3.2. Metabolism and clearance

Vitamin E is a lipophilic vitamin. Hemodialysis membranes remove only hydrophilic substances, so that alpha-tocopherol cannot be cleared by hemodialysis. It should be unlikely that vitamin E levels should be low in these patients as long as the intake is adequate, but abnormalities in absorption and metabolism of alpha-tocopherol have been reported.

Tocopherol is metabolized to carboxyethyl-hydroxychromans (CEHC), which are watersoluble compounds excreted by the kidneys. These metabolites accumulate in uremic patients, but as they are water soluble, they might be removed by dialysis membranes also. This could be an explanation for the results of a study from USA that found that even though CEHC levels increased after 30 days of alpha-tocopherol supplementation, they did not increase any more with further treatment [4, 7].

A reduction of vitamin E in cellular membranes has been noted in HD patients, suggesting that a decreased uptake of alpha-tocopherol by different tissues is happening, but the mechanism is not known. Some studies showed a disproportion between plasma tocopherol and lipids, as well as a low level of gamma-tocopherol and CEHC accumulation in patients undergoing chronic hemodialysis.

Vitamin E might directly inhibit 5-lipoxygenase in peripheral blood monocytes and partially

Vitamin E in Hemodialysis Patients

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http://dx.doi.org/10.5772/intechopen.78792

Early studies showed that vitamin E acts as a scavenger for ROS in hemodialysis patients. Other researchers found that gamma-tocopherol is a detoxifier of peroxynitrile radicals. More recent in vitro studies found that vitamin E-coated dialysis membranes reduce intracellular ROS in monocytes and maintain normal activity of Cu/Zn superoxide dismutase [4, 10–12].

Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of endothelial nitric oxide (NO) synthase and it is increased in hemodialysis patients. Vitamin E acts as an inhibitor of

Pertosa et al. demonstrated that vitamin E-coated dialysis membranes reduce activation of Jun

Vitamin E acts at the cellular level interfering with reactions implied in the progression of

• inhibits platelet aggregation and monocyte adhesion induced by superoxide anions;

control the lipid peroxidation and oxidative stress [8, 9].

Figure 2. Effects of vitamin E on hemodialysis patients.

ADMA and increases the activity of NO synthase [13, 14].

N-terminal kinase [15].

atherosclerosis such as:

4.2. Antiatherosclerotic effect

• reduces smooth muscle cell proliferation;

• reduces lipids peroxidation in monocytes;

• reduces activation of Jun-N terminal kinase;

• decreases oxidized low-density lipoproteins uptake;
