Abstract
People are at high risk of exposure to endogenous and exogenous acrolein (ACR). ACR can cause a multitude of illnesses, including cardiovascular disease, Alzheimer's disease, and diabetes. In this study, we investigated the reaction pathway of cardamonin (CAR) or alpinetin (ALP) with ACR and the interconversion of CAR and ALP in vitro at 37 °C in phosphate-buffered saline using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Subsequently, ACR adducts of CAR, ALP, and their metabolites, for example, CAR-ACR-1, ALP-ACR, mono-ACR-pinocembrin chalcone (PIN-ACR), and mono- and di-ACR-naringenin (NAR-ACR and NAR-2ACR), were detected in urine samples, but only CAR-ACR-1 and ALP-ACR were detected in fecal samples from the CAR- and ALP-treated mouse groups using ultraperformance liquid chromatography-MS/MS, respectively. Quantitative analyses showed that CAR, ALP, and their metabolites markedly scavenged ACR in a dose-dependent manner in vivo. Furthermore, we also found that the metabolites of CAR or ALP remained and promoted the ACR-trapping ability.
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