Iron-induced oxidation of (all-E)-β-carotene under model gastric conditions: kinetics, products, and mechanism.

The stability of (all-E)-β-carotene toward dietary iron was studied in a mildly acidic (pH 4) micellar solution as a simple model of the postprandial gastric conditions. The oxidation was initiated by free iron (Fe(II), Fe(III)) or by heme iron (metmyoglobin, MbFe(III)). Fe(II) and metmyoglobin were much more efficient than Fe(III) at initiating β-carotene oxidation. Whatever the initiator, hydrogen peroxide did not accumulate. Moreover, β-carotene markedly inhibited the conversion of Fe(II) into Fe(III). β-Carotene oxidation induced by Fe(II) or MbFe(III) was maximal with 5-10 eq Fe(II) or 0.05-0.1 eq MbFe(III) and was inhibited at higher iron concentrations, especially with Fe(II). UPLC/DAD/MS and GC/MS analyses revealed a complex distribution of β-carotene-derived products including Z-isomers, epoxides, and cleavage products of various chain lengths. Finally, the mechanism of iron-induced β-carotene oxidation is discussed. Altogether, our results suggest that dietary iron, especially free (loosely bound) Fe(II) and heme iron, may efficiently induce β-carotene autoxidation within the upper digestive tract, thereby limiting its supply to tissues (bioavailability) and consequently its biological activity.