Mechanism of mitigating effect of wheat germ peptides on lead-induced oxidative damage in PC12 cells.

It is well known that lead-induced neurotoxicity is closely related to oxidative stress. According to previous reports, wheat germ peptides (WGPs) isolated from wheat germ have been shown to have potent antioxidant capacity. This study hypothesized that WGPs could protect PC12 cells from lead-induced oxidative stress. Here, the protecting-efficacies of WGPs were investigated in PC12 cells that were pretreated with WGPs (200 µM, 4 h) and exposed to lead (10 µM, 24 h). The antioxidant capacity was assessed by cell viability, ROS, MDA, SOD, CAT, GR, GPx, GSH, and GSSG. The experimental results showed that WGP3, WGP8, and WGP9 could reverse the reduction of cell viability caused by lead exposure. Lead exposure causes oxidative stress by increasing the levels of ROS and MDA. Moreover, the decrease in the levels of SOD, CAT, GPx, GR, and GSH/GSSG could be observed. However, WGP3, WGP8, and WGP9 can protect PC12 cells against lead-induced oxidative stress by reversing these phenomena. The protein expression of TXNIP, Keap1, and Nrf2 was characterized by western blotting, and the results illustrated that lead exposure up-regulated the expression of TXNIP and Keap1 and down-regulated the expression of Nrf2, and WGP3, WGP8, and WGP9 could improve the antioxidant capacity of PC12 cells by reversing this phenomenon. Therefore, the present study demonstrated that WGP3, WGP8, and WGP9 may protect against lead-induced oxidative stress in PC12 cells by regulating the TXNIP/Keap1/Nrf2 pathway.

Protective effects of folic acid on oxidative damage of rat spleen induced by lead acetate.

Lead (Pb) is a heavy metal environmental pollutant that can cause functional damage and anemia of immune organs. More and more evidence indicate that the toxicity of lead was related to apoptosis driven by oxidative stress and endoplasmic reticulum stress. This article mainly discusses the protective effect and mechanism of folic acid intervention on lead-induced spleen injury and apoptosis. In this study, Sprague-Dawley rats were randomly divided into control group, lead exposure group (0.2% lead acetate), folic acid + lead group (0.4 mg/kg folic acid and 0.2% lead acetate), and folic acid group (0.4 mg/kg folic acid). By recording and calculating the rat's initial body weight, final body weight, net weight gain, daily weight gain, and spleen index, observe the rat's weight change and spleen weight. And adopt the immunofluorescence staining method to determine the expression level of NrF2, HO-1, GRP78, CHOP protein in the spleen. The results showed that The 0.4 mg/kg folic acid diet did not significantly improve in the body weight and spleen index of lead-exposed rats (P > 0.05). While compared with the control group, the expression levels of HO-1 and CHOP protein were significantly increased in the lead exposure group (P < 0.05), and the expression levels of HO-1 and CHOP protein were significantly reduced in the folic acid intervention group (P < 0.05). In conclusion, lead exposure increased the expression levels of HO-1 and CHOP in the spleen of rats, and caused damage to the spleen. Folic acid down-regulated the expression levels of HO-1 and CHOP proteins through the two pathways of NrF2/HO-1 and GRP78/CHOP, thereby exerting a certain protective effect and alleviating the spleen caused by lead-induced oxidative stress and endoplasmic reticulum stress damage.

An ultrasensitive, homogeneous fluorescence quenching immunoassay integrating separation and detection of aflatoxin M1 based on magnetic graphene composites.

A homogeneous fluorescence quenching immunoassay is described for simultaneous separation and detection of aflatoxin M1 (AFM1) in milk. The novel assay relies on monoclonal antibody (mAb) functionalized Fe3O4 decorated reduced-graphene oxide (rGO-Fe3O4-mAb) as both capture probe and energy acceptor, combined with tetramethylrhodamine cadaverine-labeled aflatoxin B1 (AFB1-TRCA) as the energy donor. In the assay, AFB1-TRCA binds to rGO-Fe3O4-mAb in the absence of AFM1, quenching the fluorescence of TRCA by resonance energy transfer. Significantly, the immunoassay integrates sample preparation and detection into a single step, by using magnetic graphene composites to avoid washing and centrifugation steps, and the assay can be completed within 10 min. Under optimized conditions, the visual and quantitative detection limits of the assay for AFM1 were 50 and 3.8 ng L-1, respectively, which were significantly lower than those obtained by fluorescence polarization immunoassay using the same immunoreagents. Owing to its operation and highly sensitivity, the proposed assay provides a powerful tool for the detection of AFM1.

Synthesis and characterization of a new soy protein isolate/Polyamic acid salt blend films.

In this study, a new method was developed to produce biodegradable material using soy protein isolate (SPI) as matrix. The blend films were successfully prepared by casting the aqueous dispersions of SPI and polyamic acid salt (PAS) solution. The effects of blending and PAS content on the structure of the resultant films were investigated by Fourier transform infrared spectroscopy (FTIR), X-ray diffraction (XRD), differential scanning calorimetry (DSC) analyses, scanning electron microscopy (SEM). Furthermore, film thickness, water vapor permeability (WVP), water barrier and mechanical properties were measured. The result showed that there exists strong intermolecular interactions between SPI and PAS, which played an important role in forming a homogeneous structure of the blend films. Moreover, the incorporation of PAS enhanced the water barrier and mechanical properties of the films. This is a simple way to prepare biodegradable films compared with other methods and the blend films have the potentiality to be used as food packaging and biomedical materials instead of synthetic polymer.

The Pea Oligosaccharides Could Stimulate the In Vitro Proliferation of Beneficial Bacteria and Enhance Anti-Inflammatory Effects via the NF-κB Pathway.

The oligosaccharides extracted from the seeds of peas, specifically consisting of raffinose, stachyose, and verbascose, fall under the category of raffinose family oligosaccharides (RFOs). The effect of RFOs on intestinal microflora and the anti-inflammatory mechanism were investigated by in vitro fermentation and cell experiments. Firstly, mouse feces were fermented in vitro and different doses of RFOs (0~2%) were added to determine the changes in the representative bacterial community, PH, and short-chain fatty acids in the fermentation solution during the fermentation period. The probiotic index was used to evaluate the probiotic proliferation effect of RFOs and the optimal group was selected for 16S rRNA assay with blank group. Then, the effects of RFOs on the inflammatory response of macrophage RAW264.7 induced by LPS were studied. The activity of cells, the levels of NO, ROS, inflammatory factors, and the expression of NF-κB, p65, and iNOS proteins in related pathways were measured. The results demonstrated that RFOs exerted a stimulatory effect on the proliferation of beneficial bacteria while concurrently inhibiting the growth of harmful bacteria. Moreover, RFOs significantly enhanced the diversity of intestinal flora and reduced the ratio of Firmicutes-to-Bacteroides (F/B). Importantly, it was observed that RFOs effectively suppressed NO and ROS levels, as well as inflammatory cytokine release and expression of NF-κB, p65, and iNOS proteins. These findings highlight the potential of RFOs in promoting intestinal health and ameliorating intestinal inflammation.

Changes in physio-biochemical metabolism, phenolics and antioxidant capacity during germination of different wheat varieties.

Changes in physio-biochemical metabolism, phenolics and antioxidant capacity during germination were studied in eight different wheat varieties. Results showed that germination enhanced sprout growth, and caused oxidative damage, but enhanced phenolics accumulation. Ferulic acid and p-coumaric acid were the main phenolic acids in wheat sprouts, and dihydroquercetin, quercetin and vitexin were the main flavonoids. The phenolic acid content of Jimai 44 was the highest on the 2th and 4th day of germination, and that of Bainong 307 was the highest on the 6th day. The flavonoid content of Hei jingang was the highest during whole germination. The enzymes activities of phenylalanine ammonia lyase (PAL), cinnamic acid 4-hydroxylase (C4H) and 4-coumarate coenzyme A ligase (4CL) were up-regulated. The activities of catalase, polyphenol oxidase and peroxidase were also activated. Antioxidant capacity of wheat sprouts was enhanced. The results provided new ideas for the production of naturally sourced phenolic rich foods.

Differential expression of SLC30A10 and RAGE in mouse pups by early life lead exposure.

BACKGROUND: SLC30A10 and RAGE are widely recognized as pivotal regulators of Aß plaque transport and accumulation. Prior investigations have established a link between early lead exposure and cerebral harm in offspring, attributable to Aß buildup and amyloid plaque deposition. However, the impact of lead on the protein expression of SLC30A10 and RAGE has yet to be elucidated. This study seeks to confirm the influence of maternal lead exposure during pregnancy, specifically through lead-containing drinking water, on the protein expression of SLC30A10 and RAGE in mice offspring. Furthermore, this research aims to provide further evidence of lead-induced neurotoxicity. METHODS: Four cohorts of mice were subjected to lead exposure at concentrations of 0 mM, 0.25 mM, 0.5 mM, and 1 mM over a period of 42 uninterrupted days, spanning from pregnancy to the weaning phase. On postnatal day 21, the offspring mice underwent assessments. The levels of lead in the blood, hippocampus, and cerebral cortex were scrutinized, while the mice's cognitive abilities pertaining to learning and memory were probed through the utilization of the Morris water maze. Furthermore, Western blotting and immunofluorescence techniques were employed to analyze the expression levels of SLC30A10 and RAGE in the hippocampus and cerebral cortex. RESULTS: The findings revealed a significant elevation in lead concentration within the brains and bloodstreams of mice, mirroring the increased lead exposure experienced by their mothers during the designated period (P < 0.05). Notably, in the Morris water maze assessment, the lead-exposed group exhibited noticeably diminished spatial memory compared to the control group (P < 0.05). Both immunofluorescence and Western blot analyses effectively demonstrated the concomitant impact of varying lead exposure levels on the hippocampal and cerebral cortex regions of the offspring. The expression levels of SLC30A10 displayed a negative correlation with lead doses (P < 0.05). Surprisingly, under identical circumstances, the expression of RAGE in the hippocampus and cortex of the offspring exhibited a positive correlation with lead doses (P < 0.05). CONCLUSION: SLC30A10 potentially exerts distinct influence on exacerbated Aß accumulation and transportation in contrast to RAGE. Disparities in brain expression of RAGE and SLC30A10 may contribute to the neurotoxic effects induced by lead.

The Impact of High Temperature on Microbial Communities in Pork and Duck Skin.

Pork skin and duck skin are highly favored by consumers in China, and high-temperature processing methods are widely employed in cooking and food preparation. However, the influence of high-temperature treatment on the microbial communities within pork skin and duck skin remains unclear. In this study, a high-temperature treatment method simulating the cooking process was utilized to treat samples of pork skin and duck skin at temperatures ranging from 60 °C to 120 °C. The findings revealed that high-temperature treatment significantly altered the microbial communities in both pork skin and duck skin. Heat exposure resulted in a decrease in microbial diversity and induced changes in the relative abundance of specific microbial groups. In pork skin, high-temperature treatment led to a reduction in bacterial diversity and a decline in the relative abundance of specific bacterial taxa. Similarly, the relative abundance of microbial communities in duck skin also decreased. Furthermore, potential pathogenic bacteria, including Gram-positive and Gram-negative bacteria, as well as aerobic, anaerobic, and facultative anaerobic bacteria, exhibited different responses to high-temperature treatment in pork skin and duck skin. These findings highlighted the substantial impact of high-temperature processing on the composition and structure of microbial communities in pork skin and duck skin, potentially influencing food safety and quality. This study contributed to an enhanced understanding of the microbial mechanisms underlying the alterations in microbial communities during high-temperature processing of pork skin and duck skin, with significant implications for ensuring food safety and developing effective cooking techniques.

Evaluating the Potential Safety Risk of Plant-Based Meat Analogues by Analyzing Microbial Community Composition.

Plant-based meat analogues offer an environmentally and scientifically sustainable option as a substitute for animal-derived meat. They contribute to reducing greenhouse gas emissions, freshwater consumption, and the potential risks associated with zoonotic diseases linked to livestock production. However, specific processing methods such as extrusion or cooking, using various raw materials, can influence the survival and growth of spoilage and pathogenic microorganisms, resulting in differences between plant-based meat analogues and animal meat. In this study, the microbial communities in five different types of plant-based meat analogues were investigated using high-throughput sequencing. The findings revealed a diverse range of bacteria, including Cyanobacteria, Firmicutes, Proteobacteria, Bacteroidota, Actinobacteriota, and Chloroflexi, as well as fungi such as Ascomycota, Basidiomycota, Phragmoplastophyta, Vertebrata, and Mucoromycota. Additionally, this study analyzed microbial diversity at the genus level and employed phenotype prediction to evaluate the relative abundance of various bacterium types, including Gram-positive and Gram-negative bacteria, aerobic, anaerobic, and facultative anaerobic bacteria, as well as potential pathogenic bacteria. The insights gained from this study provide valuable information regarding the microbial communities and phenotypes of different plant-based meat analogues, which could help identify effective storage strategies to extend the shelf-life of these products.

GABA Application Enhances Drought Stress Tolerance in Wheat Seedlings (Triticum aestivum L.).

In this study, the effects of γ-aminobutyric acid (GABA) on physio-biochemical metabolism, phenolic acid accumulation, and antioxidant system enhancement in germinated wheat under drought stress was investigated. The results showed that exogenous GABA reduced the oxidative damage in wheat seedlings caused by drought stress and enhanced the content of phenolics, with 1.0 mM being the most effective concentration. Six phenolic acids were detected in bound form, including p-hydroxybenzoic acid, vanillic acid, syringic acid, p-coumaric acid, ferulic acid, and sinapic acid. However, only syringic acid and p-coumaric acid were found in free form. A total of 1.0 mM of GABA enhanced the content of total phenolic acids by 28% and 22%, respectively, compared with that of drought stress, on day four and day six of germination. The activities of phenylalanine ammonia lyase (PAL), cinnamic acid 4-hydroxylase (C4H) and 4-coumarate coenzyme A ligase (4CL) were activated by drought stress plus GABA treatment. Antioxidant enzyme activities were also induced. These results indicate that GABA treatment may be an effective way to relieve drought stress as it activates the antioxidant system of plants by inducing the accumulation of phenolics and the increase in antioxidant enzyme activity.

Effect of 2'-Fucosyllactose on Beige Adipocyte Formation in 3T3-L1 Adipocytes and C3H10T1/2 Cells.

2'-Fucosyllactose (2'-FL), the functional oligosaccharide naturally present in milk, has been shown to exert health benefits. This study was aimed to investigate the effect of 2'-fucosyllactose (2'-FL) on the browning of white adipose tissue in 3T3-L1 adipocytes and C3H10T1/2 cells. The results revealed that 2'-FL decreased lipid accumulations with reduced intracellular triglyceride contents in vitro. 2'-FL intervention increased the mitochondria density and the proportion of UCP1-positive cells. The mRNA expressions of the mitochondrial biogenesis-related and browning markers (Cox7a, Cyto C, Tfam, Ucp1, Pgc1α, Prdm16, Cidea, Elovl3, Pparα, CD137, and Tmem26) were increased after 2'-FL intervention to some extent. Similarly, the protein expression of the browning markers, including UCP1, PGC1α, and PRDM16, was up-regulated in the 2'-FL group. Additionally, an adenosine monophosphate-activated protein kinase (AMPK) inhibitor, compound C (1 µM), significantly decreased the induction of thermogenic proteins expressions mediated by 2'-FL, indicating that the 2'-FL-enhanced beige cell formation was partially dependent on the AMPK pathway. In conclusion, 2'-FL effectively promoted the browning of white adipose in vitro.

Folic acid alleviates lead acetate-mediated cardiotoxicity by down-regulating the expression levels of Nrf2, HO-1, GRP78, and CHOP proteins.

The purpose of this study was to explore the interventional effects of folic acid on the heart damage caused by lead acetate exposure. Twenty-four 60-day-old male Sprague-Dawley (SD) rats were randomly divided into 4 groups with 6 rats in each group. The control group (C group) was normal rats; the lead exposure group (L group) rats drank 0.2% lead acetate solution freely for 14 days. The rats in the intervention group (T group) were given 0.2% lead acetate solution for 14 days, respectively, and 0.4 mg/kg BW folic acid solution was given to the rats by gavage on the 7th day of lead administration. The rats in the folic acid group (group E) were given 0.4 mg/kg BW folic acid solution by gavage. To weigh rat body weight and heart weight, calculate heart index, and observe the expression level of nuclear factor erythroid 2-related factor 2(Nrf2), heme oxygenase 1(HO-1), glucose-regulated protein 78/binding immunoglobulin protein (GRP78), and C/EBP-homologous protein (CHOP) by immunofluorescence method. The results showed that compared with group C, serum lead levels in group L and T were significantly increased (P < 0.05); superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSH-PX) levels in group L were significantly decreased (P < 0.05), and malondialdehyde (MDA) content was significantly higher increased (P < 0.05), and the GSH-PX content in group T were significantly increased in group L (P < 0.05), and the MDA content in group T was significantly lower than that in group L (P < 0.05). Compared with group C, the expression of Nrf2, HO-1, GRP78, and CHOP in group L increased significantly, and the difference was statistically significant (P < 0.05). Compared with the L group, the expression of Nrf2, HO-1, GRP78, and CHOP in the T group was reduced. Therefore, folic acid has a certain protective effect on the oxidative damage of lead-exposed rat heart tissue. Lead exposure will increase ROS, NO, MDA, and other oxidizing substances and reduce the level of GSH, SOD, CAT, GPx, and other antioxidant factors, which will lead to cardiac hypertrophy, cardiac index increase, oxidative stress, Nrf2, and HO-1. The expression of stress-related proteins such as GRP78 and CHOP also increased, leading to cardiomyocyte apoptosis. After a folic acid intervention, these changes can be significantly reversed.

The effects of lead exposure on the expression of IGF1R, IGFBP3, Aß40, and Aß42 in PC12 cells.

BACKGROUND: To investigate the effects of lead exposure and IGF1R inhibitor AG1024 on the expression of IGF1R and IGFBP3 in PC12 cells. It is clear that the mechanism of the related proteins inducing AD is regulated by them, thus providing theoretical guidance for the prevention and treatment of lead poisoning. METHODS: This study is mainly used PC12 neuron cell to cultivate and establish a corresponding lead exposure model, deal with cells with different concentrations of lead acetate respectively, divide the experiment into control group, 1 µmoL/L PbAc, 10 µmoL/L PbAc group, IGF1R inhibitor (AG1024) group, IGF1R inhibitor group (AG1024) + 1 µmoL/L PbAc group, IGF1R inhibitor group (AG1024) + 10 µmoL/L PbAc group, respective contamination's three periods of time 24 h, 48 h, and 72 h. Lead exposure dose on cell proliferation was examined by MTT. The protein expression of IGF1R and IGFBP3 in PC12 cells were tested by western blotting and immunohistochemistry, The expression of Aß40 and Aß42 in cell supernatant was determined by ELISA. RESULTS: Compared with the control group, the proliferation of the cells in the high-dose lead-exposed group was significantly inhibited (P < 0.05), and the expression of IGF1R and IGFBP3 was significantly decreased (P < 0.05); the contents of Aß40 and Aß42 were not statistically significant among the groups (P > 0.05). CONCLUSION: This study shows that lead can obviously down-regulate the expression of IGF1R and IGFBP3, lead and inhibitor can inhibit the proliferation of cells, promote the tendency of apoptosis, and damage the nervous system.

Effects of folic acid on oxidative damage of kidney in lead-exposed rats.

Introduction: Lead (Pb) has many applications in daily life, but in recent years, various problems caused by lead exposure have aroused people's concern. Folic acid is widely found in fruits and has received more attention for its antioxidant function. However, the role of folic acid in lead-induced kidney injury in rats is unclear. This study was designed to investigate the effects of folic acid on oxidative stress and endoplasmic reticulum stress in the kidney of rats caused by lead exposure. Methods: Forty specific pathogen-free male Rattus norvegicus rats were randomly divided into control, lead, intervention, and folic acid groups. The levels of SOD, GSH-Px, GSH, and MDA were measured by biochemical kits. The protein levels of Nrf2, HO-1, CHOP, and GRP78 were measured by immunofluorescence. Results: This study showed that lead exposure increased the blood levels of lead in mice. However, the intervention of folic acid decreased the levels of lead, but the difference was not statistically significant. Lead exposure causes oxidative stress by decreasing kidney SOD, GSH-Px, and GSH levels and increasing MDA levels. However, folic acid alleviated the oxidative damage caused by lead exposure by increasing the levels of GSH-Px and GSH and decreasing the levels of MDA. Immunofluorescence results showed that folic acid intervention downregulated the upregulation of kidney Nrf2, HO-1, GRP78, and CHOP expression caused by lead exposure. Discussion: Overall, folic acid alleviates kidney oxidative stress induced by lead exposure by regulating Nrf2 and HO-1, while regulating CHOP and GRP78 to mitigate apoptosis caused by excessive endoplasmic reticulum stress.

Alleviating Effects of Black Soybean Peptide on Oxidative Stress Injury Induced by Lead in PC12 Cells via Keap1/Nrf2/TXNIP Signaling Pathway.

Many researchers have found that Pb exposure can cause oxidative stress damage to the body's tissue. Black soybean peptide (BSP) has a variety of physiological functions, especially in terms of oxidative stress. Nevertheless, the mitigation function of BSPs on Pb-induced oxidative stress damage in PC12 cells has not been clearly defined. In this study, cell viability was detected by CCK8. Oxidative stress indicators, such as ROS, GSH/GSSG, MDA, SOD, CAT, GPx, and GR, were tested with biochemical kit. Protein expression of Keap1, Nrf2, and TXNIP was measured by Western blot. Compared with the control group, Pb reduced the cell viability of PC12 cells. However, BSP treatment significantly increased the viability of PC12 cells induced by lead exposure (p < 0.05). Lead can enrich the contents of MDA and ROS, but decrease the amount of CAT, SOD, GR, GPx, and GSH/GSSG in PC12 cells, while BSP can alleviate it (p < 0.05). Lead can enhance the expression of Keap1 and TXNIP proteins, but reduce Nrf2 expression. In contrast, BSPs reversed this phenomenon (p < 0.05). BSPs can alleviate oxidative stress injury induced by lead in PC12 cells through the Keap1/Nrf2/TXNIP signaling pathway.

Alleviating effects of pea peptide on oxidative stress injury induced by lead in PC12 cells via Keap1/Nrf2/TXNIP signaling pathway.

Background: Lead poisoning causes an oxidative stress response - a key "bridge" connecting various pathways - in the human body. Oxidative stress usually implies an imbalance between pro-oxidants and antioxidants. Moreover, Nrf2, Keap1, and TXNIP proteins play an essential role in oxidative stress. Some studies showed that pea peptides could alleviate the oxidative stress response. However, the effect and mechanism of pea peptide on oxidative stress response induced by lead in PC12 cells has not been reported. Aim: Investigating the effect and mechanism of pea peptides in alleviating oxidative damage in PC12 cells induced by lead. Methods: In this study, cell viability was measured by CCK8 (Cell Counting Kit-8). Superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx), reactive oxygen species (ROS), and lipid peroxidation (MDA) were measured using the corresponding Biochemical kits. The Keap1, Nrf2, and TXNIP protein expressions were tested using Western blot. Results: Pea peptides PP3, PP4, and PP6 could reverse the decrease of cell viability caused by lead exposure (P < 0.05), the elevation of ROS and MDA caused by lead exposure, and the decrease of CAT, SOD, GR, GPx, and GSH/GSSG caused by lead exposure (P < 0.05). Moreover, PP3, PP4, and PP6 could reduce the elevated expression of Keap1 and TXNIP caused by lead exposure; and increase the expression of Nrf2 (P < 0.05). Conclusion: PP3, PP4, and PP6 can alleviate lead-induced oxidative stress damage in PC12 cells, and the Nrf2/Keap1/TXNIP signaling pathway may play an essential role in this process.

Peptide amphiphile inspired self-assembled, ordered gold nanocomposites for improved sensitivity of electrochemical immunosensor: Applications in determining the total aflatoxin amount in food stuffs.

In peptide amphiphile, The positively charged amino acid arginine can inspire the ordered self-assembly of gold nanocomposites (AuNPs), transfer positive charge to AuNPs, and weaken the aggregation of AuNPs by electrostatic repulsion, whereas hydrophobic fatty acid chains regulate the self-assembly of AuNPs through hydrophobic interaction, which may be a novel strategy to overcome disordered arrangement and aggregation of AuNPs to obtain an ultra-sensitive electrochemical immunosensor for determining the total aflatoxin amount. In this study, a peptide amphiphile (C14R5), composed of five arginine residues as the hydrophilic chain and myristic acid as the hydrophobic chain, inspired AuNPs to form monodispersed hollow raspberry-like AuNPs (rasAuNPs). rasAuNPs could captured and immobilized large amounts of aflatoxin antigens via the Au-S bonds, resulting in binding to more anti-aflatoxin antibodies. In the absence of aflatoxins, the enriched antigens bound to abundant antibodies, resulting in a low blank signal current. By contrast, in the presence of aflatoxins, enough antibodies could bind to the targets and less antibodies could recognize the antigens, increasing the detection signal intensity. Under the optimal conditions, the developed sensor demonstrated a wide linear range (0.13-29.06 pg mL-1) and a low limit of detection for total aflatoxins (0.05 pg mL-1) using a mixed standard (AFB1: AFB2: AFG1: AFG2 with a weight ratio of 1:1:1:1) in peanut, peanut milk, and maize powder samples. Hence, this novel strategy improves the sensitivity of electrochemical sensors and can be easily applied to detect other small molecule compound for the purpose of food safety.

[Effects of maternal lead exposure on the expression of Abeta40 in the hippocampus of the filial mice].

OBJECTIVE: To investigate the lead exposure of pregnant and lactating mice on the expression of beta-amyloid 40 (Abeta40) in the hippocampus of filial mice, in order to reveal the mechanism of neurotoxicity induced by lead. METHODS: Lead exposure was conducted through freely drinking lead acetate solution with dosages of 0.3 g/L, 1.0 g/L and 3.0 g/L respectively. The contents of lead in blood and hippocampus of the filial mice (10 mice in each group) were determined 7, 14 and 21 days after their birth. The expression of Abeta40 in hippocampus of all filial mice in various dosage groups was determined on the 21st day after birth by immunohistochemical assay. RESULTS: The lead levels in blood and hippocampus of 7, 14 and 21 day-old filial mice in lead exposure groups were higher than those in control group (P < 0.05). The results of immunohistochemistry showed that Abeta40 was mainly located in the cytoplasm. The area density of positive immune reaction of Abeta40 in CA1 field of hippocampus in three lead exposure groups were higher than that in the control group (P < 0.05), but the average gray value of Abeta40 positive immune reaction in CA1 field of hippocampus in lead exposure groups was lower than that in control group (P < 0.05). CONCLUSION: Maternal lead exposure may induce the accumulation of lead in filial mice, and enhance the aggregation of Abeta40 in hippocampus of their offspring, which might cause learning and memory damage of filial mice.

Perinatal Lead Exposure Alters Calsyntenin-2 and Calsyntenin-3 Expression in the Hippocampus and Causes Learning Deficits in Mice Post-weaning.

Calsyntenin-2 (Clstn2) and calsyntenin-3 (Clstn3) are the members of the cadherin superfamily and function to regulate the postsynaptic activity. Both proteins are known to play an important role in memory and learning. This study was designed to test the hypothesis that exposure of mothers to Pb in drinking water may alter the expression of Clstn2 and Clstn3 in offspring, which contributes to the Pb-induced learning deficiency. Pregnant mice were exposed to Pb in drinking water as Pb acetate from gestation to weaning. At the postnatal day 21, the learning and memory ability of pups was tested by Morris water maze, and the blood and brain tissues from pups were collected for metal and protein analyses. Data showed that perinatal Pb exposure resulted in a dose-dependent increase of Pb concentrations in blood (6-20-fold), hippocampus (2-7-fold), and cerebral cortex (2-8-fold) in offspring, as compared to controls (p < 0.05).The ability of learning and memory was decreased in lead exposure group, as compared to controls (p < 0.05). Both immunofluorescence and Western blot analyses revealed a striking difference in the expression of Clstn2 vs. Clstn3 following perinatal Pb exposure. In pregnant mice exposed to 0.1%, 0.2%, and 0.5% Pb, the expression of Clstn2 in offspring showed a Pb dose-related decrease by 39.2%, 76.5%, and 96.1% in hippocampus and by12.5%, 59.4%, and 78.1% in cerebral cortex, respectively (p < 0.05). In contrast, Clstn3 expression in these offspring brain regions was significantly increased (p < 0.05), after perinatal Pb exposure. The nature of Pb differential effect on Clstn2 and Clstn3 remains unknown. These observations suggest that Clstn2 and Clstn3 may have different roles in synaptic development and differentiation. Pb-induced learning defects may partly relate to the altered expression of calsyntenin proteins.

Optimization of the Antimicrobial Effects of Surfactin against Bacillus cereus Spores.

ABSTRACT: The purpose of this study was to establish a three-variable bactericidal model of temperature, time, and concentration to determine the optimal conditions for Bacillus cereus spore inactivation by surfactin. To obtain the binary regression equation of the inactivated spore model, a total of 17 simulations were performed using response surface methodology. The experimental results showed that the three factors each had a discernible but nonequal impact on the inactivation response value. Multiple regression analysis of experimental results using Design-Expert software yielded the following equation: Y = 1.47 + 0.39ξ1(temperature) + 0.38ξ2(time) + 0.39ξ3(concentration) - 0.20ξ1ξ2 + 0.22ξ1ξ2 - 0.12ξ2ξ3 - 0.23ξ12 - 0.11ξ22 - 0.40ξ32. Optimal inactivation of spores was achieved by treatment with surfactin at a concentration of 4 mg/mL for 40 h at 53°C, with the response value reaching 1.8. The spores were treated with surfactin under these conditions; the microstructural changes of spores were observed by use of scanning electron microscopy. We found that the structures of the outer wall of the spores were damaged, whereas the spores in the control sample showed no visible damage.