Alpha-tocopherol transport in the lung is affected by the apoE genotype--studies in transgenic apoE3 and apoE4 mice.

Apolipoprotein E (apoE) is a major constituent of lipoproteins mediating peripheral uptake of lipids including the lipid-soluble vitamin alpha-tocopherol (alpha-toc). In a recent study, we observed significant lower alpha-toc concentrations in the lung of apoE4 compared with apoE3 transgenic mice. In this study, we determined the mRNA levels of genes encoding for proteins centrally involved in the uptake, export, and degradation of vitamin E. Receptors of alpha-toc uptake including scavenger receptor B1 (SR-B1), LDL receptor (LDLrec), and LDLrec-related protein 1 (LRP1) were lower in apoE4 when compared with apoE3 mice with statistical significance for SR-B1 and LRP1. Lung mRNA levels of the ATP-binding cassette A1 and the multidrug resistance transporter 1, surfactant proteins mediating the export of alpha-toc, were lower in apoE4 than in apoE3 mice. In addition, the mRNA levels of cytochrome P450 3A, a microsomal enzyme family involved in the degradation of alpha-toc, tended to be higher in the apoE4 when compared with the apoE3 genotype. Current data indicate that genes encoding for proteins involved in peripheral alpha-toc transport and degradation are affected by the apoE genotype probably accounting for thelower alpha-toc tissue concentration as observed in apoE4 mice.