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Retinal Apo-carotenal

Retinyl esters /

(storage form) &

Retinoic acid

Retinoic acid

FIGURE 1. Cleavage pathways for b-carotene leading to either two molecules of retinal (central cleavage) or to one molecule of b-apo-carotenal and one molecule of b-ionone. Both products represent intermediates, as retinal is reduced to retinol to be subsequently bound to proteins or stored as retinyl esters in the liver. b-Apo-carotenals can be shortened to RA in a process similar to b-oxidation.

or the interaction of both enzymes may modify carotenoids to yield certain apo-carotenoid products. The debate about monooxygenase versus dioxy-genase was solved by Woggon and coworkers (Leuenberger et al., 2001), who clearly could show by labeling experiments with 17O and 18O that the enzyme catalyzes the oxidative cleavage in a monooxygenase reaction type. Therefore, the gene symbol was changed from Bcdo1 to Bcmo1 for b-carotene 15,15'-monooxygenase 1 and the EC number was changed to 1.14.99.36.

Vitamin A deficiency increases b-carotene cleavage activity whereas vitamin A supplementation downregulates the monooxygenase activity. Lutein, lycopene, 15,15'-dehydro-b-carotene, and astaxanthine inhibit the cleavage activity of Bcmo1, in which lycopene and 15,15'-dehydro-b-carotene acted in a competitive manner, while lutein and astaxanthine activity also included a noncompetitive component. Also the nutritional status—especially the vitamin A level—influences the conversion of b-carotene to retinal. Rats with low vitamin A plasma level showed higher Bcmo1 activity, while those with a

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