期刊：
Ecotoxicology and Environmental Safety,2022年236:113436 ISSN：0147-6513
通讯作者：
Fei Yang
作者机构：
[Cai, Danping] Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, University of South China, Hengyang, China. Electronic address: 20202014210994@stu.usc.edu.cn;[Wei, Jia] Xiangya School of Public Health, Central South University, Changsha, China. Electronic address: wjcindy@csu.edu.cn;[Huang, Feiyu] The First People's Hospital of Jingzhou, Jingzhou, China. Electronic address: huangfeiyu@csu.edu.cn;[Feng, Hai] Xiangya School of Public Health, Central South University, Changsha, China. Electronic address: Fenghai@csu.edu.cn;[Peng, Tangjian] Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, University of South China, Hengyang, China. Electronic address: pengtangjian@usc.edu.cn
通讯机构：
[Fei Yang] H;Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, University of South China, Hengyang, China<&wdkj&>Xiangya School of Public Health, Central South University, Changsha, China
作者：
Liu, Haohao;Zeng, Xin;Ma, Ya;Chen, Xinghai;Losiewicz, Michael D.;...
期刊：
Ecotoxicology and Environmental Safety,2022年236:113454 ISSN：0147-6513
通讯作者：
Yang, F.;Zhang, H.
作者机构：
[Ma, Ya; Zhang, Shiyu; Liu, Haohao; Zhang, Huizhen; Zeng, Xin; Du, Xingde; Tian, Zhihui; Shi, Linjia] Zhengzhou Univ, Coll Publ Hlth, Zhengzhou 450001, Henan, Peoples R China.;[Chen, Xinghai; Losiewicz, Michael D.] St Marys Univ, Dept Chem & Biochem, San Antonio, TX USA.;[Yang, Fei] Univ South China, Sch Publ Hlth, Hengyang Med Sch, Hunan Prov Key Lab Typ Environm Pollut & Hlth Haz, Hengyang 421001, Hunan, Peoples R China.;[Yang, Fei] Cent South Univ, Xiangya Sch Publ Hlth, Hunan Prov Key Lab Clin Epidemiol, Changsha 410008, Hunan, Peoples R China.
通讯机构：
[Zhang, H.] C;[Yang, F.] H;College of Public Health, Henan, China;Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, Hunan, China
作者机构：
[Li, Yanfang; Si, Sisi; Li, Huimin; Liu, Song] Institute of Chemical Biology and Nanomedicine (ICBN), State Key Laboratory of Chemo/Biosensing and Chemometrics, College of Chemistry and Chemical Engineering, Hunan University, Changsha;410082, China;[Yang, Fei] Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, University of South China, Hengyang;421001, China;[Huang, Feiyu; Wei, Jia] Hunan Provincial Key Laboratory of Clinical Epidemiology, Xiangya School of Public Health, Central South University, Changsha
通讯机构：
[Fei Yang] H;[Huimin Li; Song Liu] I;Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, University of South China, Hengyang 421001, PR China<&wdkj&>Institute of Chemical Biology and Nanomedicine (ICBN), State Key Laboratory of Chemo/Biosensing and Chemometrics, College of Chemistry and Chemical Engineering, Hunan University, Changsha 410082, PR China
通讯机构：
[Lei Zhang] D;[Yi Cao] H;Department of Chemical Engineering and Waterloo Institute for Nanotechnology, University of Waterloo, 200 University Avenue West, Waterloo, Ontario N2L 3G1, Canada<&wdkj&>Hunan Province Key Laboratory of Typical Environmental Pollution and Health Hazards, School of Public Health, University of South China, Hengyang 421001, China
关键词：
3D brain organoids;Endoplasmic reticulum (ER) stress;Graphene oxide (GO);Lipidomics;Transcriptomics
摘要：
The potential uses of graphene-based nanomaterials (NMs) in various fields lead to the concern about their neurotoxicity, considering that graphene-based NMs are capable to cross blood brain barrier (BBB) and enter central nervous system (CNS). Although previous studies reported the possibility of graphene-based NM exposure to alter lipid homeostasis in animals or cultured neurons, recent studies suggested the need to use 3D human brain organoids for mechanism-based toxicological studies as this model might better recapitulate the complex human brains. Herein, we used multi-omics techniques to investigate the mechanisms of graphene oxide (GO) on lipid homeostasis in a novel 3D brain organoid model. We found that 50 μg/mL GO induced cytotoxicity but not superoxide. RNA-sequencing data showed that 50 μg/mL GO significantly up-regulated and down-regulated 80 and 121 genes, respectively. Furthermore, we found that GO exposure altered biological molecule metabolism pathways including lipid metabolism. Consistently, lipidomics data supported dose-dependent alteration of lipid profiles by GO in 3D brain organoids. Interestingly, co-exposure to GO and endoplasmic reticulum (ER) stress inhibitor 4-phenylbutyric acid (4-PBA) decreased most of the lipid classes compared with the exposure of GO only. We further verified that exposure to GO promoted ER stress marker GRP78 proteins, which in turn activated IRE1α/XBP-1 axis, and these changes were partially or completely inhibited by 4-PBA. These results proved that direct contact with GO disrupted lipid homeostasis through the activation of ER stress. As 3D brain organoids resemble human brains, these data might be better extrapolated to humans.
通讯机构：
[Dingxin Long; 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<&wdkj&>Key Laboratory of Environment-Friendly Chemistry and Application of Ministry of Education, Laboratory of Biochemistry, College of Chemistry, Xiangtan University, Xiangtan, China<&wdkj&>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：
Vascular smooth muscle cells (VSMCs), the main cells constructing blood vessels, are important in the regulation of the pathophysiology of vascular systems; however, relatively few studies have investigated the influence of nanomaterials (NMs) on VSMCs. In this study, we found that the interaction between graphene oxide and human VSMCs led to the cytotoxicity and morphological changes of cells. Because transcriptomic data suggested that graphene oxide decreased anti-viral signaling pathways via decreasing Toll-like receptor 3 (TLR3), we further verified that graphene oxide decreased interferon induced protein with tetratricopeptide repeats 1 (IFIT1) and the radical S-adenosyl methionine domain containing 2 (RSAD2), and TLR3-downstream genes involved in anti-viral responses. Due to the involvement of RSAD2 in lipid dysfunction, we also verified that graphene oxide disrupted lipid homeostasis and increased adipose triglyceride lipase (ATGL). Adding TLR3 agonist polyinosinic:polycytidylic acid (Poly IC) partially increased TLR3-downstream protein interleukin-8 (IL-8) and some lipid classes, particularly lysophosphatidylcholine (LPC) and lysophosphatidylethanolamine (LPE), in graphene oxide-exposed VSMCs. In mice receiving repeated intravenous injection of graphene oxide, significantly decreased TLR3, IFIT1 and RSAD2 but increased ATGL proteins were observed in aortas. We conclude that graphene oxide altered anti-viral signaling pathways and lipid metabolism via decreasing TLR3 in VSMCs.
通讯机构：
[Zhaohui Zhang; Xinyun Xu] S;School of Public Health, University of South China, Hengyang, China<&wdkj&>School of Public Health, University of South China, Hengyang, China<&wdkj&>Shenzhen Center for Disease Control and Prevention, Institute of environment and health, Shenzhen, China
期刊：
World Journal of Microbiology and Biotechnology,2022年38(10):1-10 ISSN：0959-3993
通讯作者：
Guowen Peng
作者机构：
[Shu, Yangzhen; Peng, Guowen] Univ South China, Sch Resources Environm & Safety Engn, Hengyang 421001, Hunan, Peoples R China.;[Xie, Jingxi; Peng, Guowen] Univ South China, Sch Chem & Chem Engn, Hengyang 421001, Hunan, Peoples R China.;[Chen, Luyao; Cheng, Conghui; Guo, Kexin] Univ South China, Sch Publ Hlth, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Guowen Peng] S;School of Resources Environment and Safety Engineering, University of South China, Hengyang, People’s Republic of China<&wdkj&>School of Chemistry and Chemical Engineering, University of South China, Hengyang, People’s Republic of China
关键词：
Biological;Genetic engineering;Uranyl;Protein DSR A
作者机构：
[Yang, Shengyuan; Tong, Xuezhi] Univ South China, Sch Publ Hlth, Hengyang Med Sch, Dept Publ Hlth Lab Sci, Hengyang 421001, Hunan, Peoples R China.;[Zeng, Dong; Feng, JiaLi; Fan, Xiang; Zhang, Hao; Chen, Dongyang] Hunan Prov Ctr Dis Control & Prevent, Changsha 410005, Hunan, Peoples R China.;[Tan, Shan] Changsha Med Univ, Sch Publ Hlth, Dept Gen Med, Changsha 410219, Hunan, Peoples R China.
通讯机构：
[Shengyuan Yang] D;[Dongyang Chen] H;Hunan Provincial Center for Disease Control and Prevention, Changsha, Hunan 410005, China<&wdkj&>Department of Public Health Laboratory Sciences, School of Public Health, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China
摘要：
Extracellular polymeric substances (EPS) participate in heavy metal adsorption in the aquatic environments. Extracellular DNA (eDNA) is an essential component of EPS, but its involvement in metal binding remains ambiguous. Herein, the role of eDNA in Cd(II) and Ni(II) adsorption was described using a combination of semi-quantitative and qualitative approaches. EPS were extracted from Burkholderia sp. MBR-1 and eDNA accounted for 6.9% of the total mass of EPS. The eDNA in the extracted EPS was digested using the DNase II to prepare an eDNA-free EPS sample. Potentiometric titration unveiled that the number of total binding sites of the eDNA-free EPS was 19% lower than the untreated EPS. The Cd(II) and Ni(II) adsorption capacity of the eDNA-free EPS was lower than the untreated EPS at the pH range of 4-7. At pH7, the results of batch adsorption experiments showed that removing eDNA from EPS resulted in declines of 12.6% and 15.7% in the adsorption capacities for Cd(II) and Ni(II), respectively. Furthermore, Fourier transform infrared spectroscopy (FTIR) and Raman spectroscopy unraveled that the phosphoryl groups and purines of eDNA are responsible for Cd(II) and Ni(II) complexation. The results demonstrated that eDNA plays an essential role in heavy metal adsorption.
关键词：
Cascade signal amplification;Convenient operation;Multi-enzyme biosensor;Pesticide;Smartphone-based sensing
摘要：
Monitoring of pesticide residues in food and environmental matrices is undoubtedly crucial to guarantee food safety and ecological health, yet how to realize their sensitive and convenient detection is still challenging. Herein, we propose an all-in-one test strip that elaborately integrates bioenzyme, nanozyme and chromogen together, and achieve the highly sensitive and convenient sensing of pesticide residues assisted by a smartphone. A sequential self-assembly strategy was first explored to acquire an integrative bioenzyme-nanozyme-chromogen assembly, and then the assembly was confined in a biocompatible hydrogel to construct the test strip. Thanks to both the proximity and confinement effects, a ∼1.2-fold improvement of the cascade catalytic efficiency was gained to benefit high-sensitivity detection. More importantly, since all the sensing elements, including target recognition units and signal amplification modules, were rationally integrated in the test strip, detection operation was significantly simplified, making it possible for in-field rapid analysis. Besides, the microenvironment provided by the alginate hydrogel carrier endowed the test strip with an excellent sensing stability. By taking paraoxon as a typical pesticide, high-performance detection of the target was accomplished via the smartphone-assisted all-in-one test strip. Moreover, the test strip was successfully applied for paraoxon detection in various real samples and exhibited good correlations with commercial kits, demonstrating its great prospect for practical applications. Our work not only offers a new tool for the high-sensitivity and convenient monitoring of pesticide residues, but will also inspire the development of efficient multi-enzyme sensing platforms.
摘要：
Inhalation of beryllium and its compounds can cause lung injuries, resulting from inflammation and oxidative stress. Multivesicular bodies (MVB), such as exosomes, are membrane vesicles produced by early and late endosomes that mediate intercellular communications. However, the role of exosomes in beryllium toxicity has not been elucidated. This current study aimed to investigate the functional role of exosomes in lung injury resulting from beryllium sulfate (BeSO(4) ). Here, Sprague-Dawley (SD) rats were exposed to 4, 8, and 12 mg/kg BeSO(4) by nonexposed intratracheal instillation. Murine macrophage (RAW 264.7) cells were pretreated with 50 nmol/L rapamycin (an mTOR signaling pathway inhibitor) for 30 min and then cultured for 24 h with 100 μg/mL exosomes, which had been previously isolated from the serum of 12 mg/kg BeSO(4) -treated SD rats. Compared with those of the controls, exposure to BeSO(4) in vivo increased LDH activity, elevated levels of inflammatory cytokines (IL-10, TNF-α, and IFN-γ) alongside inflammation-related proteins expression (COX-2 and iNOS), and enhanced secretion of exosomes from the SD rat's serum. Moreover, the BeSO(4) -Exos-induced upregulation of LDH activity and inflammatory responses in RAW 264.7 cells can be alleviated following pretreatment with rapamycin. Collectively, these results suggest that serum exosomes play an important role in pulmonary inflammation induced by BeSO(4) in RAW 264.7 cells via the mTOR pathway.
摘要：
Despite of growing evidence linking PM(2.5) exposure to autophagic activity in various human cells, the functional significance of PM(2.5) exposure affecting autophagy in the pathogenesis of human cardiovascular disease and the underlying molecular mechanisms remain unclear. In this study, the effects of ambient PM(2.5) (with final concentration 0, 1, 5, 25µg/mL) on the autophagic activity in human umbilical vein endothelial cells (HUVECs) were systematically studied. The results showed that the internalized PM(2.5) mainly localized in the membrane-surrounded vacuoles in the cytoplasm. Compared with the negative control, dose-dependent increase of autophagosomes, puncta and protein levels of LC3-II and p62, and both dose- and time-dependent increase of AKT phosphorylation, with inversely time-dependent reduction of Beclin 1, ATG3 and ATG5 proteins, were presented in the PM(2.5)-treated HUVECs, indicating a clear impairment of autophagic degradation in the PM(2.5)-exposed HUVECs. Meanwhile, increase in lysosomes, LAMP1, proteases of CTSB and CTSD, and protein phosphorylation of ERK1/2 and TFEB was identified in the PM(2.5)-treated HUVECs, showing a PM(2.5)-mediated enhancement in lysosomal activity. A novel finding in this study is that both Sntaxin-17 and LAMP2, two key proteins involved in the control of membrane fusion between autophagosome and lysosome, were significantly decreased in the PM(2.5)-exposed HUVECs, suggesting that the fusion of autophagosome-lysosome was blocked up. Collectively, ambient PM(2.5) exposure may block up the autophagic flux in HUVECs through inhibiting the expression of Sntaxin-17 and LAMP2. Autophagic activity in HUVECs is a useful biomarker for assessing risks of environmental factors to human cardiovascular health.
摘要：
Proteomics and bioinformatics were applied to explore PM(2.5)-induced differentially expressed proteins (DEPs) in hepatocytes (L02 cells) and c-Myc-silenced hepatocytes. L02 cells and c-Myc-silenced hepatocytes were treated with PM(2.5) for 24h. Fifty-two DEPs were screened in L02 hepatocytes, of which 28 were upregulated and 24 were downregulated. Forty-one DEPs were screened in the c-Myc-silenced hepatocytes, of which 31 were upregulated and 10 were downregulated. GO analysis showed that DEPs in L02 cells were mainly concentrated in the cytosol and were involved in biological processes such as the response to metal ions. DEPs in c-Myc-silenced cells were mainly enriched in the extracellular space and were involved in lipoprotein metabolism. KEGG analysis showed that DEPs in L02 cells were mainly involved in arachidonic acid metabolism and mineral absorption. DEPs in c-Myc-silenced cells were mainly enriched in pathways involving nerve absorption, complement and coagulation cascades, and other pathways. Twenty key proteins, including Metallothionein-2A (MT2A), Metallothionein-1X (MT1X), zinc transporter ZIP10 (SLC39A10) and Serine protease 23 (PRSS23) were screened in two groups through analysis of protein-protein interactions. Based on the identification of the selected DEPs, PRSS23 and SLC39A10 might be the potential biomarker of PM(2.5)-induced carcinogenesis, which provide the scientific basis for further research into the carcinogenic mechanisms of PM(2.5).
作者机构：
[Shu, Yangzhen; Peng, Guowen] Univ South China, Sch Environm Protect & Safety Engn, Hengyang 421001, Hunan, Peoples R China.;[Xiao, Fangzhu; Cheng, Conghui; Guo, Kexin; Chen, Luoyao; Li, Shanshan] Univ South China, Sch Publ Hlth, Hengyang 421001, Hunan, Peoples R China.;[Xie, Jingxi; Peng, Guowen] Univ South China, Sch Chem & Chem Engn, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Peng, G.; Xiao, F.] S;School of Environmental Protection and Safety Engineering of University of South ChinaChina;School of Public Health, China
