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

Charlotte Sy; Olivier Dangles; Patrick Borel; Catherine Caris-Veyrat

doi:10.1016/j.freeradbiomed.2013.05.017

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

Charlotte Sy
, Olivier Dangles
, Patrick Borel
, Catherine Caris-Veyrat^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

29 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	195-206
Number of pages	12
Journal	Free Radical Biology and Medicine
Volume	63
DOIs	https://doi.org/10.1016/j.freeradbiomed.2013.05.017
State	Published - 2013
Externally published	Yes

Funding

We thank Michel Carail and Christian Giniès for their technical assistance in the UPLC/DAD/MS and GC/MS analyses, respectively. This work was supported by the European Community’s Seventh Framework Program . The funding was attributed to the project entitled “New sources of natural, gastric stable, food additives, colorants and novel functional foods” (Colorspore Project 207948), which was a small collaborative project within the work program topic “(Bio)Technologies for the production of food additives, colorants, and flavours” (KBBE-2007-2-3-03). This publication reflects only the authors’ view. The Colorspore community is not liable for any use that may be made of the results.

Funders
Seventh Framework Programme

Keywords

Carotenoid
Free radicals
Iron
Kinetics
Mechanism
Oxidation
Stability
β-Carotene

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10.1016/j.freeradbiomed.2013.05.017

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title = "Iron-induced oxidation of (all-E)-carotene under model gastric conditions: Kinetics, products, and mechanism",

abstract = "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 (FeII, FeIII) or by heme iron (metmyoglobin, MbFeIII). Fe II and metmyoglobin were much more efficient than FeIII at initiating β-carotene oxidation. Whatever the initiator, hydrogen peroxide did not accumulate. Moreover, β-carotene markedly inhibited the conversion of FeII into FeIII. β-Carotene oxidation induced by FeII or MbFeIII was maximal with 5-10 eq FeII or 0.05-0.1 eq MbFeIII and was inhibited at higher iron concentrations, especially with FeII. 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) FeII 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.",

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author = "Charlotte Sy and Olivier Dangles and Patrick Borel and Catherine Caris-Veyrat",

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doi = "10.1016/j.freeradbiomed.2013.05.017",

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T1 - Iron-induced oxidation of (all-E)-carotene under model gastric conditions

T2 - Kinetics, products, and mechanism

AU - Sy, Charlotte

AU - Dangles, Olivier

AU - Borel, Patrick

AU - Caris-Veyrat, Catherine

PY - 2013

Y1 - 2013

N2 - 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 (FeII, FeIII) or by heme iron (metmyoglobin, MbFeIII). Fe II and metmyoglobin were much more efficient than FeIII at initiating β-carotene oxidation. Whatever the initiator, hydrogen peroxide did not accumulate. Moreover, β-carotene markedly inhibited the conversion of FeII into FeIII. β-Carotene oxidation induced by FeII or MbFeIII was maximal with 5-10 eq FeII or 0.05-0.1 eq MbFeIII and was inhibited at higher iron concentrations, especially with FeII. 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) FeII 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.

AB - 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 (FeII, FeIII) or by heme iron (metmyoglobin, MbFeIII). Fe II and metmyoglobin were much more efficient than FeIII at initiating β-carotene oxidation. Whatever the initiator, hydrogen peroxide did not accumulate. Moreover, β-carotene markedly inhibited the conversion of FeII into FeIII. β-Carotene oxidation induced by FeII or MbFeIII was maximal with 5-10 eq FeII or 0.05-0.1 eq MbFeIII and was inhibited at higher iron concentrations, especially with FeII. 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) FeII 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.

KW - Carotenoid

KW - Free radicals

KW - Iron

KW - Kinetics

KW - Mechanism

KW - Oxidation

KW - Stability

KW - β-Carotene

UR - https://www.scopus.com/pages/publications/84879050401

U2 - 10.1016/j.freeradbiomed.2013.05.017

DO - 10.1016/j.freeradbiomed.2013.05.017

M3 - Article

AN - SCOPUS:84879050401

SN - 0891-5849

VL - 63

SP - 195

EP - 206

JO - Free Radical Biology and Medicine

JF - Free Radical Biology and Medicine

ER -

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

Abstract

Funding

Keywords

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