional antioxidants may ameliorate or prevent, but the optimum intake of such nutrients has yet to be established. Requirement will depend in part on the level of exposure to exogenous and endogenous reactive oxygen species. Smokers incur a sustained degree of oxidant stress from both of these sources, increasing their requirements for vitamins E and C. Male smokers (n = 50) from a Scottish population with habitually low vitamin E and vitamin C intakes consistently had lower plasma ascorbate concentrations (P < 0.02) and greater susceptibility to hydrogen peroxide-stimulated erythrocyte peroxidation in vitro (P < 0.001) than did nonsmokers (n = 50) from the same population. Erythrocyte vitamin E concentrations increased in a dose-dependent manner during 20 wk of supplementation with 70, 140, 560, and 1050 mg D-alpha-tocopherol. In smokers each dose was associated with a significant decrease in susceptibility of erythrocytes to peroxidation (P < 0.001). However, red cells of nonsmokers receiving the 1050-mg supplement had an increased susceptibility to peroxidation. Moreover, prolonged supplementation with D-alpha-tocopherol in nonsmokers induced a decline in plasma ascorbate concentration (P < 0.02) in association with an increasing erythrocyte vitamin E uptake (P < 0.001), and in nonsmokers receiving 1050 mg, the susceptibility to peroxidation also increased (P < 0.001). Thus, vitamin E may have prooxidant activity in nonsmokers at high and prolonged intakes.",
keywords = "vitamin E supplementation, lipid peroxidation, ascorbate, smoking, prooxidant, low-density-lipoprotein, lipid-peroxidation, cigarette-smoking, oxidative damage, alpha-tocopherol, free-radicals, antioxidant, acid, accumulation",
author = "Brown, {K M} and Morrice, {P C} and Duthie, {G G}",
year = "1997",
month = "2",
language = "English",
volume = "65",
pages = "496--502",
journal = "The American Journal of Clinical Nutrition",
issn = "0002-9165",
publisher = "American Society for Nutrition",
number = "2",

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TY - JOUR

T1 - Erythrocyte vitamin E and plasma ascorbate concentrations in relation to erythrocyte peroxidation in smokers and nonsmokers

T2 - dose response to vitamin E supplementation

AU - Brown, K M

AU - Morrice, P C

AU - Duthie, G G

PY - 1997/2

Y1 - 1997/2

N2 - Many human degenerative diseases involve free radical processes that nutritional antioxidants may ameliorate or prevent, but the optimum intake of such nutrients has yet to be established. Requirement will depend in part on the level of exposure to exogenous and endogenous reactive oxygen species. Smokers incur a sustained degree of oxidant stress from both of these sources, increasing their requirements for vitamins E and C. Male smokers (n = 50) from a Scottish population with habitually low vitamin E and vitamin C intakes consistently had lower plasma ascorbate concentrations (P < 0.02) and greater susceptibility to hydrogen peroxide-stimulated erythrocyte peroxidation in vitro (P < 0.001) than did nonsmokers (n = 50) from the same population. Erythrocyte vitamin E concentrations increased in a dose-dependent manner during 20 wk of supplementation with 70, 140, 560, and 1050 mg D-alpha-tocopherol. In smokers each dose was associated with a significant decrease in susceptibility of erythrocytes to peroxidation (P < 0.001). However, red cells of nonsmokers receiving the 1050-mg supplement had an increased susceptibility to peroxidation. Moreover, prolonged supplementation with D-alpha-tocopherol in nonsmokers induced a decline in plasma ascorbate concentration (P < 0.02) in association with an increasing erythrocyte vitamin E uptake (P < 0.001), and in nonsmokers receiving 1050 mg, the susceptibility to peroxidation also increased (P < 0.001). Thus, vitamin E may have prooxidant activity in nonsmokers at high and prolonged intakes.

AB - Many human degenerative diseases involve free radical processes that nutritional antioxidants may ameliorate or prevent, but the optimum intake of such nutrients has yet to be established. Requirement will depend in part on the level of exposure to exogenous and endogenous reactive oxygen species. Smokers incur a sustained degree of oxidant stress from both of these sources, increasing their requirements for vitamins E and C. Male smokers (n = 50) from a Scottish population with habitually low vitamin E and vitamin C intakes consistently had lower plasma ascorbate concentrations (P < 0.02) and greater susceptibility to hydrogen peroxide-stimulated erythrocyte peroxidation in vitro (P < 0.001) than did nonsmokers (n = 50) from the same population. Erythrocyte vitamin E concentrations increased in a dose-dependent manner during 20 wk of supplementation with 70, 140, 560, and 1050 mg D-alpha-tocopherol. In smokers each dose was associated with a significant decrease in susceptibility of erythrocytes to peroxidation (P < 0.001). However, red cells of nonsmokers receiving the 1050-mg supplement had an increased susceptibility to peroxidation. Moreover, prolonged supplementation with D-alpha-tocopherol in nonsmokers induced a decline in plasma ascorbate concentration (P < 0.02) in association with an increasing erythrocyte vitamin E uptake (P < 0.001), and in nonsmokers receiving 1050 mg, the susceptibility to peroxidation also increased (P < 0.001). Thus, vitamin E may have prooxidant activity in nonsmokers at high and prolonged intakes.

KW - vitamin E supplementation

KW - lipid peroxidation

KW - ascorbate

KW - smoking

KW - prooxidant

KW - low-density-lipoprotein

KW - lipid-peroxidation

KW - cigarette-smoking

KW - oxidative damage

KW - alpha-tocopherol

KW - free-radicals

KW - antioxidant

KW - acid

KW - accumulation

M3 - Article

VL - 65

SP - 496

EP - 502

JO - The American Journal of Clinical Nutrition

JF - The American Journal of Clinical Nutrition

SN - 0002-9165

IS - 2

ER -