Serum alpha-tocopherol and retinol concentrations were followed in four heterozygous adults and one homozygous child with familial hypercholesterolemia being treated by regular low-density lipoprotein (LDL) apheresis. Approximately 50% of plasma alpha-tocopherol was eliminated during a single apheresis procedure in the heterozygous adults, while a complete elimination of this vitamin along with LDLs was observed in the homozygous child. Absolute losses of alpha-tocopherol amounted to 13.4-22.5 mg/apheresis and are equivalent to the recommended dietary intake for 1.5 to 2 days. Despite these losses, no changes were observed either in serum alpha-tocopherol levels or in the ratio of alpha-tocopherol/total serum lipids after 12 months regular apheresis treatment. Serum retinol concentrations only showed a small decrease on apheresis, there being apparently no specific elimination of this vitamin. The absolute losses ranged from 42-422 micrograms/apheresis and were, therefore, much lower than the recommended dietary intake of the equivalent of 1500 micrograms retinol/day. It is concluded that no extra supplementation of these vitamins is required during LDL-apheresis therapy, although it may be advisable to monitor vitamin E status in patients on long-term, intensive therapy.
Using bioluminescence assays for glycerol, free fatty acids, beta-hydroxybutyrate and lactate, we were able to perform complex studies of human energy and lipid metabolism both in serum samples in vivo and in isolated fat cells in vitro. These studies would have been impossible without reliable, specific and highly sensitive luminescence methods. Oxidatively modified low density lipoprotein (LDL) has been implicated in the pathogenesis of atherosclerosis. Adaptation of a chemiluminescence assay for lipid hydroperoxides to LDL isolated by specific precipitation from serum makes it possible to measure LDL oxidation in vivo. Cell dependent chemiluminescence was used to investigate whether receptor mediated endocytosis of LDL by macrophages leads to oxygen radical production in these cells. No activation of the membrane NAD(P)H oxidase was observed.
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