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Quercetin (Q), tea polyphenols (TP), and rutin (R) are widely used plant-derived active ingredients. They possess antioxidant, anti-inflammatory, and anti-tumor properties, and can reduce the muscle damage caused by mycotoxins. However, few studies have examined the protective mechanisms of quercetin, tea polyphenols, and rutin on muscle quality. To elucidate their protective mechanisms, shrimp were exposed to both T-2 toxin and these three antioxidants for 20 days in a dose-escalating trial. The changes in the protein composition of shrimp muscle were measured. The target proteins associated with T-2 and antioxidants were screened and identified by non-labeled quantitative proteomics.The T-2 toxin induced abnormal expression of 21 target proteins, leading to the deterioration of muscle proteins in shrimp. The three antioxidants ameliorated the T-2 toxin-induced damage to muscle proteins by increasing the sarcoplasmic and myofibrillar protein content and decreasing the alkali-soluble protein content. Quercetin had the strongest protective effect. The protective processes of these antioxidants involved the upregulation of target proteins involved in carbohydrate metabolism (enolase, malate dehydrogenase), protein translation (elongation factor 1-alpha and eukaryotic translation initiation factor 2 subunit alpha), and cytoskeleton component (actin 2, fast-type skeletal muscle actin 1). Quercetin regulated the largest number of target proteins, making it the best protective agent against T-2 toxin.The T-2 toxin (4.80-24.30 mg/kg feed) induced changes in target proteins and muscle composition of shrimp, leading to a deterioration in muscle proteins. Quercetin (2.00-32.00 g/kg feed) had significant protective effects against this deterioration in muscle protein in shrimp. © 2022 Society of Chemical Industry.

As a toxic trace element commonly found in food, cadmium (Cd) can cause severe liver injury. Our previous study showed that threonine (Thr) could significantly alleviate Cd toxicity in yeast. To investigate the effect of Thr on Cd-induced liver injury in mice, twenty-four mice were randomly divided into four groups: control, Cd, and low/high dose of Thr-treatment groups (0.04 and 0.08 mmol/kg/day, respectively). After 7 days of continuous treatment, the alleviative effect of Thr on liver injury in Cd-exposed mice was assessed. The results showed that Thr significantly reduced the elevation of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in Cd-exposed mice. Histological analysis showed that Thr decreased Cd-induced hepatic steatosis, zonal necrosis, and inflammatory cell infiltration. Thr also reduced the Cd-induced malondialdehyde (MDA) and O

As a global pollutant, cadmium (Cd) can easily enter the body through food chains, threatening human health. Most Cd is initially absorbed in the gut, with the gut microbiota playing a pivotal role in reducing Cd absorption and accumulation. This study assessed the effects of three fatty acids on Cd accumulation and toxicity in Cd-exposed mice. The results showed that oleic acid (OA) was the most effective in facilitating Cd excretion in mice among these fatty acids. The use of OA led to reduced Cd accumulation in the organs and increased Cd content in the feces. The metagenomic analysis of the gut microbiota showed that the genus

As a toxic pollutant, cadmium (Cd) can cause severe liver injury. In the previous study, we found that threonine (Thr) significantly alleviated the toxic effect of Cd in yeast. To investigate the effect of Thr on Cd-induced liver damage in mice, twenty-four mice were evenly divided into control, Cd-exposed, and low/high dose of Thr-treatment groups (0.04, 0.08 mmol/kg/day) for 7 days of continuous treatment. Thr significantly reduced the aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, exhibiting alleviative effect on hepatic injury. Further investigation showed that Thr significantly reduced the Cd-induced inflammation (tumor necrosis factor-α and interleukin-6), and inhibited the increase of apoptosis factors (Bax and Caspase-3). Thr also reduced liver malondialdehyde (MDA) and O2− level, and restored superoxide dismutase (SOD) activity. In conclusion, Thr alleviated Cd-induced hepatic tissue and dysfunction through reducing the formation of free radicals O2−, lipid peroxidation, inflammation, and inhibiting the expression of Bax and Caspase-3.

Environment and food contamination with cadmium (Cd) can cause serious toxicity, posing a severe threat to agricultural production and human health. However, how amino acids contribute to defenses against oxidative stress caused by Cd in cells is not fully understood. As a model eukaryote with a relatively clear genetic background, Saccharomyces cerevisiae has been commonly used in Cd toxicity research. To gain insight into Cd toxicity and cell defenses against it, 20 amino acids were screened for protective roles against Cd stress in S. cerevisiae. The results showed that threonine (Thr, T) had the strongest protective effect against Cd-induced mortality and membrane damage in the cells. Compared to the antioxidant vitamin C (VC), Thr exhibited a higher efficacy in restoring the superoxide dismutase (SOD) activity that was inhibited by Cd but not by H2 O2 in vivo. Thr exhibited evident DPPH (2,2-diphenyl-1-picrylhydrazyl) activity but weak ABTS (2,2'-azino-bis(3-ethylbenzothiazoline-6-9 sulfonic acid)) scavenging activity, giving it a weaker effect against Cd-induced lipid peroxidation and superoxide radical O2- , compared to VC. More importantly, compared to the chelating agent EDTA, Thr showed stronger chelation of Cd, giving it a stronger protective effect on SOD against Cd than VC in vitro. The results of the in vivo and in vitro experiments revealed that the role Thr plays in cell defenses against Cd may be attributed to its protection of the SOD enzyme, predominantly through the preferential chelation of Cd. Our results provide insights into the protective mechanisms of amino acid Thr that ameliorate Cd toxicity and suggest that a supplement of Thr might help to reduce Cd-induced oxidative damage.

The mechanism of aluminum toxicity was studied in the model cells of Saccharomyces cerevisiae. Cell growth of yeast was inhibited by aluminum. The spot assay showed that the mechanism of aluminum detoxification in yeast cells was different from that of heavy metal cadmium. After treatment with aluminum, intracellular levels of reactive oxygen species, protein carbonyl, and thiobarbituric acid reactive substances were dramatically increased. Meanwhile, the percentage of aluminum-treated cells permeable to propidium iodide was augmented significantly. These data demonstrated that aluminum toxicity was attributed to oxidative stress in yeast, and it induced oxidative damage by causing lipid peroxidation, injuring cell membrane integrity. Moreover, aluminum triggered the antioxidant defense system in the cells. Glutathione levels were found to be decreased, while activities of superoxide dismutase and catalase were increased after treatment with aluminum. Additionally, an oxidative-stress-related mutation sensitivity assay showed that aluminum-induced yeast oxidative stress was closely related to glutathione. These data demonstrated that the oxidative damage caused by aluminum was different from that of hydrogen peroxide, in yeast. Aluminum could cause DNA damage, and aluminum toxicity was associated with sulfhydryl groups, such as glutathione, while it was independent of YAP1.

Nanoliposomes are ideal nanocarriers for encapsulated active compounds used in the food industry as they provide stability and controlled release. However, cholesterol may pose risks in large intake, which is the commonly-used nanoliposome stabilizers. In this study, resveratrol was used instead of cholesterol as a novel nanoliposome stabilizer to construct a resveratrol blank liposome (RBL) system. The RBL system was used to protect the bacteriocin CAMT6 to create bacteriocin-loaded nanoliposomes (BLLs). The RBLs and BLLs had favourable particle sizes (172.71 nm and 150.47 nm), polydispersity index (PDI) values (0.150 and 0.120) and zeta potentials (-41.54 mV and -43.53 mV, respectively). According to Differential scanning colourimetry (DSC) and X-ray diffraction (XRD) analyses, resveratrol altered the structure of the phospholipid layer. The phospholipid layers of the RBLs and BLLs had higher mobility when resveratrol was used as a stabilizer instead of cholesterol. Structurally, resveratrol was inserted egg yolk lecithin to constitute an RBL. CAMT6 was loaded in BLLs with spherical and shell-core structures. The BLL encapsulation efficiency was 97.32 % and exhibited three release phases, with the release rates reaching 62 %. In experiments with milk, the BLLs effectively protected the anti-Listeria activity of CAMT6. In summary, resveratrol is a suitable nanoliposome stabilizer and the proposed RBL system is an excellent way to improve the stability of water-soluble preservatives, such as bacteriocins, in complex food environments.

Amphotericin B has been the gold standard for the treatment of invasive mycosis for many years. Its resistance mechanisms are reported to be mainly related to the decrease of ergosterol content or the changes of cell wall. Previous study has shown that Saccharomyces cerevisiae strain lack of BSC2 was sensitive significantly to Amphotericin B. In the present study, the role of BSC2 on Amphotericin B resistance were investigated. We found that BSC2 enhanced the resistance of yeast cells to Amphotericin B, which was not related to cellular ergosterol content. BSC2 can maintain the permeability of mitochondrial membrane and cell membrane integrity by inhibiting the accumulation of intercellular reactive oxygen species and alleviating the production of lipid peroxidation and superoxide radical. These alterations were attributed to the enhancement of the activities of superoxide dismutase, catalase and glutathione peroxidase, and the increased glutathione content. Taken together, BSC2 inhibits oxidative damage induced by Amphotericin B through increasing activities of antioxidant enzymes and levels of GSH to alleviate the accumulation of reactive oxygen species, lipid peroxidation and superoxide radical, resulting in the maintenance of mitochondrial membrane potential and cell membrane integrity. However, Amphotericin B resistance mediated by BSC2 is independent of Yap1p, GSH1 and Hog1p. The results demonstrate for the first time that BSC2 enhances cell resistance to Amphotericin B by inhibiting oxidative damage in yeast. Our findings improve current understanding of the mechanism of Amphotericin B resistance and provide potential strategy for reducing Amphotericin B resistance.

Certain foods are known as “heating” foods in Chinese medicine. Over-consumption of these foods can lead to symptoms known as “heating up”. These symptoms have been shown to be symptoms of systemic low-grade inflammation. However, the mechanism by which these foods cause inflammation is not clear. In this preliminary study, we investigated dysbacteriosis of the gut microbiota as a possible cause of inflammation by litchi, a typical “heating” food. A human flora-associated (HFA) mouse model (donor: n = 1) was constructed. After gavaging the mice with litchi extract suspension at low, medium and high doses (400, 800, 1600 mg/kg·d−1, respectively) (n = 3) for 7 days, the serum levels of inflammatory cytokines, gut microbiota, the concentration of SCFAs and the integrity of the intestinal mucosal barrier were measured. The results revealed significant increases in the abundance of Prevotella and Bacteroides. A significant increase in the abundance of Bilophila and a decrease in Megasomonas was observed in the high-dose group. High-dose litchi intervention led to a decrease of most SCFA levels in the intestine. It also caused a more than two-fold increase in the serum TNF-α level and LPS level but a decrease in the IL-1β and IL-6 levels. Medium- and high-dose litchi intervention caused widening of the intestinal epithelial cell junction complex and general weakening of the intestinal mucosal barrier as well as reduced energy conversion efficiency of the gut microbiota. These data suggest that litchi, when consumed excessively, can lead to a low degree of systematic inflammation and this is linked to its ability to cause dysbacteriosis of the gut microbiota, decrease SCFAs and weaken the intestinal mucosal tissues.

Systemic low-grade inflammation induced by unhealthy diet has become a common health concern as it contributes to immune imbalance and induces chronic diseases, yet effective preventions and interventions are currently unavailable. The Chrysanthemum indicum L. flower (CIF) is a common herb with a strong anti-inflammatory effect in drug-induced models, based on the theory of “medicine and food homology”. However, its effects and mechanisms in reducing food-induced systemic low-grade inflammation (FSLI) remain unclear. This study showed that CIF can reduce FSLI and represents a new strategy to intervene in chronic inflammatory diseases. In this study, we administered capsaicin to mice by gavage to establish a FSLI model. Then, three doses of CIF (7, 14, 28 g·kg−1·day−1) were tested as the intervention. Capsaicin was found to increase serum TNF-α levels, demonstrating a successful model induction. After a high dose of CIF intervention, serum levels of TNF-α and LPS were reduced by 62.8% and 77.44%. In addition, CIF increased the α diversity and number of OTUs in the gut microbiota, restored the abundance of Lactobacillus and increased the total content of SCFAs in the feces. In summary, CIF inhibits FSLI by modulating the gut microbiota, increasing SCFAs levels and inhibiting excessive LPS translocation into the blood. Our findings provided a theoretical support for using CIF in FSLI intervention.

Wide range of applications of heavy metals and improperly discarded their castoffs possess serious threats to environment and human health. In this study, cytotoxicity, DNA damage and oxidative stress induced by Cd(II), Hg(II) and Cr(III) were comparatively studied in yeast Saccharomyces cerevisiae. Cd(II), Hg(II), and Cr(III) all produced strong cytotoxicity resulting in growth inhibition and cell mortality to varying degrees (Hg(II) > Cd(II) > Cr(III)). Hg(II) produced more oxidative stress. Cr(III) caused more serious DNA damage in vitro. Cd(II) also caused both obvious DNA damage and oxidative stress at higher concentration, but not as efficiently as Cd(II) and Hg(II). A further null mutation sensitivity assay showed that the relative sensitivity of rad1∆ to the metals was Cr(III) > Cd(II) > Hg(II), and that of trx1∆ to the metals was Hg(II) > Cd(II) > Cr(III). These data provide a clear evidence that the Cr(III) can cause significant DNA damage and potential genotoxicity; Hg(II) can strongly inhibit SOD activity, produce lipid peroxidation and cause serious membrane injury, suggesting these heavy metals can cause different toxic effects in different ways.

Tricothecenes-2 toxin (T-2) is a major mycotoxin that is widely distributed in aquatic feeds and poses a huge challenge to the aquatic industry, but there is scant information on the toxicokinetics of T-2 in aquatic animals. Here, we describe the development of a three-compartment toxicokinetic model for the absorption, distribution, metabolism and elimination (ADME) of T-2 in shrimp. The three compartments were central (the hemolymph), slow metabolizing and fast metabolizing compartments to account for the varying ADME rates of T-2 in different shrimp organs. The toxicokinetic model was solved by the blindfold particle swarm optimization algorithm, and the values for the model equation parameters were obtained by applying the experimental data of T-2 concentrations in shrimp. The model had a good fit with the experimental data. It was revealed through the model that after i.m. administration, T-2 was rapidly absorbed into the hemolymph and distributed into shrimp organs. The hepatopancreas and intestine belonged to the fast and muscle to the slow metabolizing compartments, respectively, while the hemolymph had no capacity to metabolize T-2. The T-2 elimination rates in the hepatopancreas and intestine were similar and quite high while that in the muscle was very low. The methods used in developing and solving the model could be used for similar toxicokinetic and pharmacokinetic studies of other animals.

Background: Certain foods are known as “heating” foods in Chinese medicine as over consumption of them can lead to symptoms known as “heating up”, which have been shown to be symptoms of systemic low-grade inflammation. However, the mechanism by which these foods cause inflammation is not clear. In this study, we investigated dysbacteriosis of gut microbiota as a possible cause of inflammation by litchi, a typical “heating” food. Human flora-associated (HFA) mice model was constructed by first sterilizing their guts by oral administration of antibiotics, and then transplantation of fecal microbial suspension from a healthy human adult. After gavaging the mice with litchi powder suspension at low, medium and high doses (400, 800, 1600 mg/kg·d-1 respectively) for 7 days, the serum level of inflammatory cytokines, gut microbiota and the integrity of intestinal mucosal barrier were measured.Result: The intervention of litchi significantly increased the diversity of mice gut flora. The ratio of Bacteroidetes/Firmicutes and the abundance of Actinobacteria increased significantly. At the genus level, the abundance of Phascolarctobacterium, Akkermansia, Megasomonas and Lactobacillus generally decreased, while the abundance of Prevotella and Bacteroides increased significantly, especially in the high litchi dose group. The abundance of Bilophila increased significantly only in high dose group. litchi intervention caused serum TNF-α level to increase by more than two times and LPS level to double, but a decrease in IL-1β and IL-6 levels. Medium and high dose litchi intervention caused a widening of intestinal epithelial cell junction complex, and general weakening of the intestinal mucosal barrier as well as reduced efficiency of gut microbiota in energy conversion. Conclusion: This study confirmed the notion in Chinese medicine that as a “heating” food, litchi when consumed excessively can lead to low degree systematic inflammation and demonstrated that this is linked to its ability to cause dysbacteriosis of the gut microbiota and weakening of the intestinal mucosal tissues.

Background: Vibrio alginolyticus is an important seafood-borne pathogen. There is increasing evidence that V.alginolyticus can also contaminate non-seafood by cross contamination and thereby cause food poisoning in humans. The growth and hemolysin production of V. alginolyticus at 30 °C in briny tilapia, shrimp, scallop, oyster, pork, chicken, freshwater fish and egg fried rice were investigated. Bacterial counts were enumerated by plate counting. Hemolysin production was evaluated by blood agar and hemolytic titer tests.Results: Based on the goodness of fit primary model statistics (R 2 , MSE, BF, AF), the modified Gompertz model was a better fit to V. alginolyticus growth in foods than the logistic model. Growth kinetic parameters of V. alginolyticus displayed a higher μ max and shorter λ in briny tilapia > shrimp > freshwater fish > egg fried rice > scallop > oyster > chicken > pork. It was notable that the V. alginolyticus counts were similar at the stationary phase, with no significant growth behavior difference between raw and cooked foods. However, higher thermostable direct hemolysin activity and hemolytic titer were observed in briny tilapia > egg fried rice > shrimp > freshwater fish > chicken > scallop > oyster > pork.Conclusion: V. alginolyticus growth was good in all food matrix types tested. Contrary to current belief, V. alginolyticus displayed a higher hemolytic activity in some non-seafoods (freshwater fish, egg fried rice and chicken) than in scallop or oyster. This is the first report of growth and toxicity of V. alginolyticus in different food matrices and confirmation that some non-seafood contaminated with V. alginolyticus can be even more pathogenic. This study will enhance the awareness of non-seafood safety and improve the V. alginolyticus risk assessment accuracy.

The mechanism of aluminum toxicity was studied in the model cells of

Toxic heavy metal cadmium wildly pollutes the environment and threats the human health. Effective treatment of cadmium-induced toxicity and organ damage is an important issue. Cadmium causes organ damage through inducing oxidative stress. Our previous study also found oleic acid (OA) synthesis-related gene can confer resistance to cadmium and alleviate cadmium-induced stress in yeast. However, its alleviation mechanism on cadmium stress especially in animals is still unclear. In this study, the alleviative effects of OA on cadmium and cadmium-induced oxidative stress in rats were investigated. Oral administration of 10, 20, and 30 mg/kg/day OA can significantly increase the survival rate of rats intraperitoneally injected with 30 mg/kg/day cadmium continuously for 7 days. Similar to ascorbic acid (AA), OA can significantly reduce the cadmium-induced lipid peroxidation in multiple organs of rats. The investigation of OA on superoxide dismutase (SOD) activity showed that OA increased the SOD activity of cadmium-treated rat organs. More important, OA reduced the level of superoxide radical O2- of cadmium-treated rat organs. And OA exhibited a strong DPPH radicals scavenging activity at dose of 10, 20 and 30 mg/mL, which may contributed to alleviating cadmium-induced oxidative stress. This study revealed that OA could significantly alleviate cadmium stress via reducing cadmium-induced lipid peroxidation and SOD activity inhibition through its radicals scavenging activity.

Water and protein are major constituents of shrimp, any changes in protein and the state of water influence the quality of shrimp. Therefore, a study to examine the law of moisture migration and protein denaturation under different freezing and thawing conditions is important. The proton density images of thawed frozen‐shrimp revealed that the water loss during quick‐freezing was much greater than that during slow freezing or microfreezing. At room temperature (25 °C), the water loss from brine‐thawing was more than still‐water thawing and still‐water thawing was more than thawing spontaneously. Freezing‐thawing resulted in uniform water redistribution in shrimp muscle. Nuclear magnetic resonance technology (low field magnetic imaging) was used to directly monitor the dynamic processes of fluidity state in shrimp and indirectly monitor protein denaturation and thereby determine the optimal method of freezing‐thawing shrimp. Our research showed that microfreezing preservation minimized weight loss, juice leakage and protein denaturation in shrimp muscle during thawing. Water is one of the major components in most organs and is an important factor that influences the shrimp muscle quality. Water migration patterns and subsequent effects on the shrimp muscle under different freezing and thawing conditions were examined using low field nuclear magnetic resonance (NMR) technology. This research provides a theoretical foundation for shrimp processing plants to improve the freezing and thawing process to obtain optimal quality and flavor of shrimp products.

Vibrio parahaemolyticus is a seafood opportunistic pathogen. There are evidences suggesting that virulence skills, including hemolytic activity and biofilm formation, are regulated by the luxM/luxS-dependent quorum-sensing system in V. parahaemolyticus, and their regulatory mechanism is not well understood. To better understand the virulence regulatory mechanism of V. parahaemolyticus, the luxM deletion (△luxM) and luxS deletion (△luxS) mutants were constructed and their impacts on growth, hemolysin activity, and biofilm were investigated. Results show that both luxM and luxS are involved in the adaptation to environmental conditions in early adaptive-log phase growth of V. parahaemolyticus. Thermostable direct hemolysin gene (tdh) was negatively regulated by luxM and positively regulated by luxS. The biofilm formation was negatively regulated by both luxS and luxM. This study provides an insight into some aspects of V. parahaemolyticus virulence regulation by luxM/luxS-dependent quorum-sensing system.

The use of a direct arene-exchange method for the synthesis of benzyl-tethered arene/Ru/TsDPEN complexes for use in asymmetric transfer hydrogenation is reported. A series of complexes tethered through a three-carbon linear chain was also prepared. The arene-exchange approach significantly simplifies the synthetic approach to this class of catalyst and permits the ready formation of modified analogues. The approach also provides a route to racemic catalysts for use in general reductions with either hydrogen or transfer hydrogenation.

The objective of this work was to determine the bacterial strains and factors that most efficiently degrade T-2 toxin in foods or animal feed. To determine the most efficient strain and optimal incubation times for degradation of T-2, the rate of T-2 removal by three lactic acid bacteria strains was quantified by liquid chromatography plus tandem mass spectrometry after incubation in de Man Rogosa Sharpe broth with 50 ng mL

Although highly accurate molecular processes and various messenger RNA (mRNA) quality control and ribosome proofreading mechanisms are used by organisms to transcribe their genes and maintain the fidelity of genetic information, errors are inherent in all biological systems. Low-level translation errors caused by an imbalance of homologous and nonhomologous amino acids caused by stress conditions are particularly common. Paradoxically, advantageous phenotypic diversity can be generated by such errors in eukaryotes through unknown molecular processes. Here, we found that the significant cadmium-resistant phenotype was correlated with an increased mistranslation rate of the mRNA in Saccharomyces cerevisiae. This phenotypic change was also related to endogenous sulfur amino acid starvation. Compared with the control, the mistranslation rate caused by cadmium was significantly increased (p < .01). With the increase of cysteine contents in medium, the mistranslation rate of WT(BY4742a) decreased significantly (p < .01). This demonstrates that cadmium treatment and sulfur amino acid starvation both can induce translation errors. Although cadmium uptake is independent of the Sul1 transporter, cadmium-induced mRNA mistranslation is dependent on the sulfate uptake of the Sul1p transporter. Furthermore, cadmium-induced translation errors depend on methionine biosynthesis. Taken together, cadmium causes endogenous sulfur starvation, leading to an increase in the mRNA mistranslation, which contributes to the resistance of yeast cells to cadmium. We provide a new pathway mediating the toxicity of cadmium, and we propose that altering mRNA mistranslation may portray a different form of environmental adaptation.

Lipopeptides possess excellent broad spectrum antimicrobial activity. Different lipopeptides have their own unique chemical structures, properties and biological activities. Quantitative analysis of the lipopeptides iturin and surfactin and their homologues produced by Bacillus natto NT–6 subjected to different culture media, shaking speed of rotary shaker, and liquid and solid fermentation methods was conducted using LC–MS. For iturins, liquid-state fermentation in Landy medium at a shaking speed of 160 r min−1 was the most suitable for maximal homologue production. Addition of 0.4% attapulgite powder increased production by 1.92-fold; activated carbon significantly reduced production. For surfactin homologues, solid-state fermentation in potato dextrose broth medium at shaking speed > 160 r min−1 was the best. Addition of 0.4% attapulgite powder increased production by 1.96-fold; activated carbon had no effect. Thus it is clear that fermentation conditions can be manipulated to maximize iturin and surfactin production.

Tea polyphenols (TP), as common antioxidants, have been widely used to mitigate for the protection and preservation of aquatic animals, but the protective effect of TP against the deterioration of shrimp muscle quality induced by aflatoxin B1 (AFB1) has not been reported. This study was designed to analyse the root cause of AFB1 induced declines in shrimp muscle quality and the protective mechanisms of TP at the molecular level. Shrimp were exposed to AFB1 and TP for 20 d following a dose-escalating trial, and changes to the muscle histopathology, basic nutrient composition, and protein composition were determined. Non-labelled quantitative proteomics was used to screen and identify differential marker proteins associated with AFB1 and TP. After 20 d of AFB1 exposure, the water content, crude protein content and crude fat content of the shrimp muscle decreased to 68.66%, 18.27% and 1.01%, respectively, while the ash content was positively correlated with AFB1 dose (R2 = 0.955). AFB1 caused damage to the shrimp muscle microstructure in a dose-dependent manner, such as significant enlargement of muscle fibre spaces, rupture of the sarcomere, inflammation and so on. AFB1 induced changes in muscle protein composition, resulting in a decrease in the content of myofibrillar, sarcoplasmic and stroma proteins, while the alkali-soluble protein content increased significantly. TP can effectively protect against the damage to shrimp muscle caused by AFB1 by inhibiting the expansion of muscle fibre spaces and inflammation. TP (0.04–0.16% feed) also had a significant protective effect against the decrease of muscle nutrients and changes in protein composition of shrimp caused by exposure to AFB1 (1.2–2.7 mg/kg feed) in the early and middle period (4–12 d), but the protective effect was weak or not noticeable in the late period (16–20 d). Eleven proteins were identified and screened as biomarker proteins of AFB1 induced quality decline and TP protection, which were involved in energy metabolism (fructose 1,6-bisphosphatase; transaldolase; fructose-bisphosphate aldolase; arginine kinase), redox reaction (hydroxyphenylpyruvate reductase; prostaglandin reductase 1; protein arginine N-methyltransferase 8), anti-inflammatory responses (5′-nucleotidase; actin-depolymerizing factor) and protein translation/folding (eukaryotic translation initiation factor 3; peptidyl-prolyl cis-trans isomerase). This study provides a better understanding of AFB1 induced damage to shrimp quality and technical guidance for the use of TP to prevent the damage during the culture and processing of Penaeus vannamei.

Trivalent chromium [Cr(III)] has been shown as an essential trace element for human health. Previous studies depict that Cr(III) plays important roles in maintaining normal glucose and lipid metabolism, whereas its effect on the hepatic lipid metabolism is still unknown. In the present study, we investigated the effects and underlying mechanisms of Cr on hepatic steatosis induced by oleic acid (OA) in human hepatoma SMMC-7721 cells. Hepatic steatosis model was co-administered with Cr. Indexes of lipid accumulation were determined and associated genes expression were analyzed. The data showed that OA could induce lipid accumulation and triglyceride (TG) content in SMMC-7721 cells, and significantly increase the expression of cluster of differentiation 36 (CD36) and diacylglycerol acyltransferase 2 (DGAT2). This steatosis effect of OA was ameliorated by Cr. The TG accumulation and up-regulation of CD36 and DGAT2 genes followed steatosis induction were inhibited by Cr. After the treatment of Cr, excessive intracellular OA content was also attenuated. Furthermore, Cr still performed inhibitory effect of DGAT2 expression at the presence of DGAT2 agonist or inhibitor, which indicated that the inhibitory effect of Cr on lipogenesis is associated with the downregulation of DGAT2 expression. These findings demonstrate that Cr alleviates hepatic steatosis via suppressing CD36 expression to prevent fatty acid uptake, as well as suppressing DGAT2 expression to inhibit TG synthesis. It suggests that CD36 and DGAT2 might become the novel drug targets for their properties in hepatic steatosis. Most importantly, Cr may be a potential anti-steatosis candidate to offer protective effects against liver damage.