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The present study evaluated the effects and underlying mechanisms of light salting on quality properties of tilapia fillets during repeated freezing-thawing. Light salting was found to improve water-holding capacity and decelerated texture softening in tilapia fillets during repeated freezing-thawing. Instead of tissue distortion and heterogeneous aggregates in control groups, light salting promoted myofibril disassembly and formation of an ordered protein network with the solubilized myofibrillar proteins. The myofibrils presented an overall amorphous appearance with the loss of M-lines, removing the restraints to myofibril swelling and solubilization from A-binds in salted groups during repeated freezing-thawing. The structural rearrangement caused by light salting facilitated the enlargement of water-holding space, transformation of tissue water, and tissue recoverability, improving water-holding capacity and texture properties of tilapia fillets during freezing-thawing. The finding provided novel insight into the improvement of quality properties of tilapia fillets by light salting when subjected to drastic temperature fluctuations.

Rosa roxburghii seed oil is obtained from the seeds left following pressing of the juice from R. roxburghii fruit. The total oil content of R. roxburghii seed was around 9.30%. The fatty acid profile of the oil was determined by gas chromatography (GC). Among the 11 fatty acids identified in the oil, seven were unsaturated fatty acids (UFAs) (92.6%); four were saturated fatty acids (SFAs) (7.17%). Then, the kinetics of formation of trans‐fatty acids was studied by GC. Heat treatment of R. roxburghii seed oil showed an increase in the relative percentage of linoleic acid and α‐linolenic acid isomers with increasing temperature and time. The formation of linoleic acid and α‐linolenic acid isomers followed a zero‐order reaction. The presence of O2 enhanced the isomerization of these UFAs. In addition, the rate constants and activation energies for the geometrical isomerization of UFAs in R. roxburghii seed oil were presented. Overall, R. roxburghii seed oil contains high UFA contents. Heating temperature and duration and the presence of O2 should be considered to reduce the formation of trans‐fatty acids during thermal treatment of R. roxburghii seed oil.

Background Maillard reaction in foods gives rise to toxic byproducts such as heterocyclic amines (HCAs), acrylamide (AA) and advanced glycation end products (AGEs). Inhibition of their formation during thermal processing is the most practical way to minimize their dietary exposure and thus the associated health risks. Various effective strategies have been proposed, especially with the use of exogenous additives such as polyphenols and emerging hydrocolloids. Hydrocolloids have attracted increasing attention due to their unique structural diversities that enable them to actively participate in Maillard reaction to mitigate the formation of toxic byproducts. They also have the potential to attenuate the harmful effects of these toxic byproducts. Hence, hydrocolloids represent an important class of food ingredients with dual beneficial potential, whereas a systematic review is currently lacking. Scope and approach This review summarizes influencing factors (precursors, processing methods and parameters, and exogenous additives) of thermally induced toxicants (HCAs, AA and AGEs) formation, as well as inhibitory strategies emphasizing on the effects and potential inhibitory mechanism of hydrocolloids. The ability of hydrocolloids to attenuate their harmful effects is also highlighted. Key findings and conclusions Hydrocolloids, alone or in combination with other purported inhibitors of harmful Maillard reaction products (MRPs), may be used in form of powders or aqueous solution for pretreatment of food. Moreover, their water-holding and gelling properties render them suitable for application in form of coatings that may offer additional benefits (e.g. reduction of oil uptake during frying) besides inhibiting the formation of hazardous MRPs. Although a reasonable number of studies have demonstrated the effectiveness of hydrocolloids against both the formation and the harmful effects of Maillard byproducts, more detailed and systematic analyses are needed to clearly characterize their structure-activity relationships and their mechanisms of action.

Home cooking has been considered as an indoor pollution problem since cooking oil fumes contain various toxic chemicals such as aldehydes. Fortifying edible oils with docosahexaenoic acid (DHA) has been applied to enhance the nutritional value of oils. This study designed a frying simulation system and examined the effect of oil type, DHA fortification, heating time, and addition of natural antioxidant on the emissions of aldehydes from heated oils. Results showed that linseed oil had the highest total aldehyde emissions, followed by soybean oil, peanut oil, and palm oil. Fortifying soybean oil with DHA increased the toxic aldehydes emitted. Quercetin, a flavonoid, significantly reduced aldehydes emitted from DHA-fortified soybean oil (by up to 39.80%) to levels similar to those of normal soybean oil. Further analysis showed that DHA-fortified soybean oil with quercetin had a significantly higher DHA and unsaturated fatty acids (UFAs) content than the control oil at each heating time point. The result indicated that quercetin inhibited emissions of aldehydes, at least in part, by protecting UFAs from oxidation. Collectively, quercetin could be used as a natural additive in DHA-fortified and normal cooking oils to reduce aldehyde emissions, indoor air pollution, and preserve functional DHA and other UFAs.

In this research, we studied the antioxidative properties and chemical changes of quercetin in fish oil during accelerated storage at 60 °C for 5 days. Gas chromatography (GC) analysis showed that quercetin inhibited aldehyde formation and unsaturated fatty acid oxidation in fish oil significantly; however, the inhibitory effects decreased gradually with prolonged heating time. Moreover, quercetin was consumed with increasing heating time. Some new phenolic derivatives were discovered in the fish oil with quercetin, with their structures fully elucidated by LC-MS/MS and comparison with newly synthesized ones (characterized by MS and NMR spectroscopy). Based on their chemical structures, we proposed that quercetin reacted with EPA and DHA to form the corresponding quercetin fatty acid esters in fish oil. In addition, the newly formed quercetin-3-O-eicosapentaenoate and quercetin-3-O-docosahexaenoate showed weaker DPPH and ABTS radical cation scavenging activity but much improved lipophilicity, higher cell membrane affinity, and hence enhanced cellular antioxidant activity compared with the parent quercetin. Overall, quercetin could be used as a safe dietary polyphenol to inhibit lipid oxidation. The newly formed quercetin-polyunsaturated fatty acid esters may render improved bioactivity to humans, which needs further investigation.

Styryl flavonoids can be formed during the thermal processing of meats and flavonoid-enriched foods, showing high potentials in the prevention of different diseases. In this study, the protective effects of several styryl flavonoids against advanced glycation end product (AGE)-induced inflammation were evaluated, with 6-C-(E-phenylethenyl)-naringenin (6-PN) showing the strongest activity among them. The results indicated that 6-PN significantly ameliorated AGE-induced damages in human umbilical vein endothelial cells, including inhibition of pro-inflammatory cytokines and reactive oxygen species (ROS) production through downregulating the protein levels of the receptor for AGEs (RAGE) and NADPH oxidase. Notably, 6-PN possessed a much higher bioavailability than its parental compound, naringenin. Furthermore, 6-PN also promoted the activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway that was suppressed by AGEs, and the anti-inflammatory effects of 6-PN disappeared when the cells were treated with ML385, a Nrf2 inhibitor. Hence, 6-PN might inhibit AGE-induced inflammation by the RAGE/ROS/Nrf2 signaling pathway.

The effects of the deacetylation degree (DD) of chitosan on heterocyclic aromatic amine formation were investigated in chemical models and beef patties. The results in model systems showed that at lower addition levels (10 mg), chitosan with 85% DD showed the strongest inhibitory effect against 2-amino-1-methyl-6-phenylimidazo[4,5

The effects of Perilla frutescens leaf extract (PLE) on the quality of surimi fish balls were investigated in the present study. Firstly, the extract was prepared by solvent extraction using 95% ethanol. Then, the phenolics in the extract were analyzed by instrumental analysis. The total phenolic content in the PLE was found to be 14.51 mg gallic acid equivalent (GAE)/g dry weight (DW). The amount of caffeic acid, ferulic acid, rosmarinic acid, quercetin, and apigenin, determined by high‐performance liquid chromatography (HPLC), was 4.80, 5.10, 2.95, 6.46, and 3.93 mg/g DW, respectively. Furthermore, the PLE was found to show high free radical scavenging activity toward DPPH and ABTS radicals with IC50 values of 12.15 and 7.26 μg/ml, respectively. When PLE was fortified into surimi fish balls at 0.03% and stored at 4°C, it was found to slow down lipid and protein oxidation during storage of surimi fish balls as evidenced by the significant reduction in TBARS values and protein carbonyl contents (p

Dielectric loss (e″) represents the ability to convert electromagnetic energy into heat, which may further affect the degree of Maillard reaction (MR). Based on the differences in electromagnetic response between lysine (Lys) and glucose (Glu), this study aims to verify the e″ -mediated intervention of microwave heating (MW) on different stages of MR by using different reaction solvents. Compared to conventional heating (CV), the systems with MW showed greater e″ and absorbance at both 294 nm (A294nm) and 420 nm (A420nm). Changing the solvent from pure water to a mixture (1:1 vol ratio of water to glycerol), thereby dramatically increasing e″ (by 6.02), compared to pure water (CV), the systems treated with the mixture under MW demonstrated large increases at both A294nm and A420nm, increasing by 0.35 at 10 min and 1.35 at 60 min, respectively. These results suggest that increasing e″ contributes to the promotion of MW during different stages of the MR.

Exposure to acrolein, one environmental and dietary pollutant, has been shown to cause inflammation. Here, we reported for the first time that acrolein aggravated lipopolysaccharide (LPS)-induced inflammation in Human umbilical vein endothelial cells (HUVEC) as evidenced by the further increased mRNA expression of three pro-inflammatory cytokines, including interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-α). Acrolein also further increased the generation of reactive oxygen species (ROS) and decreased the activity of glutathione peroxidase (GSH-Px) in LPS-pretreated HUVEC. Moreover, acrolein treatment further increased the nucleotide oligomerization domain-like receptor protein 3 (NLRP3) and apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC) expression, caspase-1 cleavage, and downstream matures interleukin 18 (IL-18) and IL-1β level in LPS-pretreated HUVEC. Acrolein treatment also further increased the expressions of high-mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), and phospho-NF-κB P65 (P-P65) in the LPS pre-treated HUVEC. Thus, acrolein aggravated LPS-induced HUVEC inflammation through induction of oxidative stress, and activation of NLRP3 inflammasome and HMGB1/MYD88/NF-κB signaling pathway. In addition, apigenin and apigenin-7, 4'-O-dioctanoate attenuated acrolein-aggravated inflammation by targeting the above signaling pathways. Our findings could help to develop potential therapeutic strategies against acrolein-enhanced inflammation.

In this research, we studied the inhibitory mechanism of quercetin, one popular phenolic compound, against aldehyde formation in thermally treated soybean oil. It was found that quercetin reduced unsaturated aldehyde formation significantly, with the inhibitory effect decreased with the extension of the heating time. Meanwhile, quercetin had minimum effects on the fatty acid profile compared to untreated samples. Some new phenolic derivatives were formed in thermally treated soybean oil with quercetin, further analyzed by liquid chromatography-tandem mass spectrometry, and compared to newly synthesized derivatives (characterized by mass spectrometry and nuclear magnetic resonance spectroscopy). On the basis of their chemical structures, we proposed that quercetin reacted with 13-oxo-octadecadienoic acid, 10-oxo-hexadecenoic acid, and 10-oxo-octadecenoic acid formed from peroxidation of linoleic acid, palmitoleic acid, and oleic acid, respectively, to inhibit aldehyde formation. In addition, newly formed quercetin-3-O-hexanoate, quercetin-3-O-heptanoate, and quercetin-3-O-nonanoate showed weaker 2,2-diphenyl-1-picrylhydrazyl and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt radical cation scavenging activity and weaker antioxidant activity in soybean oil, which explained the decreased inhibitory activity of quercetin against aldehyde formation during heat treatment. More interesting, quercetin-3-O-hexanoate showed improved cellular antioxidant activity compared to the parent quercetin. Overall, quercetin inhibited the formation of lipid oxidation products in thermally treated soybean oil by reacting with early intermediates in the lipid oxidation reaction, and quercetin derivatives formed in the process could be with enhanced cellular antioxidant activity. Our results provide novel insight into the inhibitory mechanism of quercetin against the formation of lipid oxidation products.

Rosa roxburghii seed oil is obtained from the seeds left following pressing of the juice from R. roxburghii fruit. The total oil content of R. roxburghii seed was around 9.30%. The fatty acid profile of the oil was determined by gas chromatography (GC). Among the 11 fatty acids identified in the oil, seven were unsaturated fatty acids (UFAs) (92.6%); four were saturated fatty acids (SFAs) (7.17%). Then, the kinetics of formation of trans‐fatty acids was studied by GC. Heat treatment of R. roxburghii seed oil showed an increase in the relative percentage of linoleic acid and α‐linolenic acid isomers with increasing temperature and time. The formation of linoleic acid and α‐linolenic acid isomers followed a zero‐order reaction. The presence of O2 enhanced the isomerization of these UFAs. In addition, the rate constants and activation energies for the geometrical isomerization of UFAs in R. roxburghii seed oil were presented. Overall, R. roxburghii seed oil contains high UFA contents. Heating temperature and duration and the presence of O2 should be considered to reduce the formation of trans‐fatty acids during thermal treatment of R. roxburghii seed oil., Rosa roxburghii seed oil was of high quality in terms of its high amount of unsaturated fatty acids. Heat treatment of R. roxburghii seed oil showed an increase in the relative percentage of linoleic acid and linolenic acid isomers with increasing temperature and time. The formation of linoleic acid and linolenic acid isomers followed a zero order reaction.

The inhibitory effects of seven polyphenols on 3-chloropropane-1,2-diol fatty acid esters (3-MCPDE) formation were investigated in palm oil models. Results showed that there was not a positive significant correlation between the free-radical scavenging activities of the tested compounds and their 3-MCPDE-formation inhibitory activities; puerarin, with weak antioxidant activity, showed the highest inhibitory capacity. Moreover, puerarin reduced the content of glycidol and glycidyl esters (GEs), two key intermediates of 3-MCPDE formation in the oil models; and a puerarin-adduct was discovered in the oil fortified with glycidol or GEs, with its structure elucidated by LC-MS/MS and comparison with newly synthesized ones. Based on its chemical structure, we proposed that puerarin, at least in part, reacted with glycidol and GEs to inhibit 3-MCPDE formation. In addition, the formed compound, puerarin-7-O-propanediol was identified in the potato chips frying system, further confirming reacting with glycidol/GEs as a key mechanism of puerarin to inhibit 3-MCPDE formation.

Brosimone I is an isoprenoid-substituted flavonoid from Artocarpus heterophyllus. Here, we reported for the first time that brosimone I induced cell cycle G1 phase arrest and apoptosis in HCT116 human colon cancer cells. Brosimone I treatment increased the cytosolic Ca2+ level, and subsequently activated the CaMKKβ-AMPK pathway. STO-609, a CaMKKβ inhibitor, and compound C, an AMPK-specific inhibitor, attenuated brosimone I-induced loss of cell viability in HCT116 cells. Furthermore, brosimone I enhanced ER stress. Salubrinal, an ER stress inhibitor, reduced brosimone I-induced cell growth inhibition. In addition, brosimone I was found to increase ROS generation and the inhibition of ROS formation by NAC, a ROS inhibitor, attenuated brosimone I-induced cell death, cytosolic Ca2+ increase, and ER stress markers. Collectively, our findings reveal that brosimone I induces cell cycle G1 phase arrest and apoptosis via the induction of ROS-mediated increased cytosolic Ca2+, ER stress, and the activation of the CaMKKβ-AMPK signaling pathway.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is the most abundant mutagen/carcinogen produced in high temperature treated protein food. Quercetin has been shown to inhibit PhIP formation by trapping phenylacetaldehyde to form two human beneficial adducts 6-C-(E-phenylethenyl)quercetin (6-CEPQ) and 8-C-(E-phenylethenyl)quercetin (8-CEPQ). Here we studied the formation of PhIP as well as the phenylacetaldehyde-trapping ability of quercetin in microwave heating and conventional heating systems. LC-MS was applied for the comparison of PhIP formed in chemical models using microwave heating and conductive heating. Results showed that PhIP was produced time dependently under both heating conditions. Microwave heating produced a smaller amount of PhIP compared with conductive heating. Moreover, quercetin showed a more potent inhibitory effect on PhIP formation in microwave heating systems than in conductive heating models. The amount of 6-CEPQ and 8-CEPQ produced in chemical models and onion/beef soup using microwave heating was about 5 and 1.5 times more than using conductive heating, respectively. Our results demonstrate that microwave heating was a much safer and healthier thermal processing technology than conventional heating in terms of formation of less mutagenic PhIP and production of more human beneficial compounds 6-CEPQ and 8-CEPQ.

Heterocyclic aromatic amines (HAAs) are mutagens and rodent carcinogens. Flavonoids have attracted considerable attention for development into effective inhibitors against the formation of genotoxic HAAs in thermally processed foods.; Results: The inhibitory effect of dihydromyricetin (DMY) on the formation of key HAAs, including 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), 2-amino-3,8-dimethylimidazo[4,5-f]-quinoxaline (MeIQx), and 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (4,8-DiMeIQx), was significant. In chemical models, DMY (0.05 mmol, 0.1 mmol, and 0.2 mmol) significantly decreased the amount of PhIP formed (43.0%, 54.7%, and 75.7% respectively). A significant inhibitory effect on the formation of MeIQx and 4,8-DiMeIQx was also observed. Moreover, DMY (0.05%, 0.1%, and 0.2%) reduced the generation of PhIP (by 48.0%, 59.0%, and 80.1% respectively) and that of MeIQx (by 45.8%, 62.0%, and 76.7% respectively) in fried beef patties.; Conclusion: The results indicate that DMY could be converted into myricetin during thermal processing, and both DMY and myricetin could trap phenylacetaldehyde, a major Strecker aldehyde of phenylalanine, in a similar manner to thus inhibit the generation of PhIP. This study provides valuable information for the development of effective strategies to minimize HAA content in thermally processed foods and also sheds light on the mechanism that accounts for the inhibitory effect. © 2017 Society of Chemical Industry.; © 2017 Society of Chemical Industry.

// Yueliang Zhao 1 , Edmund T.S. Li 1 and Mingfu Wang 1 1 School of Biological Sciences, The University of Hong Kong, Hong Kong, China Correspondence to: Mingfu Wang, email: mfwang@hku.hk Keywords: alisol B 23-acetate, autophagy, apoptosis, ROS, JNK Received: March 29, 2017 Accepted: June 16, 2017 Published: July 26, 2017 ABSTRACT Alisol B 23-acetate (AB23A), a natural triterpenoid from the rhizome of Alisma orientale , a Chinese medicinal herb, has multiple physiological activities including anticancer. However, its effect on human colon cancer and the underlying mechanism are not clear. Here, we reported for the first time that AB23A induced cell cycle G 1 phase arrest and apoptotic cell death in colon cancer cells. Autophagy also occurred in AB23A-treated HCT116 cells as evidenced by the accumulation of microtubule-associated protein 1 light chain 3 form II (LC3-II) and degradation of SQSTM1/p62. An autophagy inhibitor, 3-methyladenine (3-MA) was found to attenuate AB23A-mediated autophagy, apoptosis, and cell death, indicating that AB23A-induced apoptotic response was dependent on the induction of autophagy. In addition, the treatment of HCT116 cells with AB23A resulted in the generation of reactive oxygen species (ROS) and phosphorylation of c-Jun N-terminal kinase (JNK). A ROS scavenger, N-acetylcysteine (NAC) and a JNK-specific inhibitor, SP600125 attenuated AB23A-induced autophagy and apoptotic cell death. Moreover, NAC was able to eliminate AB23A-induced JNK phosphorylation. This finding provides a novel mechanism of action of AB23A in colon cancer HCT116 cells that AB23A induces autophagic-dependent apoptotic cell death in colon cancer cells, at least in part, though the accumulation of intracellular ROS and subsequent activation of JNK.

Big eye tuna (Thunnus obesus), Atlantic salmon (Salmo salar) and bighead carp (Aristichthys nobilis) are three representative marine and fresh water fishes. In this study, the content of total lipids (TL), triglyceride (TG) fraction, and the fatty acid profiles in the corresponding fish heads were analyzed. Meanwhile, their complicated TG molecular species were further characterized. The results showed that TG was the major lipid in these three fish heads (60.58&ndash, 86.69%). Compared with other two fish heads, big eye tuna head was the most abundant in polyunsaturated fatty acids, among which eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA) accounted for 64.29% and 32.77% in the TL and TG fraction, respectively. It is also worth noting that EPA+DHA/total fatty acid (TFA) value of TL and TG fraction from bighead carp head showed no significant difference with Atlantic salmon head, a typical marine fish. There were 146 TG molecules detected in big eye tuna head, 90 in Atlantic salmon and 87 in bighead carp heads. DHA or EPA accounted for 56.12%, 22.88%, and 5.46% of the total TG molecules in these three fish heads, respectively. According to principal component analysis, orthogonal projection to latent structures-discriminant analysis and the constructed heat map, the three samples could be completely differentiated based on their TG molecule fingerprints. This study is the first to compare marine and fresh water fish from the perspective of their heads&rsquo, fatty acid and TG molecule profiles.

6-C-(E-phenylethenyl)naringenin (6-CEPN) is a small molecule found in naringenin fortified fried beef. It has been shown to suppress colon cancer cell proliferation, but the underlying mechanisms are not fully understood. Here we demonstrate that 6-CEPN suppresses tumour cell proliferation through cell cycle arrest in G1 phase, induces necrotic cell death and autophagy in colon cancer cells. Blockade of autophagy by knockdown of the essential autophagy proteins, Atg7 or beclin-1, resulted in aggravated cell death in response to 6-CEPN treatment. In addition, genome-wide transcriptome expression profiling by RNA-sequencing revealed that 6-CEPN-mediated gene expression pattern was extremely similar to the transcriptome response induced by a RAS inhibitor salirasib (farnesylthiosalicylic acid [FTS; salirasib]). Subsequent molecular biological and biochemical experiments demonstrated that 6-CEPN indeed strongly inhibited RAS activation, leading to the inhibition of the downstream effector pathways c-Raf/mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase kinase and phosphoinositide 3-kinase/AKT/mammalian target of rapamycin. More importantly, our computational molecular docking data showed that 6-CEPN could bind to the active site of isoprenylcysteine carboxyl methyltransferase (Icmt), a critical enzyme for the activation of RAS. Icmt activity assay showed that 6-CEPN inhibited its activity significantly. Knockdown of Icmt by siRNA attenuated 6-CEPN-mediated autophagy and cell death. The present study demonstrates that 6-CEPN induces cell growth inhibition and cytoprotective autophagy in colon cancer cells, at least in part, though inhibition of the Icmt/RAS signalling pathways.

Gamma irradiation can be performed alone or in combination with other preservatives such as dehydroacetic acid (DHA) and sodium dehydroacetate (DHA-Na) to achieve an enhanced level of food safety. Here, we studied the effect of gamma irradiation on the stability and degradation of DHA and DHA-Na in aqueous solution and pear juice. The degradation rate of DHA and DHA-Na was found to increase with increasing irradiation time and decreasing initial solute concentration in aqueous solution. The degradation rate of DHA-Na was higher than that of DHA under the same irradiation conditions. The degradation process of DHA and DHA-Na followed first-order reaction kinetics. The main radiolytic product of DHA and DHA-Na was identified as heptane-2,4,6-trione by GC-MS/MS, and the possible degradation pathway was proposed. Quantum chemical calculation results further confirmed that DHA-Na was much easier to be degraded than DHA. In addition, radiolytic degradation of DHA-Na happened in pear juice, but with a much lower degradation rate than that in aqueous solution.

Heterocyclic amines (HAs) are food-borne mutagenic compounds formed during food preparation and processing. They are considered as significant health risk in the long term and inhibiting their formation represents one of the most effective approaches to attenuate their potential health hazards. Hydrocolloids are long-chain high-molecular-weight hydrophilic polymers. In this study, the effects of six hydrocolloids, including alginic acid, sodium carboxymethylcellulose (CMC-Na), chitosan, carrageenan, konjac glucomannan (KGM) and xanthan gum, on major HAs formation (PhIP, MeIQx and 4,8-DiMeIQx) in both chemical model systems and roast beef patties were investigated. The influence of addition method (marinating) was also evaluated. HPLC-PDA and UPLC-MS analysis showed that all the six tested hydrocolloids added in form of powders in chemical models effectively inhibited PhIP formation by 19.3–42.7% at relatively lower doses (5 and 10 mg), while they exhibited better inhibitory effects against MeIQx formation at higher dose (30 mg). Among them, CMC-Na had the strongest inhibitory effect, followed by chitosan in roast beef patties. Further analysis showed chitosan, but not CMC-Na, synergized with a polyphenol, phloridzin to inhibit the formation of HAs, particularly PhIP. Marination with CMC-Na solution led to even greater inhibitory effects on HA formation with the contents of PhIP, MeIQx and 4,8-DiMeIQx being reduced by over 90%, 80% and 70%, respectively. These findings suggest that hydrocolloids are potent HA formation inhibitors and their application in meat preparation and processing could effectively reduce human dietary exposure to mutagenic HAs.

The effects of quercetin and cinnamaldehyde, two popular dietary phytochemicals from vegetables and spices on the general nutrient content and whole chemical profile of beef soup during stewing were investigated by routine chemical analysis and an UPLC-MS/MS based untargeted metabolomics analysis. It was found that quercetin decreased the content of total sugar and methionine, and increased solid matters, unsaturated fatty acids and zinc content in beef soup. Cinnamaldehyde decreased total sugar, aspartic acid and zinc content, but increased total fatty acids in beef soup. Metabolomics results showed that a total of 204 metabolites were assigned to putative molecular classes. 12 metabolite species were summarized based on the chemical structure using HMDB. Cinnamaldehyde decreased the content of most of the molecule species in beef soup while quercetin did not have significant effect. In general, cinnamaldehyde decreased the nutritional value of beef soup, thus spices rich in cinnamaldehyde may not be suitable used for preparing meat soup due to its negative effect on nutrient contents in beef soup. This work could help to fully understand the effects of quercetin and cinnamaldehyde on the nutritional value of beef soup.

The inhibitory effect of caffeic acid on the formation of 2-amino-1-methyl-6-phenylimidazo[4,5-b] pyridine (PhIP) was investigated in chemical model systems under microwave heating (MW). A mechanistic study was subsequently carried out to identify the inhibitory mechanism. The results showed that both for conductive heating (CV) and MW, the inhibition of PhIP increased with the concentration of caffeic acid but decreased with the prolongation of heating time. The inhibition on PhIP under MW was always higher than under CV, which were dominated by the difference in dielectric loss (e″). UPLC-MS analysis showed that caffeic acid releases a CO2 molecule to produce 4-vinylcatechol which can form adducts with phenylacetaldehyde, thus reducing its availability for PhIP formation. The structure of adduct was characterized as 3-(3,4-dihydroxyphenyl)-2-phenylbutanal with a molecular weight of 256. The findings indicate that trapping of phenylacetaldehyde by 4-vinylcatechol is a key mechanism of caffeic acid in inhibiting PhIP formation.

Colon cancer is one of the major causes of morbidity and mortality worldwide. Dietary phytochemicals have been drawing increasing attention for colon cancer prevention and treatment due to their chemical diversity, biological activity, easy availability, lack of toxic effects, and ability to modulate various signal transduction pathways and cell processes. The chemoprotective effects elicited by phytochemicals include antioxidative and anti-inflammatory activities, induction of phase II enzymes, cell cycle arrest, apoptosis, autophagy, and changes in gut microbiota. The present review summarizes the main chemopreventive properties of selected phytochemicals (carotenoids, flavonoids, flavonolignan, proanthocyanidin, isothiocyanates, terpenoids, peptides, and medicinal plant extracts) against colon cancer. It is found that these phytochemicals exhibit their anti-colon cancer activity through the modulation of various signaling pathways involved in the regulation of chronic inflammation, cell cycle, autophagy, apoptosis, metastasis, and angiogenesis. These phytochemicals could be helpful starting points in the design and development of novel colon cancer chemopreventive agents.

Recently, there is a growing interest in fortifying food products with flavonoids to enhance health benefits. Naringenin, naringin, hesperetin, and dihydromyricetin are four typical flavonoids constituting a natural part of our diet. In the present work, they were fortified into a chia oil cookie model to evaluate their thermal stability during baking as well as their impact on antioxidant capacity and toxicant formation. Among them dihydromyricetin was the most unstable one (only 36.1% of which was left after baking at 180 &deg, C for 20 min) and led to a loss of brightness in cookie. However, the antioxidant capacity of cookie fortified with dihydromyricetin was significantly enhanced compared with untreated cookie, on the other hand, dihydromyricetin showed the strongest effect to attenuate lipid and protein oxidation as well as decrease the level of fluorescent advanced glycation endproducts and carboxymethyl lysine in cookie model. Overall, among the four selected flavonoids, dihydromyricetin might be the most promising functional bakery additive enhancing the antioxidant capacity while decreasing the formation of toxicants.