This study compared the loading ability of various carotenoids into liposomal membrane, lipid peroxidation inhibition capacity, storage stability and in vitro release behavior in simulated gastrointestinal (GI) media. It was found that carotenoids exhibited various incorporating abilities into liposomes ranging from the strongest to the weakest: lutein > β-carotene > lycopene > canthaxanthin. A similar trend was also observed in their antioxidant activities against lipid peroxidation during preparation. Storage measurements demonstrated that a liposomal membrane can strongly retain β-carotene and lutein, whereas this effect was not pronounced for lycopene and canthaxanthin. In vitro release experiments showed that lutein and β-carotene were hardly released in a simulated gastric fluid, while displaying a slow and sustained release in a simulated intestinal fluid. By contrast, lycopene and canthaxanthin underwent fast and considerable release in GI media. Dynamic light scattering indicated that carotenoid incorporation strongly affected the particle stability and dispersion during preparation and GI incubation. The differences in molecular release may be attributed to the different modulating effects of carotenoids. Our results may guide the potential application of liposomes as carriers for the controlled delivery of carotenoids in nutraceutical and functional foods.

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The increased adsorbing of ketones could be attributed to the unfolding of secondary structures by revealing new binding sites, including thiol groups and hydrophobic binding sites. The decreased binding capacity was related to the refolding and aggregation of protein. The results suggested that microwave powers had obvious effects on the flavour retention and proteins structures in muscle foods. © 2017 Society of Chemical Industry.

In order to clarify the influence of curing agents on the flavor of duck, the effect of pH on the surface hydrophobicity, secondary structures, and adsorption capacity of myofibrillar proteins to alcohols, aldehydes, ketones, and esters was assessed using Raman spectroscopy, gas chromatography-mass spectrometer, and other methodologies. The hydrophobicity decreased as pH increased from 5.0 to 8.0; β-turn turned into α-helix and random coil as pH increased from 5.0 to 7.0, while α-helix and random coil turned into β-sheet and β-turn as pH increased from 7.0 to 8.0. With the increase of pH, the decreased adsorbing of alcohols could depend on hydrogen bonds. As pH increased from 5.0 to 8.0, the increase of aldehydes and esters was attributed to the unfolding of myofibrillar proteins and decreased hydrophobicity. The decreased adsorbing of ketones was due to the decreased hydrophobicity as pH increased from 5.0 to 8.0. The present work provided information about the correlation between structure and adsorption capacity of myofibrillar proteins to flavor compounds.

Xanthine oxidase (XOD) and paraoxonase 1 (PON1) are important enzymes in redox reactions in vivo, and are predominantly synthesized by the liver. The aim of the present study was to investigate the redox state in nonalcoholic fatty liver disease, and determine the association between the activities of XOD and PON1 and the severity of NAFLD. Sprague‑Dawley rats were randomly divided into control, model and α‑lipoic acid (high and low dose) groups. The rats in the NAFLD model were induced by feeding a high fat diet for 12 weeks and the in vitro cell model of hepatocyte steatosis was induced by treating L‑02 cells with oleic acid for 24 h. The body weight, liver function, lipid and oxidative stress indices, and histological features of the liver were examined in the rats. Compared with the control group, the rats in the NAFLD model group showed impaired liver function, lipid disorders and damage from oxidative stress. The serum activity of XOD increased significantly from the 4th week and was markedly higher, compared with that in the control group, reaching a peak in the 12th week. The activity of PON1 was negatively correlated with that of XOD. Compared with the control cells, the activity of XOD and levels of free‑fatty acids were significantly higher, and the activity of PON1 was significantly lower in the NAFLD L‑02 cell model. All the above indicators were significantly improved by treatment with the antioxidant, α‑lipoic acid. The activities of XOD and PON1 may be promising as markers in a noninvasive approach for detecting the severity of NAFLD clinically. α‑lipoic acid had protective effects on the NAFLD rats, and the potential mechanism may be associated with the inhibition of oxidative stress and lipid peroxidation.

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