Yogurt is a healthy dairy food fermented by lactic acid bacteria (LAB). Because consumers demand healthier and more nutritious yogurt, numerous substances have been used to supplement yogurt. Chia seed has been reported to contain abundant phenolic compounds, dietary fiber, and n-3 fatty acids and therefore is a potential functional food additive. The aim of this study was to investigate the influence of chia seed extracts on the physicochemical and bioactive properties of set-type yogurt. Yogurt was fortified with chia seed water extract (CSWE) or chia seed ethanol extract (CSEE) at 0.05 or 0.1% (vol/vol). Results showed that supplementation with CSWE or CSEE significantly accelerated the fermentation rate and growth of LAB. Both CSWE and CSEE improved the viscosity, syneresis, and water-holding capacity of yogurt. The radical scavenging activity of yogurt was increased with both extracts, and the 0.1% CSEE yogurt exhibited the highest radical scavenging activity. Furthermore, 0.1% CSEE yogurt significantly inhibited lipopolysaccharideinduced production of hydrogen peroxide in human colon cells. Addition of chia seed extract improves the growth of LAB, the physiochemical properties, and the health-beneficial effects of set-type yogurt.
BACKGROUND: Aluminum (Al) is the most abundant and ubiquitous metal in the environment. The main route of human exposure to Al is through food and water intake. Although human exposure to Al is common, the influence of Al on the gastrointestinal tract remains poorly understood. OBJECTIVES: We aimed to further understand the toxic effect of Al and to elucidate the underlying cellular mechanisms in the intestinal barrier. METHODS: The human intestinal epithelial cell line HT-29 and C57BL6 mice were exposed to AlCl 3 at 0-16 mM (1-24 h) and 5-50 mg=kg body weight (13 weeks), respectively. In cell culture experiments, intracellular oxidative stress, inflammatory protein and gene expression, and intestinal epithelial permeability were measured. In animal studies, histological examination, gene expression, and myeloperoxidase (MPO) activity assays were conducted. RESULTS: Cellular oxidative stress level (superoxide production) in AlCl 3-treated cells (4 mM, 3 h) was approximately 38-fold higher than that of the control. Both protein and mRNA expression of tight junction (TJ) components (occludin and claudin-1) in AlCl 3-treated cells (1-4 mM, 24 h) was significantly lower than that of the control. Transepithelial electrical resistance (TEER) decreased up to 67% in AlCl 3-treated cells (2 mM, 24 h) compared with that of the control, which decreased approximately 7%. Al activated extracellular signal-regulated kinase 1/2 and nuclear factor-kappa B (NF-jB), resulting in mRNA expression of matrix metalloproteinase-9, myosin light-chain kinase, and inflammatory cytokines [tumor necrosis factor alpha (TNF-a), interleukin-1b (IL-1b), and IL-6] in HT-29 cells. Moreover, oral administration of AlCl 3 to mice induced pathological alteration, MPO activation, and inflammatory cytokine (TNF-a, IL-1b, and IL-6) production in the colon. CONCLUSION: Al induced epithelial barrier dysfunction and inflammation via generation of oxidative stress, down-regulation of the TJ proteins, and production of inflammatory cytokines in HT-29 cells. In addition, Al induced toxicity in the colon by increasing the levels of inflammatory cytokines and MPO activity and induced histological damage in a mouse model. Our data suggest that Al may be a potential risk factor for human intestinal diseases.
The aim of this study was to investigate the oxidative status and quality characteristics of four animal skin-derived fats extracted using an identical extraction method. Pressurized hot water extraction, a green extraction method, was used to extract animal skin fats (duck, chicken, swine, and bovine skin). Multiple experiments were performed during accelerated storage at 60°C for 90 days. Quality characteristics, such as extraction yield, iodine value (IV), fatty acid composition, and fat viscosity were determined. In addition, indicators for oxidative status, including acid value (AV), peroxide value (PV), p -anisidine value ( p -AV), thiobarbituric acid reactive substances (TBARS), conjugated dienes (CD), and total oxidation (totox) values were evaluated. The fat extraction yield was highest in bovine fat, followed by duck, swine, and chicken fats. The IV was higher in duck and chicken fats. Duck fats contained the most unsaturated fats and the least saturated fats. Fat oxidation indicators, such as PV, TBARS, and totox values, were relatively higher in duck fats during storage compared to the other fats. Other indicators, including AV, p -AV, and CD, were similar in duck, chicken, and swine fats. Viscosity was similar in all the tested fats but markedly increased after 70 days of storage in duck fats. Our data indicate that duck skin fat was more vulnerable to oxidative changes in accelerated storage conditions and this may be due to its higher unsaturated fatty acid content. Supplementation with antioxidants might be a reasonable way to solve the oxidation issue in duck skin fats.
Zearalenone (ZEN) is a mycotoxin produced by Fusarium species; however, its mechanisms of action in human livers have not been fully elucidated. Thus, we investigated the toxic mechanisms of ZEN in human liver cells. HepG2 cells were treated with ZEN (0–40 μg/mL) for up to 24 h. A significant decrease in cell viability was observed after treatment with 20 and 40 μg/mL of ZEN, including a significant increase in apoptosis and reactive oxygen species production. ZEN increased GRP78 and CHOP, and eIF2α phosphorylation, indicating ER stress; elevated transcription of the autophagy-associated genes, beclin1 and LC3, and translation of LC3; and increased phase I metabolism by increasing PXR and CYP3A4. The protein expression level of CYP3A4 was higher with ZEN treatment up to 20 μg/mL, but remained at the control level after treatment with 40 μg/mL ZEN. In phase II metabolism, Nrf2 activation and UGT1A expression were increased with ZEN treatment up to 20 μg/mL. Treating cells with an ER stress inhibitor alleviated ZEN-induced cell death and autophagy, and inhibited the expression of phase I/II enzymes. Overall, high ZEN concentrations can modulate the expression of phase I/II enzymes via ER stress and reduced protein levels in human liver cells.
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