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EC number: 604-195-9
CAS number: 1406-66-2
permeated after a very long lag time ( ca. 48 hr), and the permeation
profiles were not consistent. Although the average profile increased
with time, the individual permeation profile were quite variable.
Initially, it was suspected that this small permeation rate might be due
to the low solubility (Cs: 18 mg/ml) of vitamin E
in the receptor solution (40 % PEG). When 5 mM Tween-80 solution was
a receptor solution( Cs: 2.26 mg/ml), which raised the solubility of
vitamin E by a
100, the same skin permeation profile was obtained. This suggested that the
low skin permeation rate of vitamin E is not due to its low solubility
in receptor solution. To characterize the long lag times and small
permeation profiles a permeation experiment of vitamin E was conducted
using radiolabeled as well as non-labeled vitamin E.
of skin permeation profiles of vitamin E between HPLC and radiotracer
determined the total amount of radioactivity to permeate the skin while
HPLC analysis can separate vitamin E from other metabolites. The
radiolabeled vitamin E promptly penetratetd the skin, while non-labeled
vitamin E appeared after a remarkably long time lag (ca.48 hr). If
the long time lag observed in HPLC analysis is caused by skin binding,
also increased lag time, the permeation profile of radiolabeled vitamin
E should be similar to that from HPLC analysis. This was not the case.
It is therefore suggested that the long time lag may be due to
significant metabolism of vitamin E during the initial period of time,
when the enzyme responsible for vitamin E metabolism was still very
active. During the initial period of time, most vitamin E in the
skin may be metabolized. When the time elapsed the enzymes are
and intact vitamin E appeared.
of Vitamin E and its metabolites during skin permeation:
Most of the
radioactivity of radiolabeled vitamin E was recovered with the same
retention time as vitamin E, and so this tritium-labeled vitamin E was
used for this study. With this technique, it was possible to exclude the
interference caused by endogenous skin compounds that may leach out from
the skin. This technique also allowed for the metabolic pathway of
radiolabeled alpha tocopherol during the skin permeation
be traced. The authors conclude that vitamin E was metabolized to a more
hydrophilic metabolite, which may be an alpha tocopherol quinone. The
disappearance of peaks from time to time in the HPLC chromatograms,
implied that there was some interaction between the dermis of the skin
and vitamin E in receptor solution. This may be caused by back diffusion
or further metabolism taking place by the enzyme leached from the
dermis. The authors stated that the skin is capable of
vitamin E metabolism and that vitamin E is metabolized toits more
hydrophilic metabolites which may be more easily excreted from the body.
Metabolism of vitamin E (alpha-tocopherol) in hairless mouse skin was
investigated. An in vitro skin permeation study was performed with
[3H]-1,3 -alpha-tocopherol. hairless mous skin was mounted betwee the
half cells of the Valia-Chien diffusion cell, and the total
radioactivity in the receptor solution as a function of time was
identified with HPLC in line with a UV spectrometer and a liquid
scintillation counter. Significant amounts of radioactivity were
recovered as alpha-tocopherol quinone and more hydrophilic metabolites.
To confirm the metabolism of vitamin E in the skin, a stability study of
vitamin E in the receptor solution without skin was performed, and most
of the radioactivity was recovered as alpha-tocopherol, suggesting that
major metabolism takes place in the skin, not in the receptor solution.
The present study suggests that vitamin E undergoes very extensive
metabolism during the skin permeation process and that the skin
possesses the enzymes responsible for vitamin E metabolism like other
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