| Three experiments were conducted to study lutein uptake and its effects on mammary cancer development and in vivo pim-1 gene activation. Female 8-wk-old BALB/c mice were used in all experiments. In experiment 1, mice were fed for 28 d a diet containing 0, 0.05. 0.1, 0.2 or 0.4% lutein. Lutein was rapidly absorbed into plasma, liver and spleen increased in a dose- and time-dependent manner. The liver is a major storage organ for lutein. Experiment 2 studied the efficacy of dietary lutein against mammary tumor development. Mice were fed a diet containing 0, 0.002, 0.02,0.2 or 0.4% lutein. After 14d, mice were inoculated with a mammary tumor cell line and tumor growth measured daily for 70 d. Lutein in plasma, liver, spleen and tumor increased dose-dependently, especially with dietary lutein levels from 0 to 0.2%. Dietary lutein decreased mammary incidence, tumor volume/weight and lipid peroxidation in tumors and increased tumor latency. The final experiment studied the effect of dietary carotenoids on pim-1 expression in splenocytes. Mice were fed 0, 0.02 or 0.4% of astaxanthin, {dollar}beta{dollar}-carotene and lutein for 2 wk. Blood, liver and spleen were obtained. Concentrations of each carotenoid increased rapidly in the plasma and liver of supplemented mice. However, dramatic differences exist in the relative absorption of these carotenoids, with astaxanthin concentrations in plasma averaging 3 to 50 fold higher than that of lutein and {dollar}beta{dollar}-carotene, respectively. Mice fed lutein showed a dose-related increase in pim-1 mRNA expression. Astaxanthin and {dollar}beta{dollar}-carotene did not have similar effects. Therefore, lutein is rapidly absorbed into plasma, liver and spleen in mice, has potent anticancer activities against the initiation and growth of a transplantable mammary tumor; the latter mode of action is (among others) mediated through pim-1 gene regulation. |
