Acrylamide-Aggravated Liver Injury by Activating Endoplasmic Reticulum Stress in Female Mice with Diabetes.

Acrylamide (ACR) is a common industrial contaminant with endocrine-disrupting toxicity. Numerous studies have indicated that females and diabetics are more sensitive to environmental contaminants. However, it remains unknown whether female diabetics are susceptible to ACR-induced toxicity and its potential mechanisms. Thus, the female ACR-exposure diabetic Balb/c mice model was established to address these issues. Results showed that ACR could induce liver injury in normal mice and cause more serious inflammatory cell infiltration, hepatocyte volume increase, and fusion in diabetic mice liver. Meanwhile, ACR could lead to exacerbation of diabetic symptoms in diabetic mice by disturbing the glucose and lipid metabolism in the liver, which mainly manifests as the accumulation of liver glycogen and liver lipids, the reduction of the activity/content of glycolytic and metabolizing enzyme as well as pentose phosphatase, upregulation of the gene expression in fatty acid transporter and gluconeogenesis, and downregulation of the gene expression in fatty acid synthesis and metabolism. Moreover, ACR exposure could induce oxidative stress, inflammation, and endoplasmic reticulum stress in the liver by a decrease in hepatic antioxidant enzyme activity and antioxidant content, an increase in inflammatory factor levels, and a change in the related protein expression of endoplasmic reticulum stress (ERS) and apoptosis-related pathways in diabetic mice. Statistical analysis results revealed that ACR-induced liver injury was highly correlated with inflammation and oxidative stress, and ERS and diabetic mice had a higher risk of liver injury than normal mice. Overall results suggested that female diabetic mice easily suffer from ACR-induced toxicity, and the reason was that ACR could induce further damage to the liver by worsening the condition of inflammation, oxidative stress, and ERS in the liver.

A review of cumulative toxic effects of environmental endocrine disruptors on the zebrafish immune system: Characterization methods, toxic effects and mechanisms.

Environmental endocrine disrupting chemicals (EDCs), are a type of exogenous organic pollutants, are ubiquitous in natural aquatic environments. Currently, in addition to neurological, endocrine, developmental and reproductive toxicity, ecotoxicology studies on immunotoxicity are receiving increasing attention. In this review, the composition of immune system of zebrafish, the common indicators of immunotoxicity, the immunotoxicity of EDCs and their molecular mechanism were summarized. We reviewed the immunotoxicity of EDCs on zebrafish mainly in terms of immune organs, immunocytes, immune molecules and immune functions, meanwhile, the possible molecular mechanisms driving these effects were elucidated in terms of endocrine disruption, dysregulation of signaling pathways, and oxidative damage. Hopefully, this review will provide a reference for further investigation of the immunotoxicity of EDCs.

RNA-Seq analysis offers insight into the TBBPA-DHEE-induced endocrine-disrupting effect and neurotoxicity in juvenile zebrafish (Danio rerio).

Tetrabromobisphenol A bis(2-hydroxyethyl) ether (TBBPA-DHEE) is the major TBBPA derivative. It has been detected in different environmental samples. Previous studies show that TBBPA-DHEE caused neurotoxicity in rats. In this study, juvenile zebrafish were exposed to various concentrations of TBBPA-DHEE to ascertain the potential neurotoxicity of TBBPA-DHEE, the chemical, and its possible molecular mechanism of action. Behavioral analysis revealed that TBBPA-DHEE could significantly increase the swimming distance and speed in the 1.5 mg/L group compared to the control. In contrast, the swimming distance and speed were significantly reduced in the 0.05 and 0.3 mg/L groups, affecting learning, memory, and neurodevelopment. Similarly, TBBPA-DHEE exposure caused a concentration-dependent significant increase in the levels of excitatory neurotransmitters, namely, dopamine, norepinephrine, and epinephrine, which could be attributed to the change observed in zebrafish behavior. This demonstrates the neurotoxicity of TBBPA-DHEE on juvenile zebrafish. The concentration-dependent increase in the IBR value revealed by the IBR index reveals the noticeable neurotoxic effect of TBBPA-DHEE. Transcriptomic analysis shows that TBBPA-DHEE exposure activated the PPAR signaling pathways, resulting in a disturbance of fatty acid (FA) metabolism and changes in the transcript levels of genes involved in these pathways, which could lead to lipotoxicity and hepatotoxicity. Our findings demonstrate a distinct endocrine-disrupting response to TBBPA-DHEE exposure, possibly contributing to abnormal behavioral alterations. This study provides novel insights into underlying the mechanisms and effects of TBBPA-DHEE on aquatic organisms, which may be helpful forenvironmental/human health risk assessments of the emerging pollutant.

Role of autonomic nervous system in BDE-209 maternal exposure induced immunotoxicity in female offspring.

Decabrominated diphenyl ether (BDE-209) is a typical persistent organic pollutant that can cross the placental barrier, increasing the exposure risk for offspring. Norepinephrine (NE) from nerve terminals and acetylcholine (Ach) can bind to specific receptors on immune cells, inhibit the immune function of the body then cause immunotoxicity. However, whether maternal exposure to BDE-209 could lead to immunotoxicity in the offspring by acting on the sympathetic and parasympathetic nervous systems remains unclear. In view of this, the pregnancy and lactation rat BDE-209 exposure model was established and the results demonstrated that pregnancy and lactation BDE-209 exposure could induce immunotoxicity to female offspring via affecting immunopathology (hematological and biochemical parameters, organ indices, and spleen histopathological), decreasing humoral immunity (serum hemolysin, immunoglobulins, and cytokine productions), damaging cellular immunity (splenic lymphocytes and spleen cytokine productions), and restraining nonspecific immunity. Moreover, a dramatically significant correlation was observed between spleen nerve indices and immunity indices. Additionally, the mechanism revealed that maternal BDE-209 exposure caused offspring immunotoxicity through (1) activating MHC/PKCθ/NF-κB pathway; (2) promoting sympathetic nervous pathway, by upregulating the expression of ß2AR protein, which in turn elevating cAMP, following activate PKA and phosphorylate CREB, ultimately leading to immunotoxicity;(3) activating parasympathetic nerve pathway by reducing the binding with Ach and α7nAchR, upregulating the expression of JAK2 and phosphorylating STAT3, induced immunotoxicity of female offspring.

Overview of deltamethrin residues and toxic effects in the global environment.

Pyrethroids are synthetic organic insecticides. Deltamethrin, as one of the pyrethroids, has high insecticidal activity against pests and parasites and is less toxic to mammals, and is widely used in cities and urban areas worldwide. After entering the natural environment, deltamethrin circulates between solid, liquid and gas phases and enters organisms through the food chain, posing significant health risks. Increasing evidence has shown that deltamethrin has varying degrees of toxicity to a variety of organisms. This review summarized worldwide studies of deltamethrin residues in different media and found that deltamethrin is widely detected in a range of environments (including soil, water, sediment, and air) and organisms. In addition, the metabolism of deltamethrin, including metabolites and enzymes, was discussed. This review shed the mechanism of toxicity of deltamethrin and its metabolites, including neurotoxicity, immunotoxicity, endocrine disruption toxicity, reproductive toxicity, hepatorenal toxicity. This review is aim to provide reference for the ecological security and human health risk assessment of deltamethrin.

Emerging bio-dispersant and bioremediation technologies as environmentally friendly management responses toward marine oil spill: A comprehensive review.

Marine oil spills emanating from wells, pipelines, freighters, tankers, and storage facilities draw public attention and necessitate quick and environmentally friendly response measures. It is sometimes feasible to contain the oil with booms and collect it with skimmers or burn it, but this is impracticable in many circumstances, and all that can be done without causing further environmental damage is adopting natural attenuation, particularly through microbial biodegradation. Biodegradation can be aided by carefully supplying biologically accessible nitrogen and phosphorus to alleviate some of the microbial growth constraints at the shoreline. This review discussed the characteristics of oil spills, origin, ecotoxicology, health impact of marine oils spills, and responses, including the variety of remedies and responses to oil spills using biological techniques. The different bioremediation and bio-dispersant treatment technologies are then described, with a focus on the use of green surfactants and their advances, benefits/drawbacks. These technologies were thoroughly explained, with a timeline of research and recent studies. Finally, the hurdles that persist as a result of spills are explored, as well as the measures that must be taken and the potential for the development of existing treatment technologies, all of which must be linked to the application of integrated procedures.

Purification and characterization of Se-enriched Grifola frondosa glycoprotein, and evaluating its amelioration effect on As3+ -induced immune toxicity.

BACKGROUND: Selenium (Se)-enriched glycoproteins have been a research highlight for the role of both Se and glycoproteins in immunoregulation. Arsenic (As) is a toxicant that is potentially toxic to the immune function and consequently to human health. Several reports suggested that Se could reduce the toxicity of heavy metals. Moreover, more and more nutrients in food had been applied to relieve As-induced toxicity. Hence glycoproteins were isolated and purified from Se-enriched Grifola frondosa, and their preliminary characteristics as well as amelioration effect and mechanism on As3+ -induced immune toxicity were evaluated. RESULTS: Four factions, namely Se-GPr11 (electrophoresis analysis exhibited one band: 14.32 kDa), Se-GPr22 (two bands: 20.57 and 31.12 kDa), Se-GPr33 (three bands: 15.08, 20.57 and 32.78 kDa) and Se-GPr44 (three bands: 16.73, 32.78 and 42.46 kDa), were obtained from Se-enriched G. frondosa via DEAE-52 and Sephacryl S-400 column. In addition, Se-GPr11 and Se-GPr44 are ideal proteins that contain high amounts of almost all essential amino acids. Thereafter, the RAW264.7 macrophage model was adopted to estimate the effect of Se-GPr11 and Se-GPr44 on As3+ -induced immune toxicity. The results showed that the pre-intervention method was the best consequent and the potential mechanisms were, first, by improving the oxidative stress state (enhancing the activity of superoxide dismutase and glutathione peroxidase, decreasing the levels of reactive oxygen species and malondialdehyde); secondly, through nuclear factor-κB and mitogen-activated protein kinase-mediated upregulation cytokines (interleukin-2 and interferon-γ) secretion induced by As3+ . CONCLUSION: The results suggested Se-enriched G. frondosa may be a feasible supplement to improve health level of the As3+ pollution population. © 2021 Society of Chemical Industry.

Typical neurobehavioral methods and transcriptome analysis reveal the neurotoxicity and mechanisms of di(2-ethylhexyl) phthalate on pubertal male ICR mice with type 2 diabetes mellitus.

In the present study, the neurotoxicity and mechanisms of di-(2-ethylhexyl) phthalate (DEHP) exposure on pubertal normal (P-normal) and pubertal type 2 diabetes mellitus (P-T2DM) mice were investigated by typical neurobehavioral methods and transcriptome analysis. Pubertal male ICR mice were orally exposed to DEHP (0.18, 1.8, 18 and 180 mg/kg/d) for 3 weeks. In Open field test, DEHP significantly increased the time in central area staying and decreased the total distance and clockwise (CW) rotation of P-normal and P-T2DM mice. Morris water maze showed that DEHP significantly increased the latency in locating platform and decreased the original platform quadrant and residence time in target quadrant of P-normal and P-T2DM mice. Transcriptome analysis results revealed the effects of DEHP exposure on neural signaling pathway including biogenic amines neurotransmitters, nerve receptors, neurobiological processes, etc. Enzyme-linked immunosorbent assay (ELISA) and western blotting results showed that DEHP significantly decreased the contents of 5-HT, cAMP, GABA and Ca2+, the levels of CREB, phosphorylation of PKA, ERK1/2 and CREB, increased the levels of CaM and phosphorylation of CaMKII in P-normal and P-T2DM mice. Factorial analysis results showed that P-T2DM mice were more sensitive than those of P-normal mice. The potential neurotoxicity mechanism of DEHP may be synergistically mediated by the cAMP-PKA-ERK1/2-CREB signaling and the Ca2+ signaling pathway.

Transcriptome analysis revealed the mechanism of the metabolic toxicity and susceptibility of di-(2-ethylhexyl)phthalate on adolescent male ICR mice with type 2 diabetes mellitus.

The prevalence of adolescent type 2 diabetes mellitus (A-T2DM) is increasing year by year. Di-(2-ethylhexyl)phthalate (DEHP), a widely used plasticizer, could exacerbate type 2 diabetes mellitus (T2DM). The study aimed to investigate the metabolic toxicity, susceptibility and mechanism of DEHP exposure to A-T2DM. DEHP was administered orally (0, 0.18, 1.8, 18, and 180 mg/kg/day) for 3 weeks to adolescent normal mice (A-normal mice) and established A-T2DM mice. The results of fasting blood glucose (FBG) and glycated hemoglobin (HbA1c) levels showed that the susceptibility of A-T2DM mice to DEHP exposure was more significant than that of A-normal mice. DEHP, interfering with glucose and lipid metabolism of A-normal and A-T2DM mice, caused the body weight increase of A-normal mice and decrease of A-T2DM mice. Besides, DEHP could cause more injury of cardiovascular, hepatic and renal function to A-T2DM mice than A-normal mice. Hepatic transcriptome analysis revealed that DEHP exposure interfered with the biological feedback adjustment of endocrine and metabolic system in A-T2DM mice and then led to the development of T2DM. According to the transcriptome results, insulin signaling transduction pathway was applied and researched by immunoassay. It was discovered that DEHP reduced insulin sensitivity and disturbed insulin signaling transduction, glucose utilization, lipid synthesis and protein synthesis. Collectively, DEHP could disturb the endocrine and metabolic functions and increase the insulin resistance in adolescent mice. Moreover, the adolescent T2DM mice are more sensitive to DEHP-induced endocrine and metabolic toxicity than the healthy adolescent mice.

Chromium malate alleviates high-glucose and insulin resistance in L6 skeletal muscle cells by regulating glucose uptake and insulin sensitivity signaling pathways.

Previous study revealed that chromium malate improved the regulation of fasting blood glucose and insulin resistance in type 2 diabetic rats. In this study, the effect of chromium malate on anti-high-glucose and improve insulin resistance activities in L6 skeletal muscle cells with insulin resistance and its acting mechanism were investigated. Chromium malate showed direct anti-high-glucose activity in vitro. The glucose levels had a significant downward trend compared to chromium trichloride. Compared with model group, chromium malate could significantly promote the secretion levels of GLUT-4, Akt, Irs-1, PPARγ, PI3K and p38-MAPK, promote AMPKß1 phosphorylation, and reduced the level of p-Irs-1 in L6 cells with insulin resistance. And the relate mRNA expression of chromium malate was significantly increased. Chromium malate is more effective at improving the related proteins and mRNA expression than those of chromium trichloride and chromium picolinate. Pretreatment with the specific p38MAPK inhibitor completely inhibited the GLUT-4 and Irs-1 proteins and mRNA expression induced by the chromium malate when compared with model group, but GLUT-4 and Irs-1 proteins and mRNA expression was partially inhibited after inhibiting p38MAPK/PI3K expression. The results suggested that chromium malate had a beneficial influence on the improvement of controlling glucose levels and insulin resistance in L6 cells with insulin resistance by regulating proteins production and genes expression in glucose uptake and insulin sensitivity signaling pathways. The signaling pathways of glucose uptake and insulin sensitivity. This study shown that chromium malate could significant increase in the production levels of GLUT-4, p-AMPKß1, Akt, Irs-1, PPARγ, PI3K and p38-MAPK proteins and mRNA in L6 cells with insulin resistant. Pretreatment with the specific p38MAPK inhibitor completely inhibited the GLUT-4 and Irs-1 proteins and mRNA expression induced by the chromium malate compared to model group, but the proteins and mRNA were partially inhibited after inhibiting p38MAPK/PI3K. Therefore, chromium malate had beneficial influence on improvement of controlling glucose levels and insulin resistant in L6 cells by regulating proteins production and genes expression in glucose uptake and insulin sensitivity signaling pathways. The key proteins of glucose uptake and insulin sensitivity signaling pathways were p38MAPK, PI3K and PPARγ.

Large-scale isolation of high-purity anthocyanin monomers from mulberry fruits by combined chromatographic techniques.

Anthocyanins have attracted attention over the past several decades because of their beneficial health effects. In this research, a strategy combining column chromatography and high-speed countercurrent chromatography was developed for the separation of high-purity anthocyanin monomers from mulberry fruits. After purification using Amberlite XAD-7HP column with 80% ethanol (0.1% HCl), a fraction of anthocyanins mixtures with a purity of 68.6% was obtained. High-speed countercurrent chromatography with a biphasic solvent system of n-butanol/methyl tert-butyl ether/acetonitrile/water/trifluoroacetic acid (30:10:10:50:0.05, v/v) was used to separate the anthocyanin monomers. Three monomers of delphinidin-3-O-rutinoside, cyanidin-3-O-rutinoside, and cyanidin-3-O-glucoside were obtained, and identified by 1 H and 13 C NMR spectroscopy and high-performance liquid chromatography with electrospray ionization-mass spectrometry. The method developed in this work can be used to conduct large-scale separations of anthocyanin monomers from mulberry fruits and other plants.

Modulation of N-Methyl-D-Aspartate Receptors (NMDAR), Bcl-2 and C-Fos Gene Expressions on Exposure to Individual and Mixtures of Low Concentration Metals in Zebrafish (Danio rerio).

Currently, there is limited information on the toxicity of low concentration of metal mixtures in the environment. Of particular interest is the effect of low levels of metal mixtures on neurodevelopment of aquatic organisms. This study reports the neurological gene expressions after exposing zebrafish embryos to low concentration toxic heavy metals, 120 h post fertilization (hpf). Embryos were exposed to low concentration individual and mixtures of lead (Pb), mercury (Hg), arsenic (As), and cadmium (Cd). Quantitative real-time PCR was used to assess gene expressions. The findings of this study confirmed that exposure to low concentration heavy metals upregulated N-methyl-D-aspartate (NMDA) receptor subunits NMDAR2A (NR2A), NMDAR2B (NR2B), and NMDAR2D (NR2D) and B cell lymphoma (Bcl-2) genes. NR2A genes were significantly upregulated by 90 and 74%, respectively, on exposure to Pb + As and Pb + Cd. NR2B genes were upregulated by 85.3, 68.6, 62.7, and 62.7% on exposure to As, Pb + Hg, Pb + As, and Pb + Cd, respectively. Exposure to As, Pb + Cd, and Pb + Hg + As significantly upregulated Bcl-2 genes by 2.01-, 1.84-, and 1.80-fold, respectively. NR1A and C-fos gene expressions were not significantly different from control. Upregulation of NMDAR subunits and Bcl-2 genes in this study was largely a counter measure against insults from exposure to low concentration heavy metals. Principal component analysis confirmed the influence of low concentration individual and mixtures of Pb, Hg, As, and Cd on gene expression of NMDAR subunits and Bcl-2. These data suggest that altered expression of NMDA receptor subunits and Bcl-2 genes may explain toxicity of low concentration individual and mixtures of Pb, Hg, As, and Cd.

A multivariate assessment of innate immune-related gene expressions due to exposure to low concentration individual and mixtures of four kinds of heavy metals on zebrafish (Danio rerio) embryos.

Concerns over the potential health effects of mixtures of low concentration heavy metals on living organisms keep growing by the day. However, the toxicity of low concentration metal mixtures on the immune system of fish species has rarely been investigated. In this study, the zebrafish model was employed to investigate the effect on innate immune and antioxidant-related gene expressions, on exposure to environmentally relevant concentrations of individual and mixtures of Pb (0.01 mg/L), Hg (0.001 mg/L), As (0.01 mg/L) and Cd (0.005 mg/L). Messenger-RNA (mRNA) levels of IL1ß, TNF-α, IFNγ, Mx, Lyz, C3B and CXCL-Clc which are closely associated with the innate immune system were affected after exposing zebrafish embryos to metals for 120 h post fertilization (hpf). Individual and mixtures of metals exhibited different potentials to modulate innate-immune gene transcription. IL1ß genes were significantly up regulated on exposure to Pb + As (2.01-fold) and inhibited on exposure to Pb + Hg + Cd (0.13-fold). TNF-α was significantly inhibited on exposure to As (0.40-fold) and Pb + As (0.32-fold) compared to control. Metal mixtures generally up regulated IFNγ compared to individual metals. Additionally, antioxidant genes were affected, as CAT and GPx gene expressions generally increased, whiles Mn-SOD and Zn/Cu-SOD reduced. Multivariate analysis showed that exposure to individual metals greatly influenced modulation of innate immune genes; whiles metal mixtures influenced antioxidant gene expressions. This suggests that beside oxidative stress, there may be other pathways influencing gene expressions of innate immune and antioxidant-related genes. Low concentration heavy metals also affect expression of development-related (wnt8a and vegf) genes. Altogether, the results of this study clearly demonstrate that low concentration individual and mixtures of metals in aquatic systems will greatly influence the immune system. It is indicative that mechanisms associated with toxicity of metal mixtures is complex, however, further studies to elucidate them are ongoing in our research laboratory.

Isolation, purification and characterisation of selenium-containing polysaccharides and proteins in selenium-enriched Radix puerariae.

BACKGROUND: Selenium (Se) is an essential dietary mineral and Radix puerariae (RP) (the dried root of Pueraria lobata Willd.) is a botanical supplement widely used as a nutraceutical. Food enriched with Se provides a feasible and economic approach for production of organic Se compounds. However, little is known about Se-enriched RP and the structure of Se-containing polysaccharides and proteins derived from Se-enriched RP. RESULTS: The organic form of Se accounted for 82.42% of total content. Purification by DEAE-52 and Sephadex G-100 column chromatography yielded three single fractions--RP-SeP-11, RP-SeP-22 and RP-SeP-33--with Se contents of 0.9562 × 10⁻³, 0.6113 × 10⁻³ and 0.3827 × 10⁻³ g kg⁻¹, respectively. RP-SeP-11 (3.5 kDa) was made of glucose, RP-SeP-22 (19.6 kDa) was composed of xylose and glucose, and RP-SeP-33 (97.9 kDa) was made up galactose, mannose and glucose. Two Se-containing proteins were obtained with Se content of 3.175 × 10⁻³ and 4.328 × 10⁻³ g kg⁻¹, respectively. One appeared as three subunits with molecular masses of 43.0, 29.0 and 17.8 kDa while the other appeared as two subunits with molecular masses of 43.0 and 26.3 kDa. CONCLUSION: The results provide a basis for promoting the utilisation of RP resources enriched with Se as a promising tool for the food industry and are significant for its contribution to Se biochemistry in plants.

Association of tetrabromobisphenol A (TBBPA) with micro/nano-plastics: A review of recent findings on ecotoxicological and health impacts.

Despite the diverse research into the environmental impact of plastics, several stones have yet to be unraveled in terms of their ecotoxicological potential. Moreover, their detrimental impacts have become terrifying in recent years as the understanding of their tendency to associate and form cohorts with other emerging contaminants grew. Despite the hypothesis that microplastics may potentially adsorb organic pollutants, sequestering and making them not bioavailable for enhanced toxicity, evidence with pollutants such as Tetrabromobisphenol A (TBBPA) defers this assertion. TBBPA, one of the most widely used brominated flame retardants, has been enlisted as an emerging contaminant of serious environmental and human health concerns. Being also an additive to plasticware, it is not far to suspect that TBBPA could be found in association with micro/nanoplastics in our environment. Several pieces of evidence from recent studies have confirmed the micro/nanoplastics-TBBPA association and have exposed their compounded detrimental impacts on the environment and human health. This study, therefore, presents a comprehensive and up-to-date review of recent findings regarding their occurrence, factors that foster their association, including their sorption kinetics and isotherms, and their impacts on aquatic/agroecosystem and human health. The way forward and prospects for future studies were presented. This research is believed to be of significant interest to the readership due to its relevance to current environmental challenges posed by plastics and TBBPA. The study not only contributes valuable insights into the specific interaction between micro/nanoplastics and TBBPA but also suggests the way forward and prospects for future studies in this field.

Protective Effect of Protocatechuic Acid on Oxidative Damage and Cognitive Impairment in Pb-Induced Rats.

Protocatechuic acid (PCA), a class of water-soluble phenolic acid abundant in the human diet, has been shown to be of great nutritional interest and to have medicinal value. However, the protective effects against lead (Pb)-induced body injury have not been elucidated. In this study, we explored the protective effect of PCA on Pb-induced oxidative damage and cognitive impairment in rats. The results showed that PCA could reduce the Pb content in rat bodies (blood, bone, brain, liver, and kidney) after Pb exposure. Moreover, PCA may inhibit Pb-induced oxidative damage by increasing the activity of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and decreasing the level of malondialdehyde (MDA) in the brain, liver, and kidney. In addition, PCA may alleviate Pb-induced learning and memory impairment by upregulating neurotransmitter levels; maintaining the normal function of N-methyl-D-aspartate receptors (NMDARs); and promoting Ca2+ influx, thus activating signaling molecules, related protein kinases, and transcription factors in the cAMP-PKA-CREB pathway. In general, PCA could reduce oxidative stress and ameliorate the learning and memory deficits in Pb-treated rats, indicating that PCA may be an effective preventive agent and treatment or plumbism.

Differential susceptibility of BRL cells with/without insulin resistance and the role of endoplasmic reticulum stress signaling pathway in response to acrylamide-exposure toxicity effects in vitro.

Acrylamide (ACR) is an endogenous food contaminant, high levels of ACR have been detected in a large number of foods, causing widespread concern. Since different organism states respond differently to the toxic effects of pollutants, this study establishes an insulin-resistant BRL cell model to explore the differential susceptibility of BRL cells with/without insulin resistance in response to acrylamide-exposure (0.0002, 0.02, or 1 mM) toxicity effects and its mechanism. The results showed that ACR exposure decreased glucose uptake and increased intracellular lipid levels by promoting the expression of fatty acid synthesis, transport, and gluconeogenesis genes and inhibiting the expression of fatty acid metabolism genes, thereby further exacerbating disorders of gluconeogenesis and lipid metabolism in insulin-resistant BRL cells. Simultaneously, its exposure also exacerbated BRL cells with/without insulin-resistant damage. Meanwhile, insulin resistance significantly raised susceptibility to BRL cell response to ACR-induced toxicity. Furthermore, ACR exposure further activated the endoplasmic reticulum stress (ERS) signaling pathway (promoting phosphorylation of PERK, eIF-2α, and IRE-1α) and the apoptosis signaling pathway (activating Caspase-3 and increasing the Bax/Bcl-2 ratio) in BRL cells with insulin-resistant, which were also attenuated after ROS scavenging or ERS signaling pathway blockade. Overall results suggested that ACR evokes a severer toxicity effect on BRL cells with insulin resistance through the overactivation of the ERS signaling pathway.

Effects of Freeze-Thaw Pretreatment Combined with Hot Air on Snake Gourd (Trichosanthes anguina L.).

Snake gourd is a seasonal vegetable with a high water content and medicinal value, but the short harvest period limits the large-scale application of snake gourd. Therefore, the effects of freeze-thaw pretreatment (FT) combined with hot air (HD) on the drying characteristics, active ingredients and bioactivities of snake gourd were investigated. The results showed that FT pretreatment reduced browning and shortened the drying time by 44%; the Page model was the best fit for describing the drying process. The polysaccharide contents (21.70% in alcoholic extract (TG1) and 44.34% in water extract (TG2)) and total phenol contents (1.81% in TG1 and 0.88% in TG2) of snake gourd pretreated by FT-HD were higher than those of snake gourd pretreated by the corresponding HD treatment. The FT pretreatment decreased the molecular weight of snake gourd polysaccharides and increased the molar ratio of glucose. The extracts pretreated by FT-HD showed greater chemical, cellular antioxidant capacity and α-amylase and α-glucosidase inhibition than those pretreated by HD. FT-HD can be recommended for achieving a short drying time and high quality of snake gourd and can be used for the drying of other fruits and vegetables.

A review of heavy metal risks around e-waste sites and comparable municipal dumpsites in major African cities: Recommendations and future perspectives.

In Africa, the effects of informal e-waste recycling on the environment are escalating. It is regularly transported from developed to developing nations, where it is disassembled informally in search of precious metals, thus increasing human exposure to harmful compounds. Africa has a serious problem with e-waste, as there are significant facilities in Ghana and Nigeria where imported e-waste is unsafely dismantled. however, because they are in high demand and less expensive than new ones, old electronic and electrical items are imported in large quantities, just like in many developing nations. After that, these objects are frequently scavenged to recover important metals through heating, burning, incubation in acids, and other techniques. Serious health hazards are associated with these activities for workers and individuals close to recycling plants. At e-waste sites in Africa, there have been documented instances of elevated concentrations of hazardous elements, persistent organic pollutants, and heavy metals in dust, soils, and vegetation, including plants consumed as food. Individuals who handle and dispose of e-waste are exposed to highly hazardous chemical substances. This paper examines heavy metal risks around e-waste sites and comparable municipal dumpsites in major African cities. Elevated concentrations of these heavy metals metal in downstream aquatic and marine habitats have resulted in additional environmental impacts. These effects have been associated with unfavourable outcomes in marine ecosystems, such as reduced fish stocks characterized by smaller sizes, increased susceptibility to illness, and decreased population densities. The evidence from the examined studies shows how much e-waste affects human health and the environment in Africa. Sub-Saharan African nations require a regulatory framework that includes specialized laws, facilities, and procedures for the safe recycling and disposal of e-waste.

Neurodevelopmental toxicity and molecular mechanism of environmental concentration of tetrabromobisphenol A bis (2- hydroxyethyl) ether exposure to sexually developing male SD rats.

Tetrabromobisphenol A bis (2- hydroxyethyl) ether (TBBPA-DHEE), as one of the main derivatives of Tetrabromobisphenol A, been attracted attention for its health risks. In this study, the neurotoxicity, mechanism, and susceptivity of TBBPA-DHEE exposure to sexually developing male rats were systematically studied. Neurobehavioral research showed that TBBPA-DHEE exposure could significantly affect the behavior, learning,and memory abilities of male-developing rats, and aggravate their depression. TBBPA-DHEE exposure could inhibit the secretion of neurotransmitters. Transcriptomics studies show that TBBPA-DHEE can significantly affect gene expression, and a total of 334 differentially expressed genes are enriched. GO function enrichment analysis shows that TBBPA-DHEE exposure can significantly affect the expression of genes related to synapses and cell components. KEGG function enrichment analysis shows that TBBPA-DHEE exposure can significantly affect the expression of signal pathways related to nerves, nerve development, and signal transduction. Susceptibility analysis showed that female rats were more susceptible to TBBPA-DHEE exposure than male rats. Therefore, TBBPA-DHEE exposure has neurodevelopmental toxicity to male developmental rats, and female developmental rats are more susceptible than male developmental rats. Its possible molecular mechanism is that TBBPA-DHEE may inhibit the secretion of neurotransmitters and affect signal pathways related to neurodevelopment and signal transduction.