enzyme supplements are administered orally. More severe vitamin E deficiency symptoms, including neurological abnormalities, occur if bile secretion is also impaired in the children (Cynamon et al., 1988; Elias et al., 1981; Farrell et al., 1977; Sokol et al., 1989; Stead et al., 1986; Winklhofer-Roob et al., 1996a,b). Breath ethane, a lipid peroxidation marker, and erythrocyte susceptibility to in vitro hydrogen peroxide lysis have been inversely correlated with plasma α-tocopherol concentrations in children and adults with vitamin E deficiency as defined by low plasma vitamin E concentrations (Refat et al., 1991). Moreover, both the markers (breath ethane concentrations and erythrocyte lysis) and the symptoms of neurological abnormality can be corrected with supplemental vitamin E.

The hypothesis that oxidized low-density lipoprotein (oxLDL) is a causative agent in the development of cardiovascular disease (Steinberg et al., 1989) continues to dominate experimental protocols aimed at understanding the cause, and potentially the prevention, of cardiovascular disease.

Vitamin E does inhibit LDL oxidation whether induced by cells in culture (Steinbrecher et al., 1984) or by copper ion in vitro (Dieber-Rotheneder et al., 1991; Jialal et al., 1995; Reaven et al., 1993). In addition, vitamin E could affect atherogenesis at a number of steps, based on the following in vitro observations:

• Vitamin E inhibits smooth muscle cell proliferation through the inhibition of protein kinase C (Azzi et al., 1995; Boscoboinik et al., 1991; Chatelain et al., 1993).

• Vitamin E inhibits platelet adhesion, aggregation, and platelet release reactions (Freedman et al., 1996; Higashi and Kikuchi, 1974; Ishizuka et al., 1998; Steiner and Anastasi, 1976).

• Vitamin E inhibits plasma generation of thrombin, a potent endogenous hormone that binds to platelet receptors and induces aggregation (Rota et al., 1998).

• Vitamin E decreases monocyte adhesion to the endothelium by downregulating expression of adhesion molecules (Devaraj et al., 1996; Faruqi et al., 1994; Islam et al., 1998; Martin et al., 1997; Molenaar et al., 1989) and decreasing monocyte superoxide production (Cachia et al., 1998; Islam et al., 1998).