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Lower plasma -carboxyethyl-hydroxychroman after deuterium-labeled -tocopherol supplementation suggests decreased vitamin E metabolism in smokers^1,2,3

¹ From the Linus Pauling Institute, Oregon State University, Corvallis, OR (RSB, SWL, TMB, and MGT), and Roswell Park Cancer Institute, Buffalo, NY (JL)

Background: Cigarette smoking increases the fractional disappearance rates of -tocopherol and is associated with increased oxidative stress, but its effects on -tocopherol metabolism are unknown.

Objective: We hypothesized that smokers would have less -tocopherol available and consequently lower plasma -carboxyethyl-hydroxychroman (-CEHC), the -tocopherol metabolite produced by a cytochrome P450–mediated process.

Design: Smokers and nonsmokers (n = 10 per group) were supplemented with deuterium-labeled -tocopheryl acetates (75 mg each d₃-RRR--tocopheryl and d₆-all-rac--tocopheryl acetate) from day –6 to day –1, and plasma tocopherols and CEHCs were measured (day –6 through day 17).

Results: After 6 d of supplementation, plasma d₃- and d₆--tocopherol concentrations did not differ significantly between groups. Plasma d₃- and d₆--CEHCs were detectable only from day –5 to day 5. Before supplementation, unlabeled - and -CEHCs were 60% and 40% lower, respectively, in smokers than in nonsmokers (P 0.05). In addition, d₀-, d₃-, and d₆--CEHC areas under the curves were 50% lower in smokers (P < 0.05), and smokers had lower maximal d₃--CEHC (P = 0.004) and d₆--CEHC (P = 0.0006) concentrations. Notably, 2.9–4.7 times as much -CEHC was produced from all-rac--tocopherol than from RRR--tocopherol. During supplementation, smokers had about one-half (P < 0.05) the plasma total, d₆-, or d₃--CEHC concentrations that nonsmokers did given similar -tocopherol concentrations.

Conclusions: Smoking did not increase -tocopherol disappearance through P450-mediated tocopherol metabolism. Therefore, the mechanism of increased -tocopherol disappearance in smokers likely operates through oxidation pathways, which is consistent with -tocopherol’s antioxidant function. Consequently, evaluating the molecular mechanism or mechanisms responsible for tocopherol metabolism under conditions of oxidative stress and the mechanisms that regulate -tocopherol status is warranted.

Key Words: Oxidative stress • carboxyethyl-hydroxychroman • CEHC • smokers • tocopherols • metabolism • cytochrome P450

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