α‐Tocopherol does not Accelerate Depletion of γ‐Tocopherol and Tocotrienol or Excretion of their Metabolites in Rats

From an enzyme kinetic study using rat liver microsomes, α‐tocopherol has been suggested to accelerate the other vitamin E catabolism by stimulating vitamin E ω‐hydroxylation, the late limiting reaction of the vitamin E catabolic pathway. To test the effect of α‐tocopherol on catabolism of the other vitamin E isoforms in vivo, we determined whether α‐tocopherol accelerates depletion of γ‐tocopherol and tocotrienol and excretion of their metabolites in rats. Male Wistar rats were fed a γ‐tocopherol‐rich diet for 6 weeks followed by a γ‐tocopherol‐free diet with or without α‐tocopherol for 7 days. Intake of γ‐tocopherol‐free diets lowered γ‐tocopherol concentrations in serum, liver, adrenal gland, small intestine, and heart, but there was no effect of dietary α‐tocopherol on γ‐tocopherol concentrations. The level of urinary excretion of γ‐tocopherol metabolite was not affected by dietary α‐tocopherol. Next, the effect of α‐tocopherol on tocotrienol depletion was examined using rats fed a tocotrienol‐rich diet for 6 weeks. Subsequent intake of a tocotrienol‐free diet with or without α‐tocopherol for 7 days depleted concentrations of α‐ and γ‐tocotrienol in serum and tissues, which was accompanied by a decrease in the excretion of γ‐tocotrienol metabolite. However, neither the tocotrienol concentration nor γ‐tocotrienol metabolite excretion was affected by dietary α‐tocopherol. These data showed that dietary α‐tocopherol did not accelerate the depletion of γ‐tocopherol and tocotrienol and their metabolite excretions, suggesting that the positive effect of α‐tocopherol on vitamin E ω‐hydroxylase is not sufficient to affect the other isoform concentrations in tissues.