Sepiolite-Supported Manganese Oxide as an Efficient Catalyst for Formaldehyde Oxidation: Performance and Mechanism.

The current study involved the preparation of a number of MnOx/Sep catalysts using the impregnation (MnOx/Sep-I), hydrothermal (MnOx/Sep-H), and precipitation (MnOx/Sep-P) methods. The MnOx/Sep catalysts that were produced were examined for their ability to catalytically oxidize formaldehyde (HCHO). Through the use of several technologies, including N2 adsorption-desorption, XRD, FTIR, TEM, H2-TPR, O2-TPD, CO2-TPD, and XPS, the function of MnOx in HCHO elimination was examined. The MnOx/Sep-H combination was shown to have superior catalytic activities, outstanding cycle stability, and long-term activity. It was also able to perform complete HCHO conversion at 85 °C with a high GHSV of 6000 mL/(g·h) and 50% humidity. Large specific surface area and pore size, a widely dispersed active component, a high percentage of Mn3+ species, and lattice oxygen concentration all suggested a potential reaction route for HCHO oxidation. This research produced a low-cost, highly effective catalyst for HCHO purification in indoor or industrial air environments.

Baicalein inhibits apoptosis and autophagy induced by chlorpyrifos exposure to kidney of Cyprinus carpio through activation of PI3K/AKT pathway.

Chlorpyrifos (CPF), a widely used organophosphate pesticide that has caused large-scale contamination globally, has become a major concern. Baicalein (BAI), as a flavonoid extract, shows anti-inflammatory as well as antioxidant activities. The kidneys of fish serve to excrete toxins and are major target organs for environmental contaminants. However, it is not obvious whether BAI can counteract the damage caused by CPF exposure to fish kidneys. Therefore, we conducted a 30-day simulation of CPF poisoning and/or BAI treatment by adding 23.2 µg/L CPF to water and/or 0.15 g/kg BAI to feed. In the transmission electron microscopy results, we observed obvious phenomenon of autophagy and apoptosis in the CPF group, and the TUNEL staining and immunofluorescence of LC3B and p62 double-staining results confirmed that CPF induced autophagy and apoptosis in the kidney of common carp. Furthermore, CPF induced the increase of ROS level and inhibition of PI3K and Nrf2 pathways, which in turn triggered oxidative stress, autophagy and apoptosis in carp kidney according to western blot, RT-qPCR and kit assays. However, addition of BAI significantly alleviated oxidative stress, autophagy and apoptosis due to binding to PI3K protein. Additionally, through phylogenetic tree and structural domain analyses, we also found that the binding sites of BAI and PI3K are conserved in a variety of representative species. These results suggest that BAI antagonizes CPF-caused renal impairments in carp involving the PI3K/AKT pathway and the Nrf2 pathway. Our findings provide new insights into the nephrotoxicity effects of CPF and the potential use of BAI as a detoxification agent for CPF intoxication.

Polystyrene nanoplastics induced cardiomyocyte apoptosis and myocardial inflammation in carp by promoting ROS production.

Nanoplastics (NPs) existing in aquatic ecosystem is an emerging environmental pollutant, which has become a nagging serious environmental problem. Miniaturized plastic fragments with different diameters have different penetration capabilities to body tissues, and thus may have different toxicity to the target organs. However, the specific toxicological effects and mechanisms of NPs with different particle sizes on aquatic animal hearts are still unknown. To this end, carps were directly exposed to the aqueous environment of polystyrene NPs (1000 µg/L, PS-NPs) with three particle sizes (50 nm, 100 nm and 400 nm), respectively, for 28 days. H&E and TUNEL staining displayed that exposed to PS-NPs of three diameters all caused myocardial tissue inflammation and cardiomyocyte apoptosis in carps. Of note, at the same exposure concentration, the damage caused by PS-NPs with particle size of 50 nm was more serious than that of 100 nm and 400 nm. Further research found that, in carp hearts exposed to PS-NPs, the levels of carp innate immunity-related components TLR4 and NOX2 were significantly higher than those in controls and were negatively correlated with the exposed particle size. The content of ROS increased significantly, the activities of antioxidant enzymes (CAT, SOD1 and Gpx1) decreased, and MDA accumulated. In addition, as the particle size of PS-NPs decreased, Th1 cells gradually replaced Th2 cells to dominate, the Th1/Th2 balance was dysregulated, and the expression of apoptosis-inducing pathway IGFBP3/p53/ACHE-related genes was increased, markedly. Overall, our study results demonstrated that PS-NPs exposure caused oxidative stress, resulting in inflammation and apoptosis in carp heart, and the degree of damage was negatively correlated with the particle size of PS-NPs. Our work enriched the theoretical basis for NPs toxicological research and shed new light on the risk of NPs exposure.

Cadmium exposure causes mitochondrial fission and fusion disorder in the pig hypothalamus via the PI3K/AKT pathway.

Cadmium (Cd) is the main environmental pollutant causing endocrine and nervous system dysfunction in animals. High doses of Cd cause cytotoxicity, including programmed necrosis and apoptosis, which has aroused widespread concern. Mitochondrial dynamics plays a key role in programmed necrosis and apoptosis of endocrine organs. Nevertheless, there is a lack of information on the relationship between Cd-induced programmed necrosis/apoptosis of the hypothalamus and the mitochondrial fusion-fission balance. Therefore, a hypothalamic injury model of Cd exposure was established by adding 20 mg/kg CdCl2 to the basic pig diet for 40 days. Analysis of the Cd toxicity mechanism was conducted by inductively coupled plasma mass spectrometry, hematoxylin and eosin staining, the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, and quantitative reverse transcription-polymerase chain reaction, as well as western blot analyses. The results suggested that exposure to Cd inhibited the expression of PI3K and AKT, interfered with the balance of mitochondrial fusion and division, downregulated the expression of Mfn2, Mfn1, and OPA1, and upregulated the expression of Drp1 and Mff, which led to cell apoptosis and programmed necrosis in the pig hypothalamus. This study finds that cadmium exposure leads to mitochondrial fission and fusion dysfunction in porcine hypothalamus via the PI3K/AKT pathway.

The antagonistic effect of selenium on lead-induced apoptosis and necroptosis via P38/JNK/ERK pathway in chicken kidney.

Lead (Pb), as a toxic heavy metal pollutant, has been paid much attention. Pb is often discharged into the environment through the soot, wastewater and waste residue in industrial production, which poses a great threat to animal health. Selenium (Se) is a trace element known to antagonize the toxicity caused by heavy metals. However, the interaction between Se and Pb in chicken kidney and its specific biological mechanism are still unclear. So, we constructed chicken models of Pb exposure and Pb, Se co-exposure. Therefore, we used western blot and qRT-PCR to detect the expression of related genes. The results showed that Pb activated the MAPK signaling pathway by up-regulating the expression of MARK pathway genes to induce the expression of pro-apoptotic genes and necroptosis-related genes. Se can regulate the MARK signaling pathway and attenuated the expression of MAPK pathway genes altered by Pb to reduce apoptosis and necroptosis of chicken kidney cells. Our study gives new ideas for the specific mechanism of Pb nephrotoxicity and provides a reference for comparative medicine and clinical medication.

Resveratrol relieves chlorothalonil-induced apoptosis and necroptosis through miR-15a/Bcl2-A20 axis in fish kidney cells.

Chlorothalonil (CT) is a commonly used fungicide and its excessive application seriously threatens aquatic life and human health. Resveratrol (RSV) is a natural polyphenol and can be used as a therapeutic and preventive agent for the treatment of various diseases. To explore the toxic mechanism of CT exposure on fish kidney cell, as well as the alleviation effect of RSV, we established CT poisoning and/or RSV treatment fish kidney cell models. Ctenopharyngodon idellus kidney (CIK) cell line was treated with CT (5 µg/L) and/or RSV (10 µM) for 48 h. The results showed that CT exposure activated cytochromeP450s (CYPs) including CYP1A1, CYP1B1 and CYP1C, caused malondialdehyde (MDA) accumulation, inhibited glutathione (GSH) levels and glutathione peroxidase (GPX) activities, increased the expression of miR-15a and downregulated BCL2 and TNFα-induced protein 3 (TNFAIP3, A20), triggered mitochondrial pathway mediated apoptosis and receptor interacting serine/threonine kinase (RIP)-dependent necroptosis in CIK cells. However, cell death under CT exposure could be relieved by RSV treatment through inhibiting the expression of CYP1 family genes and restoring miR-15a/BCL2-A20 axis disorders. Overall, we conclude that RSV could relieve CT-induced apoptosis and necroptosis through miR-15a/Bcl2-A20 axis in CIK cells. These results enrich the toxicological mechanisms of the CT and confirm that RSV can be used as a potential antidote for CT poisoning.

Dexmedetomidine ameliorates lipopolysaccharide-induced acute kidney injury in rats by inhibiting inflammation and oxidative stress via the GSK-3ß/Nrf2 signaling pathway.

Acute kidney injury (AKI) is a frequent and serious complication of sepsis; however, there are currently no effective therapies. Inflammation and oxidative stress are the major mechanisms implicated in lipopolysaccharide (LPS)-induced AKI. Dexmedetomidine (DEX) has been reported to have remarkable anti-inflammatory and antioxidant effects. Here, we examined the renoprotective effects of DEX and potential underlying mechanisms in rats with LPS-induced AKI. We analyzed renal function and structure; serum inflammatory cytokine; renal oxidant and antioxidant levels; and renal expression of glycogen synthase kinase-3ß (GSK-3ß)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway-related proteins in rats 4 hr after administration of LPS. Pretreatment with DEX improved renal function and significantly reduced the levels of inflammatory cytokines and oxidative stress markers. Treatment with DEX and the GSK-3ß inhibitor SB216367 promoted phosphorylation of GSK-3ß, induced Nrf2 nuclear translocation, and increased transcription of the Nrf2 target genes heme oxygenase-1 and NAD(P)H quinone oxidoreductase-1, primarily in renal tubules. Alpha-2-adrenergic receptor (α2-AR) antagonist atipamezole and imidazoline I 2 receptor (I 2 R) antagonist idazoxan reversed the effects of DEX. These results suggest that the renoprotective effects of DEX are mediated via α2-AR and I 2 R-dependent pathways that reduce inflammation and oxidative stress through GSK-3ß/Nrf2 signaling.

Dexmedetomidine alleviates lipopolysaccharide-induced acute kidney injury by inhibiting the NLRP3 inflammasome activation via regulating the TLR4/NOX4/NF-κB pathway.

Dexmedetomidine (DEX) prevents kidney damage caused by sepsis, but the mechanism of this effect remains unclear. In this study, the protective molecular mechanism of DEX in lipopolysaccharide (LPS)-induced acute kidney injury was investigated and its potential pharmacological targets from the perspective of inhibiting oxidative stress damage and the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome activation. Intraperitoneal injection of DEX (30 µg/kg) significantly improved LPS (10 mg/kg) induced renal pathological damage and renal dysfunction. DEX also ameliorated oxidative stress damage by reducing the contents of reactive oxygen species, malondialdehyde and hydrogen peroxide, and increasing the level of glutathione, as well as the activity of superoxide dismutase and catalase. In addition, DEX prevented nuclear factor-kappa B (NF-κB) activation and I-kappa B (IκB) phosphorylation, as well as the expressions of NLRP3 inflammasome-associated protein and downstream IL-18 and IL-1ß. The messengerRNA (mRNA) and protein expressions of toll-like receptor 4 (TLR4), NADPH oxidase-4 (NOX4), NF-κB, and NLRP3 were also significantly reduced by DEX. Their expressions were further evaluated by immunohistochemistry, yielding results were consistent with the results of mRNA and protein detection. Interestingly, the protective effects of DEX were reversed by atipamezole-an alpha 2 adrenal receptor (α2 AR) inhibitor, whereas idazoxan-an imidazoline receptor (IR) inhibitor failed to reverse this change. In conclusion, DEX attenuated LPS-induced AKI by inhibiting oxidative stress damage and NLRP3 inflammasome activation via regulating the TLR4/NOX4/NF-κB pathway, mainly acting on the α2 AR rather than IR.

Dexmedetomidine protects against lipopolysaccharide-induced early acute kidney injury by inhibiting the iNOS/NO signaling pathway in rats.

Increasing evidence has demonstrated that dexmedetomidine (DEX) possesses multiple pharmacological actions. Herein, we explored the protective effect and potential molecular mechanism of DEX on lipopolysaccharide (LPS)-induced early acute kidney injury (AKI) from the perspective of antioxidant stress. We found that DEX (30 µg/kg, i.p.) ameliorated the renal dysfunction and histopathological damage (tubular necrosis, vacuolar degeneration, infiltration of inflammatory cells and cast formation) induced by LPS (10 mg/kg). DEX also attenuated renal oxidative stress remarkably in LPS-induced early AKI, as evidenced by reduction in production of reactive nitrogen species, decreasing malondialdehyde levels, as well as increasing superoxide dismutase activity and glutathione content. DEX prevented activator protein-1 translocation, inhibited phosphorylation of I-kappa B (IκB) and activation of nuclear factor kappa B (NF-κB) in LPS-induced early AKI, as assessed by real-time quantitative polymerase chain reaction and protein levels of c-Jun, c-Fos, IκB and NF-κB. Notably, DEX pretreatment had the same effect as intraperitoneal injection of an inhibitor of inducible nitric oxide synthase inhibitor (1400W; 15 mg/kg), and inhibited the activity of renal inducible nitric oxide synthase (iNOS) and decreased the expression of iNOS mRNA and NO production. However, the protective effect of DEX on LPS-induced early AKI was reversed by the alpha 2 adrenal receptor (α2-AR) inhibitor atipamezole, whereas the imidazoline receptor inhibitor idazoxan did not. Taken together, DEX protects against LPS-induced early AKI in rats by inhibiting the iNOS/NO signaling pathway, mainly by acting on α2-ARs instead of IRs.

Co-exposure of decabromodiphenyl ethane and polystyrene nanoplastics damages grass carp (Ctenopharyngodon idella) hepatocytes: Focus on the role of oxidative stress, ferroptosis, and inflammatory reaction.

Decabromodiphenyl ethane (DBDPE) and polystyrene nanoplastics (PS-NPs) are emerging pollutants that seriously threaten the ecological safety of the aquatic environment. However, the hepatotoxicity effect of their combined exposure on aquatic organisms has not been reported to date. In, this study, the effects of single or co-exposure of DBDPE and PS-NPs on grass carp hepatocytes were explored and biomarkers related to oxidative stress, ferroptosis, and inflammatory cytokines were evaluated. The results show that both single and co-exposure to DBDPE and PS-NPs caused oxidative stress. Oxidative stress was induced by increasing the contents of pro-oxidation factors (ROS, MDA, and LPO), inhibiting the activity of antioxidant enzymes (CAT, GPX, T-SOD, GSH, and T-AOC), and downregulating the mRNA expressions of antioxidant genes (GPX1, GSTO1, SOD1, and CAT); the effects of combined exposure were stronger overall. Both single and co-exposure to DBDPE and PS-NPs also elevated Fe2+ content, promoted the expressions of TFR1, STEAP3, and NCOA4, and inhibited the expressions of FTH1, SLC7A11, GCLC, GSS, and GPX4; these effects resulted in iron overload-induced ferroptosis, where co-exposure had stronger adverse effects on ferroptosis-related biomarkers than single exposure. Moreover, single or co-exposure enhanced inflammatory cytokine levels, as evidenced by increased mRNA expressions of IL-6, IL-12, IL-17, IL-18, IL-1ß, TNF-α, IFN-γ, and MPO. Co-exposure exhibited higher expression of pro-inflammatory cytokines compared to single exposure. Interestingly, the ferroptosis inhibitor ferrostatin-1 intervention diminished the above changes. In brief, the results suggest that DBDPE and PS-NPs trigger elevated levels of inflammatory cytokines in grass crap hepatocytes. This elevation is achieved via oxidative stress and iron overload-mediated ferroptosis, where cytotoxicity was stronger under co-exposure compared to single exposure. Overall, the findings contribute to elucidating the potential hepatotoxicity mechanisms in aquatic organisms caused by co-exposure to DBDPE and PS-NPs.

Adverse childhood experiences predict internet gaming disorder in university students: the mediating role of resilience.

BACKGROUND: To investigate the relationship between adverse childhood experiences and internet gaming disorder (IGD) and the mediating role of resilience in the relationship between these two factors. METHODS: The adverse childhood experience scale, resilience scale and IGD Scale were administered to 9349 university students. Correlations and mediating effects were calculated among these scores. RESULTS: After controlling for sex and age, significant correlations among adverse childhood experiences, resilience and IGD were observed; resilience was a partial mediator variable in the relationship between adverse childhood experiences and IGD. CONCLUSIONS: The more adverse childhood experiences an individual has, the less their mental toughness and the greater their tendency to become addicted to internet games. Adverse childhood experiences can effectively predict IGD, and the risk of becoming addicted to the internet can be decreased by increasing one's mental toughness.

Anti-influenza activity of CPAVM1 protease secreted by Bacillus subtilis LjM2.

Bacillus spp. has been considered a promising source for identifying new antimicrobial substances, including anti-viral candidates. Here, we successfully isolated a number of bacteria strains from aged dry citrus peel (Chenpi). Of note, the culture supernatant of a new isolate named Bacillus subtilis LjM2 demonstrated strong inhibition of influenza A virus (IAV) infection in multiple experimental systems in vitro and in vivo. In addition, the anti-viral effect of LjM2 was attributed to its direct lysis of viral particles. Further analysis showed that a protease which we named CPAVM1 isolated from the culture supernatant of LjM2 was the key component responsible for its anti-viral function. Importantly, the therapeutic effect of CPAVM1 was still significant when applied 12 hours after IAV infection of experimental mice. Moreover, we found that the CPAVM1 protease cleaved multiple IAV proteins via targeting basic amino acid Arg or Lys. Furthermore, this study reveals the molecular structure and catalytic mechanism of CPAVM1 protease. During catalysis, Tyr75, Tyr77, and Tyr102 are important active sites. Therefore, the present work identified a special protease CPAVM1 secreted by a new strain of Bacillus subtilis LjM2 against influenza A virus infection via direct cleavage of critical viral proteins, thus facilitates future biotechnological applications of Bacillus subtilis LjM2 and the protease CPAVM1.

New Insights into How Melatonin Ameliorates Bisphenol A-Induced Colon Damage: Inhibition of NADPH Oxidase.

Bisphenol A (BPA) is an endocrine disruptor, widely employed, and detected in many consumer products and food items. Oral intake poses a great threat to intestinal health. Melatonin (MT) stands out as an endogenous, dietary, and therapeutic molecule with potent antioxidant capacity. To explore the protective effect of MT against BPA-induced colon damage and the role of NADPH oxidase (NOX) in this process, we established mice and colonic epithelial cell (NCM460) models of BPA exposure and treated with MT. In vitro and in vivo results showed that MT ameliorated BPA-induced oxidative stress, DNA damage, and the G2/M cell cycle arrest. MT also downregulated the expression of NOX family-related genes, reversed the inhibition of the base excision repair (BER) pathway, promoted the activation of non-homologous end-joining (NHEJ) pathway, and suppressed the mRNA and protein expression of ATM, Chk1/2, and p53. Diphenyleneiodonium chloride (DPI), a NOX-specific inhibitor, also attenuated the toxic effects of BPA on NCM460 cells. Furthermore, molecular docking revealed that MT could bind to NOX. Conclusively, our finding suggested that MT can ameliorate BPA-induced colonic DNA damage by scavenging NOX-derived ROS, which further attenuates G2/M cell cycle arrest dependent on the ATM-Chk1/2-p53 axis.

TBBPA causes apoptosis in grass carp hepatocytes involving destroyed ER-mitochondrial function.

Tetrabromobisphenol A (TBBPA) is the most-produced brominated flame retardant, which can be found in various industrial and household products. Studies have shown that TBBPA has hepatotoxicity, and could pose a risk to aquatic animals. The endoplasmic reticulum (ER) and mitochondria are two important organelles that are highly dynamic in cells, the homeostasis and orchestrated interactions of which are crucial to maintaining cellular function. The aim of this study was to explore the involvement of ER-mitochondria crosstalk in TBBPA-induced toxicity in aquatic animals' hepatocytes. Herein, we exposed grass carp hepatocytes (L8824 cells) to different concentrations of TBBPA. Our experimental results suggested that TBBPA exposure suppressed cell viability and caused apoptosis of L8824 cells. TBBPA treatment upregulated expressions of ER stress markers, increased reactive oxygen species (ROS) and mitochondrial Ca2+ levels, and reduced mitochondrial membrane potential (MMP) in L8824 cells. However, the pretreatment of 2-aminoethoxydiphenyl borate (2-APB) could alleviate TBBPA-induced cell apoptosis, ER stress, and mitochondrial dysfunction. Additionally, 2-APB pretreat relieved ER-mitochondrial contact and the expression of ER-mitochondrial function-related genes induced by high-dose TBBPA. Taken together, these results indicated that TBBPA caused grass carp hepatocyte apoptosis by destroying ER-mitochondrial crosstalk.

Melatonin attenuates bisphenol A-induced colon injury by dual targeting mitochondrial dynamics and Nrf2 antioxidant system via activation of SIRT1/PGC-1α signaling pathway.

Industrial advancement has led to an increase in the production and usage of bisphenol A (BPA), thereby resulting in serious environmental pollution problems. BPA ingestion causes multiorgan toxicity. However, the exact mechanism underlying BPA-induced colon damage remains elusive. Moreover, no safe treatment is available to alleviate BPA-induced colon injury. Therefore, the in vivo and in vitro approaches were employed to detect the protective effects of melatonin (MT) on BPA-induced colon injury and to determine the underpinning molecular mechanisms. MT treatment of mice and the colonic epithelial cells NCM460 alleviated BPA-induced colon damage by inhibiting the mitochondrial dynamic imbalance, enhancing mitochondrial respiratory chain (MRC) complexes expression, reducing reactive oxygen species (ROS) production, and suppressing apoptosis and necroptosis. MT upregulated the proteins level of silent information regulator 1 (SIRT1) and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), which further increased the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and the downstream antioxidant target genes heme oxygenase-1 (HO-1) and NAD(P)H quinone redox enzyme-1 (NQO1). Treatment with the SIRT1 inhibitor EX527 effectively reversed the MT-induced upregulation of the aforementioned protein levels. Thus, the MT-activated Sirt1/PGC-1α signaling pathway restored the mitochondrial dynamic balance and activated the Nrf2 antioxidant axis to attenuate BPA-induced colon injury. These results demonstrate that MT supplementation may potentially mitigate BPA toxicity.

New insights into brain injury in chickens induced by bisphenol A and selenium deficiency-Mitochondrial reactive oxygen species and mitophagy-apoptosis crosstalk homeostasis.

Bisphenol A (BPA), a component of plastic products, can penetrate the blood-brain barrier and pose a threat to the nervous system. Selenium (Se) deficiency can also cause nervous system damage. Resulting from the rapid industrial development, BPA pollution and Se deficiency often coexist. However, it is unclear whether brain damage in chickens caused by BPA exposure and Se deficiency is related to the crosstalk disorder between mitophagy and apoptosis. In this study, 60 chickens (1 day old) were fed with a diet that contained 20 mg/kg BPA but was insufficient in Se (only 0.039 mg/kg) for 42 days to establish a chicken brain injury model. In vitro, the primary chicken embryo brain neurons were treated for 24 h with Se-deficient medium containing 75 µM BPA. The results showed that BPA exposure and Se deficiency inhibited the expression of the mitochondrial respiratory chain complex in brain neurons, and a large number of mitochondrial reactive oxygen species were released. Furthermore, the expression levels of mitochondrial fusion proteins (OPA1, Mfn1, and Mfn2) decreased, while the expression levels of mitochondrial fission proteins (Drp1, Mff, and Fis1) increased, thus exacerbating mitochondrial division. In addition, the results of immunofluorescence and flow cytometry analysis, as well as the elevated expressions of mitophagy related genes (PINK1, Parkin, ATG5, and LC3II/I) and pro-apoptotic markers (Bax, Cytc, Caspase3, and Caspase9) indicated that BPA exposure and Se deficiency disrupted the crosstalk homeostasis between mitophagy and apoptosis. However, this crosstalk homeostasis was restored after Mito-Tempo and Rapamycin treatment. In contrast, 3-methyladenine treatment exacerbated this crosstalk disorder. In conclusion, BPA exposure and Se deficiency can induce mitochondrial reactive oxygen species bursts and disorders of mitochondrial dynamics by destroying the mitochondrial respiratory chain complex. The result is indicative of an imbalance in mitochondrial autophagy and apoptosis crosstalk homeostasis, which damages the chicken brain.

Apigenin ameliorates di(2-ethylhexyl) phthalate-induced ferroptosis: The activation of glutathione peroxidase 4 and suppression of iron intake.

Di(2-ethylhexyl) phthalate (DEHP) is a widely artificial persistent organic pollutant, the contamination of which infiltrates daily human life from many aspects, imperceptibly causing damage to multiple organs in the body, including the liver. Apigenin (APG) is widely distributed in vegetables and fruits and can relieve or prevent the injuries caused by exogenous chemicals through various pharmacological effects, such as antioxidant effects. To investigate the mechanism of DEHP-induced liver injury and the antagonistic effects of APG, we treated AML12 cells with 1 mM DEHP and/or APG. Ultrastructural morphology analysis indicated that DEHP induced typical ferroptosis-like damage. In addition, we found that DEHP exposure induced ferroptosis by enhancing reactive oxygen species (ROS) levels, disrupting iron homeostasis and lipid peroxidation, and regulating the expression of ferroptosis-related genes. Notably, supplementation with APG significantly inhibited these abnormal changes, and molecular docking further showed evidence of the activating effects of APG ligand on glutathione peroxidase 4 (GPX4). These results demonstrated that the protective effects of APG on DEHP-induced ferroptosis were achieved by activating GPX4 and suppressing intracellular iron accumulation. This information not only adds to DEHP toxicological data but also provides a basis for the practical application of APG.

Attention impedes neural representation of interpolated orientation during perceptual completion.

One of the most remarkable functional feats accomplished by visual system is the interpolation of missing retinal inputs based on surrounding information, a process known as perceptual completion. Perceptual completion enables the active construction of coherent, vivid percepts from spatially discontinuous visual information that is prevalent in real-life visual scenes. Despite mounting evidence linking sensory activity enhancement and perceptual completion, surprisingly little is known about whether and how attention, a fundamental modulator of sensory activities, affects perceptual completion. Using EEG-based time-resolved inverted encoding model (IEM), we reconstructed the moment-to-moment representation of the illusory grating that resulted from spatially interpolating the orientation of surrounding inducers. We found that, despite manipulation of observers' attentional focus, the illusory grating representation unfolded in time in a similar manner. Critically, attention to the surrounding inducers simultaneously attenuated the illusory grating representation and delayed its temporal development. Our findings disclosed, for the first time, the suppressive role of selective attention in perceptual completion and were suggestive of a fast, automatic neural machinery that implements the interpolation of missing visual information.

Autophagy flux inhibition mediated by lysosomal dysfunction participates in the cadmium exposure-induced cardiotoxicity in swine.

Cadmium (Cd), a common toxic heavy metal, is believed as a risk factor for the induction and progression of cardiovascular disease. Autophagy is a highly ordered intracellular lysosomal-mediated degradation pathway that is crucial for protein and organelle quality control. Autophagy dysfunction could develop exacerbated cardiac dysfunction. However, the role of autophagy in Cd exposure-induced cardiotoxicity remains largely unknown. In this study, the Cd-induced swine cardiotoxicity model was established by feeding with a CdCl2 suppled diet (20 mg Cd/kg diet). The results showed that Cd exposure increased the expression of endoplasmic reticulum stress-related genes (GRP78, GRP94, IRE1, XBP1, PERK, ATF4, and ATF6), increased the expression of Ca2+ release channels IP3R and RYR1 and decreased the expression of Ca2+ uptake pump SERCA1. Cd exposure upregulated the expression of autophagy-related genes (CAMKKII, AMPK, ATG5, ATG7, ATG12, Beclin1, LC3-II, and P62) and downregulated mTOR expression. Cd exposure inhibited the expression of V-ATPase and cathepsins (CTSB and CTSD), and increased the expression of cathepsins in cytoplasm. Cd exposure decreased the colocalization of autophagosome and lysosome. This study revealed that autophagy flux inhibition caused by lysosomal dysfunction participates in the cardiotoxicity induced by Cd exposure in swine.

Eucalyptol relieves imidacloprid-induced autophagy through the miR-451/Cab39/AMPK axis in Ctenopharyngodon idellus kidney cells†.

Imidacloprid (IMI) is a widely used neonicotinoid insecticide that has toxic effects on nontarget organisms. 1,8-Cineole (eucalyptol) is purified from essential oils in several aromatic plants and can prevent xenobiotic toxicity. The kidney is a major organ for xenobiotic elimination and thus has high risk of exposure. The purpose of this research was to clarify the effect of IMI exposure on autophagy in fish kidney cells, determine the potential of eucalyptol to provide cytoprotection from the toxicity of the neonicotinoid pesticide IMI, and identify its mechanism of action. Therefore, the Ctenopharyngodon idellus kidney cell line (CIK cell) was treated with 20 mg/L IMI and/or 20 µM eucalyptol for 48 h as the research objective. The results showed that IMI exposure induced autophagy accompanied by advanced autophagy markers BNIP3, Beclin1 and LC3Ⅱ/Ⅰ in CIK cells, reduced the levels of miR-451, increased the expression of Cab39 and AMPK, inhibited AKT/mTOR signaling, and activated the JNK pathway. Eucalyptol treatment alleviated IMI-induced autophagy and relieved the activation of autophagy-associated signals. These results indicate that eucalyptol could alleviate IMI-induced autophagy through the miR-451/Cab39/AMPK axis in fish kidney cells. These results partly explained the mechanism of biological threat on fish under IMI exposure and the potential application value of EUC in aquaculture.