作者机构：
[让蔚清; 姚承志; 张敏; 吴霞; Zeng, Y K; 张译匀] Department of Preventive Medicine, School of Public Health, University of South China, Hengyang 421001, China;[熊文婧] Department of Preventive Medicine, School of Public Health, University of South China, Hengyang 421001, China Department of Traditional Chinese Medicine, The First Affiliated Hospital of University of South China, Hengyang 421001, China
摘要：
To evaluate the oral toxicity of nanoparticles (NPs), it is necessary to consider the interactions between NPs and nutrient molecules. Recently, we reported that epigallocatechin gallate (EGCG), a healthy component in green tea, alleviated the toxicity of ZnO NPs to 3D Caco-2 spheroids in vitro. The present study investigated the combined effects of EGCG and ZnO NPs to mice in vivo. Mice were administrated with 35 or 105 mg/kg bodyweight ZnO NPs with or without the presence of 80 mg/kg bodyweight EGCG via gastric route, once a day, for 21 days, and the influences of EGCG on the toxicity of ZnO NPs to intestine were investigated. We found that EGCG altered the colloidal properties of ZnO NPs both in water and artificial intestine juice. As expected, ZnO NPs induced toxicological effects, such as decreased bodyweight, higher Chiu's scores, and ultrastructural changes in intestine, whereas EGCG alleviated these effects. Combined exposure to EGCG and ZnO NPs also changed trace element levels in mouse intestine. For example, the levels of Ti, Co, and Ni were only significantly elevated after co-exposure to EGCG and ZnO NPs, and Fe levels were only significantly decreased by ZnO NPs. Western blot analysis suggested that tight junction (TJ) and endoplasmic reticulum (ER) proteins were elevated by ZnO NPs, but EGCG inhibited this trend. Combined, these data suggested that gastric exposure to ZnO NPs induced intestinal damage, trace element imbalance, and TJ/ER protein expression in mouse intestine, whereas EGCG alleviated these effects of ZnO NPs. This study investigated the combined effects of EGCG and ZnO NPs to mouse intestine. EGCG altered hydrodynamic size, zeta potential, and solubility of ZnO NPs. After gastric administration, ZnO NPs induced damages to intestine, impaired trace element balance, and increased TJ and ER proteins, whereas EGCG altered the bio-effects of ZnO NPs. These data suggested a need to investigate the in vivo oral toxicity of ZnO NPs in the presence of food molecule.
期刊：
Science of The Total Environment,2023年905:167167 ISSN：0048-9697
通讯作者：
Liu, J
作者机构：
Univ South China, Sch Basic Med Sci, Hengyang Med Sch, Inst Cytol & Genet,Dept Cell Biol & Genet,Key Lab, Hengyang 421001, Hunan, Peoples R China.;Univ South China, Sch Publ Hlth, Hengyang Med Sch, Hunan Key Lab Typ Environm Pollut & Hlth Hazards, Hengyang 421001, Hunan, Peoples R China.;[Liu, Jun] 28 Changsheng West Rd, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Liu, J ] 2;28 Changsheng West Rd, Hengyang 421001, Hunan, Peoples R China.
关键词：
Liver;MCs;Mechanisms;Toxicity
摘要：
Microcystins (MCs) are a class of biologically active cyclic heptapeptide pollutants produced by the freshwater alga Microcystis aeruginosa. With increased environmental pollution, MCs have become a popular research topic. In recent years, the hepatotoxicity of MCs and associated effects and mechanisms have been studied extensively. Current epidemiological data indicate that long-term human exposure to MCs can lead to severe liver toxicity, acute toxicity, and death. In addition, current toxicological studies on the liver, a vital target organ of MCs, indicate that MC contamination is associated with the development of liver cancer, nonalcoholic fatty liver, and liver fibrosis. MCs produce hepatotoxicity that affects the metabolic homeostasis of the liver, induces apoptosis, and acts as a pro-cancer factor, leading to liver lesions. MCs mainly mediate the activation of signaling pathways, such as the ERK/JNK/p38 MAPK and IL-6-STAT3 pathways, which leads to oxidative damage and even carcinogenesis. Moreover, MCs can act synergistically with other pollutants to produce combined toxicity. However, few systematic reviews have been performed on these new findings. This review systematically summarizes the toxic effects and mechanisms of MCs on the liver and discusses the combined liver toxicity effects of MCs and other pollutants to provide reference for subsequent research. The toxicity of different MC isomers deserves further study. The detection methods and limit standards of MCs in agricultural and aquatic products will represent important research directions in the future. Standard protocols for fish sampling during harmful algal blooms or to evaluate the degree of MC toxicity in nature are lacking. In future, bioinformatics can be applied to offer insights into MC toxicology research and potential drug development for MC poisoning. Further research is essential to understand the molecular mechanisms of liver function damage in combined-exposure toxicology studies to establish treatment for MC-induced liver damage.
期刊：
INFECTION AND DRUG RESISTANCE,2023年16(Volume 16, 2023 - Issue):3157-3169 ISSN：1178-6973
通讯作者：
Yuan, XQ;Li, GL
作者机构：
[Yuan, Xiuqin; Yu, Jinjie; Yuan, XQ] Univ South China, Sch Publ Hlth, Hengyang 421001, Peoples R China.;[Deng, Lele; Zhao, Xiuqin; Liu, Haican; Li, Guilian; Yu, Jinjie; Wan, Kanglin] Natl Inst Communicable Dis Control & Prevent, Collaborat Innovat Ctr Diag & Treatment Infect Dis, Chinese Ctr Dis Control & Prevent, State Key Lab Infect Dis Prevent & Control, Beijing 102206, Peoples R China.;[Xiao, Hui; Yin, Chunjie; Liu, Mengwen; Li, Machao] Xinjiang Med Univ, Sch Publ Hlth, Urumqi 830011, Xinjiang, Peoples R China.;[Xu, Miao; Mijiti, Xiaokaiti; Wang, Quan] Xinjiang Med Univ, Affiliated Hosp 8, Urumqi 830049, Xinjiang, Peoples R China.;[Anwaierjiang, Aiketaguli] Coll Xinjiang Uyghur Med, Hetian 848000, Peoples R China.
通讯机构：
[Li, GL ] N;[Yuan, XQ ] U;Univ South China, Sch Publ Hlth, Hengyang 421001, Peoples R China.;Natl Inst Communicable Dis Control & Prevent, Collaborat Innovat Ctr Diag & Treatment Infect Dis, Chinese Ctr Dis Control & Prevent, State Key Lab Infect Dis Prevent & Control, Beijing 102206, Peoples R China.
关键词：
vitamin D receptor;VDR;polymorphism;tuberculosis;Mycobacterium tuberculosis;Beijing lineage
摘要：
BACKGROUND: The aim of the present study was to investigate the association between vitamin D receptor (VDR) gene polymorphism and tuberculosis susceptibility, as well as the potential interaction of host genetic factors with the heterogeneity of Mycobacterium tuberculosis in the population from Xinjiang, China. METHODS: From January 2019 to January 2020, we enrolled 221 tuberculosis patients as the case group and 363 staff with no clinical symptoms as the control group from four designated tuberculosis hospitals in southern Xinjiang, China. The polymorphisms of Fok I, Taq I, Apa I, Bsm I, rs3847987 and rs739837 in the VDR were detected by sequencing. M. tuberculosis isolates were collected from the case group and identified as Beijing or non-Beijing lineage by multiplex PCR. Propensity score (PS), univariate analysis and multivariable logistic regression models were used to perform the analysis. RESULTS: Our results showed that the allele and genotype frequencies of Fok I, Taq I, Apa I, Bsm I, rs3847987 and rs739837 in VDR were not correlated with tuberculosis susceptibility or lineages of M. tuberculosis. Two out of six loci of the VDR gene formed one haplotype block, and none of the haplotypes was found to correlate with tuberculosis susceptibility or lineages of M. tuberculosis infected. CONCLUSION: Polymorphisms in the VDR gene may not indicate susceptibility to tuberculosis. There was also no evidence on the interaction between the VDR gene of host and the lineages of M. tuberculosis in the population from Xinjiang, China. Further studies are nonetheless required to prove our conclusions.
作者机构：
[Shi, Xiaolu; Xu, Shiqin; Ji, Liyin] Shanxi Med Univ, Sch Publ Hlth, Taiyuan 030001, Peoples R China.;[Wu, Shuang; Qiu, Yaqun; Jiang, Min; Chen, Qiongcheng; Hu, Qinghua; Feng, Tiejian; Jiang, Yixiang; Zou, Xuan; Cai, Rui; Shi, Xiaolu] Shenzhen Ctr Dis Control & Prevent, Shenzhen 518055, Peoples R China.;[Shi, Xiaolu] Chinese Acad Med Sci, Shenzhen Res Ctr Communicable Dis Control & Preven, Shenzhen, Peoples R China.;[Wu, Jinsong; Chen, Huaisheng] Shenzhen Peoples Hosp, Shenzhen 518020, Peoples R China.;[Jin, Ying] Shenzhen Baoan Dist Songgang Peoples Hosp, Shenzhen 518105, Peoples R China.
通讯机构：
[Shi, XL ] S;Shanxi Med Univ, Sch Publ Hlth, Taiyuan 030001, Peoples R China.;Shenzhen Ctr Dis Control & Prevent, Shenzhen 518055, Peoples R China.;Chinese Acad Med Sci, Shenzhen Res Ctr Communicable Dis Control & Preven, Shenzhen, Peoples R China.
摘要：
We report a 36-year-old male patient died of V. vulnificus-induced septicaemia and multiple organ failure syndrome after oyster consumption at a restaurant. We isolated and identified V. vulnificus vv16015 from the patient’s blood sample and antibiotic susceptibility tests indicated sensitivity to all 21 antibiotics. Oyster samples were subsequently collected from the restaurant’s supplier and three strains of V. vulnificus were isolated. Whole genome sequencing and analysis revealed vv16015 to be distantly related to these strains and confirmed that V. vulnificus contamination was present in the seafood of the restaurant and supplier. Using a Galleria mellonella larvae infection model, the virulence of vv16015 was determined to be higher than that of comparison strains isolated from a surviving patient (vv15018) and an oyster (vv220015). The human and environment distribution of V. vulnificus in Shenzhen is sporadic and heterogeneous, and vv16015 is highly virulent compared to other strains.
作者机构：
[Song, Fengmei; Tang, Xiaomin; Cao, Yi; Zhao, Weichao] Univ South China, Sch Publ Hlth, Hengyang Med Sch, Hunan Prov Key Lab Typ Environm Pollut & Hlth Haza, Hengyang 421001, Peoples R China.;[Huang, Chaobo] Nanjing Forestry Univ NFU, Coll Chem Engn, Nanjing 210037, Peoples R China.;[Dai, Xuyan] Hunan Agr Univ, Econ Coll, Changsha 410128, Peoples R China.
通讯机构：
[Yi Cao] H;Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, Hengyang Medical School, University of South China, Hengyang 421001, China
摘要：
BACKGROUND: Nanoplastics (NPs) could be released into environment through the degradation of plastic products, and their content in the air cannot be ignored. To date, no studies have focused on the cardiac injury effects and underlying mechanisms induced by respiratory exposure to NPs. RESULTS: Here, we systematically investigated the cardiotoxicity of 40nm polystyrene nanoplastics (PS-NPs) in mice exposed via inhalation. Four exposure concentrations (0µg/day, 16µg/day, 40µg/day and 100µg/day) and three exposure durations (1 week, 4 weeks, 12 weeks) were set for more comprehensive information and RNA-seq was performed to reveal the potential mechanisms of cardiotoxicity after acute, subacute and subchronic exposure. PS-NPs induced cardiac injury in a dose-dependent and time-dependent manner. Acute, subacute and subchronic exposure increased the levels of injury biomarkers and inflammation and disturbed the equilibrium between oxidase and antioxidase activity. Subacute and subchronic exposure dampened the cardiac systolic function and contributed to structural and ultrastructural damage in heart. Mechanistically, violent inflammatory and immune responses were evoked after acute exposure. Moreover, disturbed energy metabolism, especially the TCA cycle, in the myocardium caused by mitochondria damage may be the latent mechanism of PS-NPs-induced cardiac injury after subacute and subchronic exposure. CONCLUSION: The present study evaluated the cardiotoxicity induced by respiratory exposure to PS-NPs from multiple dimensions, including the accumulation of PS-NPs, cardiac functional assessment, histology observation, biomarkers detection and transcriptomic study. PS-NPs resulted in cardiac injury structurally and functionally in a dose-dependent and time-dependent manner, and mitochondria damage of myocardium induced by PS-NPs may be the potential mechanism for its cardiotoxicity.
摘要：
Ferroptosis has been linked to the pathogenesis of hepatic injury induced by ischemia/reperfusion (I/R). However, the mechanistic basis remains unclear. In this study, by using a mouse model of hepatic I/R injury, it is observed that glutathione (GSH) and cysteine depletion are associated with deficiency of the reducing power of nicotinamide adenine dinucleotide phosphate (NADPH). Genes involved in maintaining NADPH homeostasis are screened, and it is identified that I/R-induced hepatic ferroptosis is significantly associated with reduced expression and activity of NADP(+)-dependent malic enzyme 1 (Me1). Mice with hepatocyte-specific Me1 gene deletion exhibit aggravated ferroptosis and liver injury under I/R treatment; while supplementation with L-malate, the substrate of ME1, restores NADPH and GSH levels and eventually inhibits I/R-induced hepatic ferroptosis and injury. A mechanistic study further reveals that downregulation of hepatic Me1 expression is largely mediated by the phosphatase and tensin homologue (PTEN)-dependent suppression of the mechanistic target of rapamycin/sterol regulatory element-binding protein 1 (mTOR/SREBP1) signaling pathway in hepatic I/R model. Finally, PTEN inhibitor, mTOR activator, or SREBP1 over-expression all increase hepatic NADPH, block ferroptosis, and protect liver against I/R injury. Taken together, the findings suggest that targeting ME1 may provide new therapeutic opportunities for I/R injury and other ferroptosis-related hepatic conditions.
摘要：
Uranyl coordination polymers have caught more and more attention due to their rich topological structures and potential practical applications in nuclear waste processing and management. In this work, four novel uranyl coordination polymers have been successfully synthesized by the utilization of a semirigid ligand and uranyl nitrate under hydrothermal reactions through the introducing of different kinds of auxiliary ligands (NaCl, oxalate acid, succinic acid). Therein, the powder X-ray diffraction, Infrared spectroscopy and luminescence properties of compounds 3 and 4 are investigated.
摘要：
Nanomaterials with enzyme-like catalytic features (nanozymes) find wide use in analytical sensing. Apart from catalytic characteristics, some other interesting functions coexist in the materials. How to combine these properties to design multifunctional nanozymes for new sensing strategy development is challenging. Besides, in nanozymes it is still a challenge to conveniently control the catalytic process, which also hinders their further applications in advanced biochemical analysis. To remove the above barriers, here we design a light-controllable multifunctional nanozyme, namely manganese-inserted cadmium telluride (Mn-CdTe) particles, that integrates oxidase-like activity with luminescence together, to achieve the fluorometric/colorimetric dual-mode detection of toxic mercury ions (Hg(2+)) at ambient pH. The Mn-CdTe exhibits a light-triggered oxidase-mimicking catalytic behavior to induce chromogenic reactions, thus enabling one to start or stop the catalytic progress easily via applying or withdrawing light irradiation. Meanwhile, the quantum dot material can exhibit bright photoluminescence, which provides the fluorometric channel to sense targets. When Hg(2+) is introduced, it rapidly leans toward Mn-CdTe through electrostatic interaction and Te-Hg bonding and induces the aggregation of the latter. As a result, the luminescence of Mn-CdTe is dynamically quenched, and the masking of active sites in aggregated Mn-CdTe leads to the decrease of light-initiated oxidase-mimetic activity. According to this principle, a new fluorometric/colorimetric bimodal method was established for Hg(2+) determination with excellent performance. A 3D-printed portable platform combining paper-based test strips and an App-equipped smartphone was further fabricated, making it possible to achieve in-field sensing of the analyte in various matrices.
摘要：
Background The protective effects of astragaloside IV (ASIV) on various diseases are well known, but its potential impact on radiation-induced bystander effect (RIBE) has remained unclear. Objective This study aimed to explore the protective mechanism of ASIV against oxidative damage caused by RIBE in LO2 cells. Methods To construct the RIBE model, the conditioned medium from HepG2 cells irradiated with radiation was transferred to nonirradiated LO2 cells. LY294002, a commonly used phosphatidylinositol 3-kinase/Akt pathway inhibitor, was added to LO2 cells 1 h before exposing HepG2 cells to radiation. LO2 cells were then collected for analyses after RIBE exposure. Results The study found that ASIV significantly improved cell proliferation and promoted the recovery of mitochondrial membrane potential while reducing the rate of apoptosis. Western blot analyses demonstrated that ASIV upregulated B-cell lymphoma 2 and downregulated B-cell lymphoma 2-related X protein and cleaved-caspase 3. Measurement of reactive oxygen species, superoxide dismutase, glutathione peroxidase, and malondialdehyde levels showed that ASIV effectively restored the oxidative stress state induced by RIBE. Additionally, immunofluorescence and western blots analyses confirmed that ASIV enhanced the translocation of Nrf2 to the nucleus and activated downstream nicotinamide adenine dinucleotide phosphate: quinine oxidoreductase 1 and heme oxygenase 1. Importantly, Akt pathway inhibitor repressed ASIV-induced activation of Nrf2 and its protective effect against RIBE. Conclusion This study demonstrates that ASIV protects LO2 cells against oxidative damage caused by RIBE through activation of the Akt/Nrf2 pathway.
摘要：
Type 2 diabetes mellitus (T2DM) is frequently associated with diabetic cognitive impairment (DCI), and recent studies have shown a strong association between DCI and hippocampal ferroptosis. In this study, we administered dihydromyricetin (DHM) or JNK inhibitor SP600125, to T2DM rats and monitored changes in blood glucose levels, conducted behavioral tests, and detected changes in JNK, inflammatory factors and ferroptosis-related indicators. Our findings demonstrated that T2DM rats displayed signs of cognitive impairment (CI), with ferrozine assays indicating elevated iron content in the hippocampus. Concurrently, there was an increase in p-JNK activity and inflammatory factors IL-6 and TNF-α in the hippocampal region of these rats. Furthermore, we observed elevated levels of Fe(2+), MDA, ROS, LPO, and ACSL4, along with a decrease in GPX4 and GSH, suggesting the occurrence of hippocampal ferroptosis. SP600125 application reversed these changes in the T2DM rats, although it exhibited no significant effects in the control group. Treatment with high and low doses of DHM led to a reduction in p-JNK expression, inflammatory factor-related proteins, and iron accumulation in the hippocampal region, effectively alleviating hippocampal ferroptosis in T2DM rats. No notable effects of DHM were observed in the control group. To conclude, our study suggests that DHM can potentially alleviate hippocampal ferroptosis of T2DM cognitive impairment rats, primarily by suppressing the JNK-inflammatory factor pathway in the hippocampus.
