Alpha-tocopherol (vitamin E), the main lipid-soluble antioxidant in bi
ological membranes, reacts readily with radical and non-radical oxidan
ts. Such reactions may lead to alpha-tocopherol consumption, defined a
s loss of antioxidant action. Irreversibly oxidized metabolites excret
ed via the bile into the feces are tocopheryl quinone, epoxyquinones,
and products of dimeric and trimeric structures. A alpha-tocopherol ba
lance cannot be calculated, due to low intestinal absorption, enterohe
patic circulation, and microbial metabolism in the intestine. For thes
e reasons physiological vitamin E requirement cannot be derived from t
he alpha-tocopherol turnover. A common approach towards dietary recomm
endations is based on the PUFA - vitamin E relationship. Recently it w
as discovered that not the Simon metabolites, but -tetramethyl-2-(2'-c
arboxyethyl)-6-hydroxy-chroman (alpha-CEHC) is the major urinary excre
tion product. Our finding that excretion of this metabolite depends on
the plasma tocopherol concentration has been reason to conclude that
alpha-CEHC may be a marker of the optimum prophylactic vitamin E intak
e.