Keto-Carotenoids Are the Major Metabolites of Dietary Lutein and Fucoxanthin in Mouse Tissues1–3

Abstract

Fucoxanthin, a xanthophyll present in brown algae consumed in Eastern Asia, can suppress carcinogenesis and obesity in rodents. We investigated the metabolism, tissue distribution, and depletion of fucoxanthin in ICR mice by comparison with those of lutein. The experiments comprised 14-d dietary supplementation with lutein esters or fucoxanthin, followed by 41- or 28-d, respectively, depletion periods with carotenoid-free diets. After lutein ester supplementation, 3′-hydroxy-ε,ε-caroten-3-one and lutein were the predominant carotenoids in plasma and tissues, accompanied by ε,ε-carotene-3,3′-dione. The presence of these keto-carotenoids in mouse tissues is reported here for the first time, to our knowledge. Lutein and its metabolites accumulated most in the liver (7.51 µmol/kg), followed by plasma (2.11 µmol/L), adipose tissues (1.01–1.44 µmol/kg), and kidney (0.87 µmol/kg). The half-life of the depletion (t1/2) of lutein metabolites varied as follows: plasma (1.16 d) < liver (2.63 d) < kidney (4.44 d) < < < adipose tissues (>41 d). Fucoxanthinol and amarouciaxanthin A were the main metabolites in mice fed fucoxanthin and partitioned more into adipose tissues (3.13–3.64 µmol/kg) than into plasma, liver, and kidney (1.29–1.80 µmol/kg). Fucoxanthin metabolites had shorter t1/2 in plasma, liver, and kidneys (0.92–1.23 d) compared with those of adipose tissues (2.76–4.81 d). The tissue distribution of lutein and fucoxanthin metabolites was not associated with their lipophilicity, but depletion seemed to be slower for more lipophilic compounds. We concluded that mice actively convert lutein and fucoxanthin to keto-carotenoids by oxidizing the secondary hydroxyl groups and accumulate them in tissues.