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Vitamin E and neurodegenerative diseases.Mol
Aspects Med. 2007 Jan 11;
Vitamin E is
essential for neurological function. This fact, together with a
growing body of evidence indicating that neurodegenerative processes
are associated with oxidative stress, lead to the convincing idea that
several neurological disorders may be prevented and/or cured by the
antioxidant properties of vitamin E. In this review, some aspects
related to the role of vitamin E against Alzheimer's disease,
Parkinson's disease, amyotrophic lateral sclerosis and ataxia with
vitamin E deficiency will be presented.
Protective
effect of vitamin E supplements on experimental atherosclerosis is
modest and depends on preexisting vitamin E deficiency.Free
Radic Biol Med. 2006 Sep 1;41(5):722-30.
Vitamin
E has failed to protect humans from cardiovascular disease outcome,
yet its role in experimental atherosclerosis remains less clear. A
previous study (Proc. Natl. Acad. Sci. USA 97:13830-13834; 2000)
showed that vitamin E deficiency caused by disruption of the alpha-tocopherol
transfer protein gene (Ttpa) is associated with a modest increase in
atherosclerosis in apolipoprotein E gene deficient (Apoe(-/-)) mice.
Here we confirm this finding and report that in Apoe(-/-)Ttpa(-/-)
mice dietary alpha-tocopherol (alphaT) supplements restored
circulating and aortic levels of alphaT, and decreased atherosclerosis
in the aortic root to a level comparable to that seen in Apoe(-/-)
mice. However, such dietary supplements did not decrease disease in
Apoe(-/-) mice, whereas dietary supplements with a synthetic vitamin E
analog (BO-653), either alone or in combination with alphaT, decreased
atherosclerosis in Apoe(-/-) and in Apoe(-/-)Ttpa(-/-) mice.
Differences in atherosclerosis were not associated with changes in the
arterial concentrations of F(2)-isoprostanes and cholesterylester
hydro(pero)xides, nor were they reflected in the resistance of plasma
lipids to ex vivo oxidation. These results show that vitamin E at best
has a modest effect on experimental atherosclerosis in hyperlipidemic
mice, and only in situations of severe vitamin E deficiency and
independent of lipid oxidation in the vessel wall.
Low plasma
vitamin E levels in major depression: diet or disease?
Eur J Clin Nutr. 2005 Feb;59(2):304-6.
OBJECTIVE:
Levels of vitamin E have been reported to be lower in patients
suffering major depression, but whether this is due to inadequate
dietary intake or the pathophysiology of depression is not known, and
was the subject of the present study. SETTING: Wollongong, Australia.
METHODS: Plasma vitamin E (alpha-tocopherol) was measured in 49 adults
with major depression, age (mean+/-s.d.): 47+/-12 y. In a subset
(n=19) usual dietary intake of vitamin E was determined by diet
history. RESULTS: Subjects had significantly lower plasma alpha-tocopherol
(4.71+/-0.13 mumol/mmol cholesterol) than has previously been reported
for healthy Australians, and plasma alpha-tocopherol was inversely
related to depression score (by Beck Depression Inventory) (r=-0.367,
P<0.009). Diet analysis indicated that 89% of subjects met or exceeded
the recommended intake for vitamin E, and dietary intake was not
related to plasma alpha-tocopherol level in this subset. CONCLUSION:
These findings suggest that plasma levels of alpha-tocopherol are
lower in depression, but this is not likely to be the result of
inability to meet recommended dietary intake.
Accumulation of
vitamin E metabolites in the blood of renal failure patients.Clin
Nutr. 2004 Apr;23(2):205-12.
BACKGROUND &
AIMS: Carboxyethyl-hydroxychromans (CEHC) are hydrosoluble vitamin E
metabolites excreted through the renal filter. In this study we
investigated the effect of the kidney damage on the blood levels of
CEHC. METHODS: Plasma levels of alpha-CEHC, gamma-CEHC and their
precursors (namely, alpha-tocopherol and gamma-tocopherol) were
measured by HPLC with electrochemical detection in chronic (CRF) and
end-stage renal failure patients on regular hemodialysis (HD) before
and after dialysis. CRF patients (n = 26) were divided into three
subgroups with different extent of kidney damage as measured by the
intervals of creatinine clearance (CrCl, in ml/min): (a) 2-10, (b)
10-20, and (c) 20-45. HD patients (n = 8) did not show residual renal
function. In all the subjects the intake of vitamin E (as alpha-tocopherol)
was assessed using a food frequency questionnaire. In the HD group,
the plasma concentrations of ascorbic and uric acid (AA and UA,
respectively), total thiols, the total antioxidant status (TAS) and
reactive carbonyls were also measured. RESULTS: The progressive
deterioration of the kidney function in the different groups of
patients produced an exponential increase of both alpha-CEHC and
gamma-CEHC in plasma. Compared with healthy controls (alpha-CEHC =
20.1+/-13.4 and gamma-CEHC = 230.6+/-83.0 nmol/l) the levels of CEHC
approximately doubled in patients with CrCl < or = 20ml/min
(42.4+/-20.2 and 424.5.5+/-174.4; P <0.05 or higher in both) and
reached a 3-fold maximum increase in HD patients (77.3+/-45.7 and
636.6+/-219.3). The hemodialysis provided a significant, but only a
transient, correction of CEHC accumulation (44.8+/-23.5,
364.2+/-189.9). The HD patients showed lower intake and levels of
vitamin E (alpha-tocopherol = 5.1+/-1.0 and gamma-tocopherol
=0.32+/-0.11 micromol/mmol cholesterol; P <0.05) compared to healthy
controls (5.8+/-0.8 and 0.43+/-0.14), but in the CRF patients
tocopherol levels were normal or only slightly decreased even though
approximately half of the subject had lowered vitamin E intake. When
the entire patient population was considered, the blood concentrations
of parental tocopherols and CEHC did not correlate. The HD patients
before dialysis showed a marked decrease of TAS/UA, AA and thiols
levels, while UA and free carbonyls significantly increased. After
dialysis, the depletion of AA and thiols further worsened and also UA
and TAS/UA decreased, but free carbonyls slightly increased.
CONCLUSIONS: The results other than to confirm the key importance of
the renal route for the excretion of CEHC, demonstrate that CEHC
cannot be reliably used to investigate vitamin E biokinetics and
transformation without a careful examination of the renal function.
CEHC accumulation does not seem to influence the antioxidant status in
the plasma of HD patients. Further studies are requested to establish
whether such an increase in blood CEHC concentrations might be harmful
or could contribute to the biological functions of the vitamin E in
uremia and dialysis patients.
Comparison of a
vitamin E-rich diet and supplemental vitamin E on measures of vitamin
E status and lipoprotein profile.Eur
J Clin Nutr. 2001 Jul;55(7):555-61.
OBJECTIVE: To
determine whether dietary modification rather than use of supplements
can raise indices of vitamin E status to potentially cardioprotective
levels. DESIGN: Eight week randomised controlled trial with parallel
treatments to compare increased use of vitamin E-rich foods,
supplementation with 200 IU of vitamin E, and a placebo. SETTING:
Dunedin, New Zealand. SUBJECTS: Ninety subjects were recruited, of
whom 82 non-smoking, free-living individuals aged 22-72 y with plasma
cholesterol <7.5 mmol/l completed the trial. MAIN OUTCOME MEASURES:
Dietary intakes, plasma alpha tocopherol, plasma alpha tocopherol/cholesterol
ratio and lipoprotein cholesterol. RESULTS: Consumption of an
additional 12 mg of vitamin E (alpha tocopherol equivalents) from
dietary sources was primarily achieved through the replacement of
saturated fat-rich foods with unsaturated fats rich in vitamin E, nuts
and vegetables. This resulted in a 3.4 micromol/l increase in plasma
alpha tocopherol at week 6 (95% CI 1.6-5.3), and 0.9 micromol/mmol in
plasma alpha tocopherol/cholesterol at weeks 4 and 6 (95% CI 0.3-1.4
and 0.4-1.4, respectively) when compared with the placebo group. In
the supplement group, plasma alpha tocopherol and plasma alpha
tocopherol/cholesterol were significantly increased within 2 weeks and
remained so throughout the 8 week intervention. CONCLUSION: Increasing
dietary vitamin E intake can increase plasma alpha tocopherol levels,
although factors other than dietary intake are also important
determinants. The extent of dietary modification required to achieve
potentially cardioprotective levels of plasma alpha tocopherol is
difficult in practice. SPONSORSHIP: The study was supported through
the Otago Medical Research Foundation Laurenson Award.
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