observations suggest that in patients with cholestatic liver disease, there is increased oxidative stress, perhaps as a result of copper accumulation in the liver (Bayliss et al., 1995).

Hemolysis, using hydrogen peroxide or other oxidants added in vitro, has been used as a test for vitamin E adequacy in subjects thought to be at risk for vitamin E deficiency (Boda et al., 1998; Farrell et al., 1977). These tests suggest that plasma α-tocopherol concentrations of 14 µmol/L (600 µg/dL) are sufficient to prevent hemolysis (Farrell et al., 1977).

SELECTION OF INDICATORS FOR ESTIMATING THE REQUIREMENT FOR α-TOCOPHEROL

Lipid Peroxidation Markers

Several biomarkers measured in plasma, urine, or breath have been used to reflect the degree of lipid peroxidation in vivo. These include thiobarbituric acid reactive substances (TBARS), malondialdehyde, conjugated dienes, pentane, ethane, and the F2-isoprostanes.

Quantification of F2-isoprostanes, isomers of prostaglandin F2, has been suggested by a number of investigators as the most reliable index of in vivo free-radical generation and oxidative lipid damage (Morrow et al., 1999). The F2-isoprostanes are formed in membranes from arachidonyl-containing lipids largely as a result of free radical-catalyzed lipid peroxidation (Klein et al., 1997; Moore and Roberts, 1998). The F2-isoprostanes are increased in vitamin E-deficient rats (Awad et al., 1994). Importantly, their excretion was depressed in humans by consuming antioxidant vitamin supplements (Delanty et al., 1996; Reilly et al., 1996). Furthermore, in an animal atherosclerosis model, the apoE-deficient mouse, vitamin E supplementation not only suppressed F2-isoprostane production but also decreased atherosclerotic lesion formation (Pratico et al., 1998).

In general, lipid peroxidation markers are elevated during vitamin E depletion and their levels can be normalized upon vitamin E repletion. However, these markers are not necessarily specific to vitamin E, since changes in intake of other antioxidants can also change the levels of these markers. At present, there is no evidence that lowering lipid peroxidation marker levels is associated with health benefits. Therefore, estimates of lipid peroxidation products have not been used for establishing α-tocopherol requirements.



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