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. & 2013 Elsevier Inc. All rights reserved. Carotenoids are one of the most important groups of natural pigments. Carotenoids are mainly synthesized in plants but have also been isolated from yeasts, fungi, marine algae, microalgae, and some bacteria. Like animals in general, humans do not synthesize carotenoids and those that are found in human blood and tissues originate from food or supplements [1–3]. To date, over 700 carotenoids have been described in nature, among which 40 are present in the human diet. Epidemiological studies have shown correlations between carotenoid consumption and a lower risk of several diseases, thus suggesting that carotenoid-rich foods play important beneficial roles in human health. In particular, carotenoids participate in reducing skin photooxidative damage, age-related macular degeneration, and the incidence of certain cancers and diseases associated with the metabolic syndrome [4–7]. Carotenoids are widely recognized as antioxidants acting in plants and possibly in animals via several mechanisms, such as quenching of singlet dioxygen and other reactive oxygen species such as peroxyl radicals and protection of LDL against cell-mediated oxidation [7–9]. They are also associated with the induction and stimulation of intercellular communication via gap junctions [10] and there is increasing evidence that some carote-noids regulate signaling pathways and gene expression [7,11]. β-Carotene is the main precursor of vitamin A [4,12] and has been widely studied for its bioactivity [4,13–16]. Increasing awareness of the potential health benefits of car-otenoids has prompted the development of functional food products enriched in carotenoids, in particular β-carotene. However, the long chain of conjugated carbon–carbon double bonds makes β-carotene highly susceptible to oxidation. Its instability during processing (extraction, thermal treatments), storage, and digestion is an important issue. The oxidation of β-carotene (mechanism, products' characterization) has been a subject of intense research [17]. Apo-carotenals are the most common oxidation products of β-carotene. A cleavage mechanism starting at either end of the conjugated system and progressing to the central (15,15′) double bond has been proposed [18]. In an oxidation catalyzed by a metalloporphyrin, Z-isomers of (all-E)-β-carotene were found to be possible intermediates in the formation of cleavage products. Indeed, dioxygen would attack preferentially on either side of the Z carbon–carbon double bond, giving epoxide intermediates and then carbonyl cleavage products (apo-carotenals and apo-carotenones) [19].