Vitamin C and vitamin E are both antioxidants and protect
against
reactive oxygen species. These substances are of parallel interest as
water-soluble vitamin C regenerates lipid soluble vitamin E in vitro (Packer et
al. 1979;
Sharma & Buettner 1993;
Wijesunara & Berger 1994). There is much evidence indicating
that
vitamins C and E may also have a physiologically relevant interaction.
In guinea pigs, vitamin C deficiency led to reduced levels of vitamin E
in the liver, kidney, spleen, and lungs (Kanazawa et al. 1981; Hruba et
al. 1982; Bendich et al. 1984).
In inherently scorbutic rats, vitamin C deficiency led to reduced
vitamin E levels in the liver, kidney, and heart (Tanaka et al. 1997).
In guinea pigs administered oxidized frying oil, large doses of vitamin
C increased the level of vitamin E in liver, kidney, heart, lung, and
spleen (Liu & Lee 1997).
In normal rats, vitamin C supplementation increased plasma vitamin E
level (Chen et al. 1980). Nevertheless, in one study, vitamin C
deficiency did not affect the plasma vitamin E level in guinea pigs
(Hruba et al. 1982), and in another, excessive doses of vitamin C
reduced plasma vitamin E levels (Chen & Chang 1979).
In studies with human subjects, vitamin C supplementation increased
plasma lipid standardized α-tocopherol (Hamilton et al.
2000).
Vitamin C supplementation also led to a higher level of vitamin E in
plasma in participants who were administered 800 mg/day of vitamin E
than in participants administered vitamin E alone (Baker et al. 1996).
In normal rats and guinea pigs, vitamin E supplementation increased the
plasma vitamin C level (Chen et al. 1980; Bendich et al. 1984).
In inherently scorbutic rats, a deficiency of vitamin E led to lower
levels of vitamin C in the plasma, liver, kidney, and heart (Tanaka et
al. 1997).
In rats, vitamin E deficiency did not affect the plasma vitamin C
level, but the muscle vitamin C level was significantly increased
(Gohil et al. 1986).
In a study with human subjects, vitamin E supplementation increased the
plasma level of vitamin C (Hamilton et al. 2000).
In smokers, but not in nonsmokers, vitamin E disappearance in plasma
was inversely related to vitamin C levels (Bruno et al. 2005)
A recent study found that a combined deficiency of vitamins C and E in
guinea pigs produced a clinical picture different from scurvy. Many of
these doubly deficient animals had paralysis of their limbs, and there
was evidence of oxidative damage in the central nervous system (Hill et
al. 2003).
In endotoxin-treated guinea pigs, simultaneous supplementation of
vitamins C and E led to higher levels of vitamin E in the liver than
vitamin E supplementation alone (Cadenas et al. 1998).
Wahli et al. (1998) found an interaction between vitamins C and E in
their effects on the susceptibility to infection of rainbow trout (pp
118, 129).
Accordingly, there is experimental data indicating that vitamin C and
vitamin E have a physiological interaction, but its significance is
poorly understood both in experimental animals and human beings.
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NOTE: All the links in the
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