Vitamin E is actually a collection of chemicals (α-, β-, γ- and δ-tocopherol, and α-, β-, γ- and δ-tocotrienol) that all share the same biological activity as α-tocopherol. Vitamin E exerts strong antioxidant activity in cell membranes because of its hydrophobic nature, and the tocopherol radical can be recycled to its reduced form by cytosolic vitamin C. The α-tocopherol isomer is the most common form of vitamin E in human tissues due to its transport on the α-tocopherol transport protein (TTP), and is the only form retained in high concentrations. Vitamin E is absorbed from the small intestine following incorporation into mixed micelles, and then subsequently packaged into chylomicrons and transported to the liver where it selectively binds to the α-TTP to be distributed to the tissues. The metabolism of α-tocopherol is controversial because most studies have been short-term and use extrapolation to estimate the half-life.
To more accurately investigate the half-life of α-tocopherol researchers1 have used a long-term tracer study using [5-14CH3]-(2R, 4’R, 8’R)-α-tocopheryl acetate in 6 healthy men and women with a mean age of 27 years. The subjects ingested 1.81nmol of the tracer and the levels of 14C in the blood plasma and red blood cells (RBC) were monitored for up to 460 days and levels of 14C in the urine and faeces were monitored for up to 21 days post supplementation. Baseline levels of α-tocopherol in the subjects were comparable with those previously reported in Americans who were not taking any α-tocopherol supplements. The faeces was the major route for elimination and accounted for 23.2% of the total 14C dose. Urine accounted for 4.26% of the excreted dose. The amount retained in the body was close to the amount of α-tocopherol absorbed in the intestines (retained = absorbed – 23.2 – 4.26).
The advantage this study had over previous ones investigating the half-life of α-tocopherol was the long duration. This is advantageous because the actual measured half-life is always more accurate that the extrapolated half-life based on shorter-duration studies. By day 460 of the study, neither the plasma nor RBC tracer levels of 14C had returned to baseline which suggested that the t1/2 of [5-14CH3]-(2R, 4’R, 8’R)-α-tocopherol was much longer than prior estimates from short-duration studies. Biochemical differences were apparent between subjects with regard half-lives, as is often the case in this sort of bioavailability study. Generally the half-life for α-tocopherol was longer in RBC compared to plasma levels. The long half-live of α-tocopherol seen in this study may reflect recycling to plasma from peripheral tissues such as adipose tissue, where roughly ≤10% of cells are removed annually and little tocopherol is mobilised.
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