Polyphenol oxidation is a chemical process impairing food freshness and other desirable qualities, which has become a serious problem in fruit and vegetable processing industry. It is crucial to understand the mechanisms involved in these detrimental alterations. o-Quinones are primarily generated by polyphenols with di/tri-phenolic groups through enzymatic oxidation and/or auto-oxidation. They are highly reactive species, which not only readily suffer the attack by nucleophiles but also powerfully oxidize other molecules presenting lower redox potentials via electron transfer reactions. These reactions and subsequent complicated reactions are capable of initiating quality losses in foods, such as browning, aroma loss, and nutritional decline. To attenuate these adverse influences, a variety of technologies have emerged to restrain polyphenol oxidation via governing different factors, especially polyphenol oxidases and oxygen. Despite tremendous efforts devoted, to date, the loss of food quality caused by quinones has remained a great challenge in the food processing industry. Furthermore, o-quinones are responsible for the chemopreventive effects and/or toxicity of the parent catechols on human health, the mechanisms by which are quite complex. Herein, this review focuses on the generation and reactivity of oquinones, attempting to clarify mechanisms involved in the quality deterioration of foods and health implications for humans. Potential innovative inhibitors and technologies are also presented to intervene in o-quinone formation and subsequent reactions. In future, the feasibility of these inhibitory strategies should be evaluated, and further exploration on biological targets of o-quinones is of great necessity.
Background Ulcerative colitis is a type of chronic inflammatory bowel disease closely associated with gut microbiota dysbiosis and intestinal homeostasis dysregulation. Barley leaf (BL) has a long history of use in Traditional Chinese Medicine with potential health-promoting effects on intestinal functions. However, its mechanism of action is not yet clear. Here, we explore the potential modulating roles of gut microbial metabolites of BL to protect against colitis and elucidate the underlying molecular mechanisms. Results Using 16S rRNA gene-based microbiota analysis, we first found that dietary supplementation of BL ameliorated dextran sulphate sodium (DSS)-induced gut microbiota dysbiosis. The mechanisms by which BL protected against DSS-induced colitis were resulted from improved intestinal mucosal barrier functions via the activation of peroxisome proliferator-activated receptor (PPAR)γ signaling. In addition, metabolomic profiling analysis showed that the gut microbiota modulated BL-induced metabolic reprograming in the colonic tissues particularly by the enhancement of glycolysis process. Notably, dietary BL supplementation resulted in enrichment of microbiota-derived purine metabolite inosine, which could activate PPARγ signaling in human colon epithelial cells. Furthermore, exogenous treatment of inosine reproduced the similar protective effects as BL to protect against DSS-induced colitis through improving adenosine 2A receptor (A2AR)/PPARγ-dependent mucosal barrier functions. Conclusions Overall, our findings suggest that the gut microbiota-inosine-A2AR/PPARγ axis plays an important role in the maintenance of intestinal homeostasis, which may represent a novel approach for colitis prevention via manipulation of the gut microbial purine metabolite.
Browning is a severe problem in the juice industry, which is tremendously affected by quinone (Q) reactivity. Here, the formation rate, electrophilicity, and oxidizing ability of different quinones were investigated. LC/MS was applied to monitor the loss of polyphenols and quinones in model systems during storage. Mathematical modeling of collected LC/MS data was conducted to derive the rate constants of various reactions. Polyphenols containing catechol or pyrogallol groups are more susceptible to oxidation. Periodic acid and quinone mediated oxidation were faster than the autoxidation of polyphenols. Chlorogenic acid (CQA) and 4‐methylcatechol (4MC) only containing B ring can hardly contribute to browning. They must combine with A ring to form yellow polymers. Furthermore, the electrophilicity and oxidizing ability order of quinone is: CQA‐Q ≈ 4MC‐Q > catechin quinone (CAT‐Q) ≈ epicatechin quinone (EC‐Q) > gallic acid quinone (GA‐Q). It was possible that CAT‐Q and EC‐Q would undergo nucleophilic addition with their A rings and GA‐Q's extra hydroxyl group might contribute to the electrons, resulting in lower reactivity. This work innovatively evaluated the reactivity of diverse polyphenols and quinones, attempting to illustrate their contributions to nonenzymatic browning. These findings provide a new perspective to restrain the browning in the juice processing industry.
BACKGROUND Acrylamide (AA) is a potential carcinogen formed in food rich in carbohydrate during heating. Recently, AA has been found in several fruit products, such as prune juice, sugarcane molasses and canned black olives. This study focused on the role of galacturonic acid (GalA), the main acid hydrolysis product of fruit pectin, in AA formation in three model systems – asparagine (Asn)/glucose (Glc), Asn/GalA, and Asn/Glc/GalA – during heating under different pH values (pH 3.8–7.8), Glc concentration (0–0.1 mol L−1), molar ratio of substrates (Asn/Glc = 1:1, 0.025–0.5 mol L−1) and temperature (120–180 °C) for 30 min, respectively. RESULTS The results suggested that the addition of 0.1 mol L−1 GalA strongly accelerated AA formation in a manner dependent on pH value and temperature (P < 0.05). AA concentration under different Glc concentration and molar ratio of substrates suggested that GalA was more reactive than Glc when reacted with Asn. Furthermore, the Amadori rearrangement product/Schiff base/oxazolidine‐5‐one were identified as the intermediates formed in the Asn/GalA model system using ultra‐performance liquid chromatography–quadrupole‐time‐of‐flight–mass spectrometry. CONCLUSION The results suggested that Maillard reaction between Asn and GalA might contribute to AA formation. This study is significant in elucidating the contribution of interaction between components for AA formation in fruit products. © 2022 Society of Chemical Industry.
Astringency is a major sensory property and plays an important role in the overall quality of juice and wines. A major contributor to astringency is condensed tannins, which can precipitate with salivary glycoproteins. And thus, it is vital to develop methods to measure the tannin accurately. Recently, the interest in the application of condensed tannin assays has been increasing in various fields. Condensed tannin assays broadly include the determination of concentration, activity, mean degree of polymerization and its derivative flavan‐3‐ol sulfonates content. In this guideline, the mechanisms and the practice of the most common condensed tannin assays applied in research labs are discussed in detail.
The browning of white fat has become a hot topic as it could help to lose weight and improve metabolic health. Therefore, this study aims to explore the in vivo browning or thermogenesis effect of 6‐gingerol (6G), a natural bioactive compound of ginger, and to clarify the underlying mechanism. The results showed that 6G limited weight gain, improved cold tolerance, and increased energy expenditure in high‐fat diet‐induced obese mice. Moreover, histological and immunohistochemical analysis revealed that 6G activated brown adipose tissue (BAT) and induced more beige cells in epididymal adipose tissue (eWAT). Meanwhile, eWAT browning was marked by appearance of multilocular lipid droplets, a higher level of uncoupling protein 1 (UCP1), and increased mitochondrial content. The potential molecular mechanism of eWAT browning was further investigated by RNA‐seq, qPCR, and western blot assays. Results indicated that 6G significantly induced the expression of beige and thermogenesis‐specific markers in eWAT and triggers thermogenesis mainly through a phosphoinositide 3‐kinase (PI3K) / protein kinase B (AKT)‐ribosomal protein S6 (RPS6) axis. Consistently, in vitro, data showed that pretreatment of primary white adipocytes with PI3K/AKT pathway inhibitor significantly counteracted the 6G‐induced effects. This study reveals, for the first time, that 6G induces browning in adipose tissue by modulating the PI3K/AKT‐RPS6 and thermogenesis pathways, thereby alleviating obesity.
Autophagy‐lysosomal pathway (ALP), a lysosome‐mediated self‐renewal process, is crucial for cell survival and death. Acrylamide (AA) is a neurotoxic compound produced during food thermal processing, and the mechanism underlying AA‐induced neurotoxicity remains elusive. In this study, we explored whether dysregulated ALP was involved in AA‐induced neurotoxicity and the underlying mechanism. We first evaluated the toxic effects of AA on the activation of apoptosis and NLRP3 pathway in human glioma U251 cells. We found that AA‐induced autophagy activation with the accumulation of an autophagy substrate P62, which implies the occurrence of autophagy‐lysosomal disorders. By using autophagy agonist PP242 and siRNA interfering ATG5, we demonstrated that ALP dysregulation contributed to AA‐induced apoptosis and NLRP3 inflammasome pathway activation. In addition, AA triggered ALP dysfunction by decreasing the expression of transcription factor EB (TFEB), and TFEB overexpression restored the lysosomal‐associated proteins and protected against AA‐induced apoptosis and inflammasome activation. Moreover, the autophagy agonist rapamycin restored AA‐induced ALP dysfunction by upregulating TFEB and prevented neurotoxicity. Overall, our study provides novel insights into the role of disrupted ALP in AA‐induced neurotoxicity and highlights that TFEB can be developed as a promising intervention target against AA‐induced neurotoxicity.
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