Epidemiological studies show that β-carotene intake and plasma levels shows an inverse association with certain forms of cancer. This protective effect may be due to the accumulation of carotenoids in the outer portion of cell membranes where they have antioxidant effects. In addition, carotenoids may increase gap cell communication which may cause apoptosis of cancerous cells. Studies generally measure the plasma levels of carotenoids, but cellular levels may present a more accurate reflection of long-term carotenoid status. This is because while plasma levels can fluctuate with daily intakes, cellular levels are less prone to fluctuations. Many studies have reported on the plasma levels β-carotene following supplementation, but there is less information comparing plasma and cellular contents. Those studies that have been performed suggest that cellular carotenoid concentrations can differ between cells.
For example, the Physicians Health Study in 1982 involved 22 071 healthy male doctors who were supplemented with aspirin, β-carotene, neither or both for 12 years. Researchers1 randomly sampled 73 of these doctors to obtain plasma samples in order to analyse them for concentrations of tocopherols and carotenoids in plasma and blood cells. The results showed that the treatment group had higher levels of β-carotene in plasma, red blood cells (RBC) and peripheral blood mononuclear cell (PBMC) as would be expected. In both the treatment and placebo group, plasma β-carotene concentrations correlated with RBC and PBMC concentrations, suggesting that the increases in plasma concentrations of β-carotene resulted in a similar increase in the concentration of β-carotene in blood cells. The increase in β-carotene in plasma and blood cells did not affect the tocopherol concentrations in these tissues.
However, in the treatment group the rank order of carotenoids in the PBMCs was β-carotene>lutein>lycopene>cryptoxanthin>α-carotene while in RBCs the rank order was lutein>β-carotene> cryptoxanthin>lycopene>α-carotene. In contrast, in the placebo group the rank order of carotenoids in both RBCs and PBMCs was the same (lutein>cryptoxanthin>β-carotene>lycopene>α-carotene). Taken as a whole, these results suggest that β-carotene supplementation may cause differences in the accumulation of carotenoids in cells. In particular, this suggests that PBMCs and RBCs have different affinities for the uptake of carotenoids. This is important because it is the cellular levels that would likely dictate the beneficial protective effects from cancer. Plasma levels in combination with cellular levels may be a better marker of carotenoid status.
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