Abstract

Acrolein (ACR) derives from the external environment and the endogenous metabolism of organisms. It has super-reactivity and can induce various diseases. We investigated the capacity of cyanidin-3-O-glucoside (C3G) and its degradants/metabolites to capture ACR during thermal processing or in vivo. Our results indicated that both C3G and its degradants, including phloroglucinaldehyde (PGA) and protocatechuic acid (PCA), could efficiently trap ACR to form adducts, such as C3G-ACR, C3G-2ACR, PGA-ACR, PGA-2ACR, PCA-ACR, and PCA-2ACR. Additionally, these adducts were detected in commercial canned red bayberry products. The adducts of C3G and its metabolites conjugated with ACR, such as C3G-ACR, C3G-2ACR, PGA-ACR, and 4-hydroxybenzoic-acid-ACR (4-HBA-ACR), were also detected in mice feces treated with C3G by oral gavage, where the adduct level was dose-dependent. A similar pattern was observed in tests on human consumption of red bayberry. In human urine, only PGA-2ACR and 4-HBA-ACR, were found, whereas C3G-ACR, C3G-2ACR, myricetin-3-O-rhamnoside-ACR (M3R-ACR), PGA-2ACR, 4-HBA-ACR and ferulic acid-ACR (FA-ACR) were detected in human feces following administration of red bayberry. Our results are the first demonstration that C3G and its metabolites can capture ACR in vitro and in vivo (mice and humans) and present a novel strategy, the development of C3G as a promising ACR inhibitor.

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