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409条结果
  • 机译 氧化铈纳米粒子的生物相容性研究–通过植入途径的局部效应,全身毒性和遗传毒性的组合研究
    摘要:An implantation study of cerium oxide nanoparticles (CeO2-NP) combined with 28-day systemic toxicity and genotoxicity studies aligned to current regulatory standards was conducted. The results suggested that local tissue reactions caused by CeO2-NP was minimal (implantation irritation index of less than 3) and was better tolerated than most other implant materials tested in our laboratory. Furthermore, CeO2-NP showed virtually no systemic toxicity or in vivo micronucleus induction in bone marrow via implantation route. Chemical analysis showed that CeO2-NP migrated from the implant sites (250 mg per site) in low levels and was deposited predominantly in liver (191.8 ± 35.1 ng g–1 of tissue; P < 0.01), lungs (263.4 ± 30.9 ng g–1 of tissue; P < 0.001), spleen (211.2 ± 6.5 ng g–1 of tissue; P < 0.001) and kidneys (272.8 ± 20.4 ng g–1 of tissue; P < 0.001). These observations provide a base line biocompatibility and toxicity data on CeO2-NP. The current findings will also be useful in defining standards for nanoparticle containing biomaterials and devices.
  • 机译 三氯生(TCS)和甲基三氯生(MTCS)对人肝细胞HepG2细胞的肝毒性和机制的比较
    摘要:Triclosan (TCS) is used as an antimicrobial agent and has been widely dispersed and detected in the environment and organisms including human samples. Methyl-triclosan (MTCS) is the predominant bacterial TCS metabolite. At present, the toxicological effects and mechanism of TCS and MTCS are still not fully understood. In this study, the cytotoxic effects of TCS and MTCS in HepG2 cells were investigated in terms of cell proliferation, comet assay, cell cycle, and apoptosis. In addition, the expressions of related proteins were detected with western blotting analysis. The results showed that TCS could significantly inhibit cell proliferation, while MTCS had no obvious effect on cell growth. Both TCS and MTCS caused oxidative injury associated with HO-1 induction and increased DNA strand breaks, which consequently initiated the damage repair process via up-regulation of DNA-PKcs. In addition, TCS blocked the HepG2 cells in S and G2/M phases of cell cycle through down-regulation of cyclin A2 and CDK; while MTCS induced cell cycle arrest at the S phase through up-regulation of cyclin A2 and CDK. Furthermore, TCS activated p53 mediated apoptosis in HepG2 cells in a caspase-independent manner, while MTCS induced apoptosis was dependent on caspase. Moreover, TCS exposure exhibited more severe toxicity in HepG2 cells as compared with MTCS exposure, indicating that the replacement of the ionizable proton in TCS by the methyl group in MTCS is correlated with the cellular toxicity and the molecular mechanism.
  • 机译 REACH数据的可靠性和相关性评估
    摘要:Regulatory authorities rely on hazard and risk assessments performed under REACH for identifying chemicals of concern and to take action. Therefore, these assessments must be systematic and transparent. This study investigates how registrants evaluate and report data evaluations under REACH and the procedures established by the European Chemicals Agency (ECHA) to support these data evaluations. Data on the endpoint repeated dose toxicity were retrieved from the REACH registration database for 60 substances. An analysis of these data shows that the system for registrants to evaluate data and report these evaluations is neither systematic nor transparent. First, the current framework focuses on reliability, but overlooks the equally important aspect of relevance, as well as how reliability and relevance are combined for determining the adequacy of individual studies. Reliability and relevance aspects are also confused in the ECHA guidance for read-across. Second, justifications for reliability evaluations were mainly based on studies complying with GLP and test guidelines, following the Klimisch method. This may result in GLP and guideline studies being considered reliable by default and discounting non-GLP and non-test guideline data. Third, the reported rationales for reliability were frequently vague, confusing and lacking information necessary for transparency. Fourth, insufficient documentation of a study was sometimes used as a reason for judging data unreliable. Poor reporting merely affects the possibility to evaluate reliability and should be distinguished from methodological deficiencies. Consequently, ECHA is urged to improve the procedures and guidance for registrants to evaluate data under REACH to achieve systematic and transparent risk assessments.
  • 机译 室内煤细颗粒物对卵清蛋白诱导的小鼠炎症因子表达水平的影响
    摘要:Objective: Cooking and heating with coal is the main source of household air pollution in acid rain-plagued areas of China and is a leading contributor to disease burden. In this study, we investigated the adverse effects of exposure to indoor fine particulate matter emission from coal combustion on the expression levels of inflammatory factors in ovalbumin (OVA)-induced mice. Methods: Forty BALB/c male mice were randomly divided into four groups (control group, PM2.5 group, OVA group, and OVA + PM2.5 group; n = 10) and treated with ovalbumin (OVA) or PM2.5, alone or together. Interleukin-4 (IL-4), interleukin-7 (IL-7), interleukin-8 (IL-8), interleukin-17 (IL-17), transforming growth factor β1 (TGF-β1), and interferon γ (IFN-γ) protein expression levels were measured in bronchoalveolar lavage fluid (BALF). Additionally, serum immunoglobulin (Ig) IgE and IgG1 levels were measured. The mRNA expression levels of IL-7 and IFN-γ in pulmonary tissue were also analyzed. Bronchoalveolar lavage (BAL), inflammatory cell counts, and histopathological examinations were also performed. Results: Exposure to PM2.5 + OVA induced abnormal pathological changes and inflammatory responses in lungs compared to the control. The levels of IL-4, IL-7, IL-8 and IL-17 in BALF from the OVA + PM2.5 group were higher than those in BALF from the control group, OVA group, and PM2.5 group (P < 0.05). PM2.5 plus OVA significantly raised the serum IgE and IgG1 levels compared with the control group. An increasing IL-7 mRNA trend was found among the treatment groups (P < 0.05). The expression level of IFN-γ mRNA was significantly higher in the control group than in the other 3 groups (P < 0.05). Conclusion: Indoor coal PM2.5 was sufficient by itself to cause inflammatory cellular infiltration of pulmonary tissue, leading to organelle injury and physiological structure change. Additionally, it promoted the occurrence and development of asthma by influencing the expression levels of IL-7 and various relevant inflammatory factors (such as IL-4 and IL-8) and changing the equilibrium between Treg and Th17 cells.
  • 机译 二烯丙基硫化物治疗可通过抑制小鼠的氧化应激,炎症和细胞凋亡来预防对乙酰氨基酚/四氯化碳诱导的急性肝损伤
    摘要:The purpose of the present study was to investigate the effects and underlying mechanisms of diallyl sulfide (DAS), an organosulfur compound extracted from garlic, on drug-induced or chemical-induced liver injury caused by acetaminophen (APAP) or carbon tetrachloride (CCl4) in mice. DAS (100, 200, or 400 μmol kg–1) was orally administered 1 hour before APAP or CCl4 intraperitoneal injection, and the serum and liver tissue were collected 24 hours after APAP or CCl4 exposure. The serum aminotransferase activities and liver histopathological examination showed that DAS exhibited obvious hepatoprotective effects against acute liver injury induced by APAP or CCl4. In addition, exposure to APAP or CCl4 resulted in an increased content of malonaldehyde as well as a decreased ratio of reduced to oxidized glutathione, and a decreased level of superoxide dismutase and catalase activity in the liver (p < 0.05); however, pretreatment with DAS restored the perturbations of the antioxidant system in the liver. Beyond that, DAS pretreatment reduced the APAP-/CCl4-induced increase in phosphorylation of inhibitor of kappa B alpha (IκBα) and p65 subunit of nuclear factor kappa B (NF-κB) expression in the cytoplasm and nucleus in the liver. DAS pretreatment also decreased the excessive level of TNF-α caused by APAP or CCl4 in serum (p < 0.05). Moreover, DAS pretreatment regulated the expression of cleaved caspase 3, Bax and Bcl-2 in the liver and suppressed APAP-/CCl4-induced hepatocyte apoptosis. In conclusion, DAS exhibits hepatoprotective effects against drug-induced and chemical-induced liver injuries induced by APAP or CCl4 in mice, probably due to its ability to reduce hepatic oxidative stress and inhibit inflammatory injury and hepatocyte apoptosis.
  • 机译 on暴露于人的支气管上皮细胞中的线粒体功能障碍和长期暴露的上皮-间质转化
    摘要:Radon is a naturally occurring radionuclide, which has a wide environmental distributed. It emits multiple high linear energy transfer (LET) alpha particles during radiative decay, and has been regarded as a human carcinogen by the International Agency for Research on Cancer. Currently, residential radon exposure is considered as the second highest cause of lung cancer and the leading cause among nonsmokers. Radon exposure leads to genomic instability, which causes the accumulation of multiple genetic changes and leads to cancer development. However, the molecular basis underlying carcinogenesis, especially the radon-induced changes to mitochondria, has not been fully elucidated. The aim of this study was to explore the dynamic changes in mitochondria along with the cell transformations induced by long-term radon exposure. A malignant transformation model of BEAS-2B cells was established with upto 40 times the usual radon exposure (20 000 Bq m–3, 30 min each time every 3 days). Long-term radon exposure induced EMT-like transformation of epithelial cells in our study, evidenced by decrease in epithelial markers and increase in mesenchymal markers, as well as the loss of cell–cell adhesion and alterations to the morphology of cells from compact shape to a spindle shaped, fibroblast-like morphology. Additionally, the proliferation and migration of cells were increased and apoptosis was decreased with long-term radon exposure. Furthermore, mitochondrial function was up-regulated and the levels of oxidative stress were repressed with long-term radon exposure. Our work explored the dynamic changes of mitochondrial in radon induced malignant transformation of lung bronchial epithelial cells, which could partially elucidate the role of mitochondria in radon induced cell malignancy.
  • 机译 可以通过消耗mTOR活性来恢复自噬来减轻砷诱导的细胞凋亡
    摘要:Arsenic and its compounds are toxic environmental pollutants and known carcinogens. We investigated here the mechanism of arsenite-induced damage in renal cells. Treating human embryonic kidney cells (HEK293) with sodium arsenite reduces cell viability in a dose- and time-dependent manner. The decline of cell viability is due to apoptotic death since arsenite treatment reduces Akt activity and the Bcl2 level but increases caspase 3 activity and the cytochrome c level. These effects can be reverted by the addition of an apoptosis inhibitor. PTEN, the upstream negative regulator of Akt activity, was also reduced with arsenite treatment. Noticeably, PTEN markedly increased in the insoluble fraction of the cells, suggesting a cell failure in removing the damaged proteins. Arsenite treatment activates a variety of signaling factors. Among them, ERK and JNK are associated with autophagy via regulating the levels of LC3 and p62. With arsenite administration, the LC3 and p62 levels increased. However, lysosomal activity was decreased and led to the decline of autophagic activity. The addition of rapamycin, the mTOR inhibitor, activated the autophagic pathway that accelerated the removal of damaged proteins. The recovery of autophagy increased the viability of arsenite-treated cells. Similar to rapamycin treatment, the knockdown of mTOR expression also enhanced the viability of arsenite-treated cells. Both rapamycin treatment and mTOR knockdown enhanced ERK activity further, but reduced JNK activity and the p62 level in arsenite-treated cells. Lysosomal activity increased with the depletion of mTOR, indicating an increase of autophagic activity. These results reveal the critical role of mTOR in regulating the cell fate of arsenite-exposed renal cells.
  • 机译 有毒物质对呼吸链的靶向作用:超出线粒体形态的毒性范围
    摘要:The mitochondrion is an important subcellular target of environmental toxicants. With environmental stress, a series of toxic effects on mitochondria are induced, which originate from the dynamic changes of mitochondrial fusion and fission, structure/membrane damage, and respiratory chain dysfunction. The toxic effects of various toxicants on mitochondrial morphology and intact membranes, and their determination of cell fate, have already been broadly studied and reported on. However, their effects on the integrity and function of the mitochondrial respiratory chain (RC) remain incompletely understood. Recently, Fan et al. and Yu et al. approached this topic by closely examining the mitochondrial toxicities, including the effect on the respiratory chain, induced by organic arsenical chemical 2-methoxy-4-(((4-(oxoarsanyl)phenyl)imino)methyl)phenol and thiourea gold(i) complexes (AuTuCl). Obviously, toxicant-induced dysfunction of the respiratory chain can hinder ATP production, and may elevate ROS generation. The increased ROS can further damage mtDNA, and consequently leads to inactivation of some RC protein-encoding mtDNA, generating a vicious circle of amplifying mitochondrial damage. We hope that these studies focused on RC structure and activity will broaden our view of mitochondrial toxicology and draw forth more profound mechanistic studies on the respiratory chain toxicity of environmental toxicants and their application in risk assessment.
  • 机译 中药(TCM)的光毒性
    摘要:Phototoxicity can cause toxic responses such as edemas and lesions, and is one of the severe adverse effects that largely limit the use of these phototoxic drugs. Some traditional Chinese medicines (TCMs) and their constituents have been reported to be phototoxic. However, to date, their phototoxicity information is still very limited, and lacks systemic investigation. This article presents the phototoxicity potential of various types of TCMs and their active components in an effort to provide valuable information for drug research and discovery to mitigate phototoxicity concerns. Some potential mechanisms of action (MoAs) of phototoxicity are discussed. In addition, in vivo and in vitro phototoxicity assays are summarized this review.
  • 机译 大数据和机器学习可改善计算毒理学及其在风险评估中的应用
    摘要:The creation of large toxicological databases and advances in machine-learning techniques have empowered computational approaches in toxicology. Work with these large databases based on regulatory data has allowed reproducibility assessment of animal models, which highlight weaknesses in traditional in vivo methods. This should lower the bars for the introduction of new approaches and represents a benchmark that is achievable for any alternative method validated against these methods. Quantitative Structure Activity Relationships (QSAR) models for skin sensitization, eye irritation, and other human health hazards based on these big databases, however, also have made apparent some of the challenges facing computational modeling, including validation challenges, model interpretation issues, and model selection issues. A first implementation of machine learning-based predictions termed REACHacross achieved unprecedented sensitivities of >80% with specificities >70% in predicting the six most common acute and topical hazards covering about two thirds of the chemical universe. While this is awaiting formal validation, it demonstrates the new quality introduced by big data and modern data-mining technologies. The rapid increase in the diversity and number of computational models, as well as the data they are based on, create challenges and opportunities for the use of computational methods.
  • 机译 产妇SSRI的经验和后代发生ASD的风险:一项综述
    摘要:Antidepressants are extensively used during pregnancy and associated with severe outcomes, including innate malformations, prematurity, and low birth weight, etc. A recent study suggested that prenatal exposure to antidepressants may impair child neurodevelopment process. Thus, the aim of this review is to investigate the potential association between prenatal use of selective 5-HT reuptake inhibitors (SSRIs) and the risk of autism spectrum disorders (ASDs). Twelve studies related to the linkage between SSRI exposure during pregnancy and ASD in children were explored and compiled. However, there is a knowledge gap concerning the potential link between gestational exposure to antidepressants and the risk of ASDs. Despite such limitations, the available data show that some signal exists and signifies that antenatal exposure to SSRIs may increase the risk of ASDs. Thus, there is a vital need for further, large and well-designed research to definitively evaluate the existence and the magnitude of this severe risk.
  • 机译 百草枯中毒导致的延迟死亡:三例病例报告和文献复习
    摘要:Paraquat (PQ) poisoning is principally reported in developing countries. However, most fatalities occur elsewhere due to the induction of multi-organ failure. PQ poisoning can hardly be managed by clinical practice, and no specific antidote has come into existence yet. Here three cases, including 17-, 20-, and 23-year-old men, who were poisoned with PQ, have been reported. Furthermore, the literature regarding biological mechanisms, clinical manifestation, and treatment of PQ-induced toxicity was reviewed. Patients who, either intentionally or accidentally, ingested PQ earlier were initially found to be stable at the emergency department (ED). Therefore, they were discharged from the hospital under a follow-up. However, after several days, the patients were referred to the hospital for the second time and despite cardiovascular resuscitation (CPR) efforts, they suddenly expired. The delayed death following exposure to PQ was reported for inducing gradual progressive pulmonary fibrosis, metabolic acidosis, neurotoxicity, renal failure, and liver injury in poisoned patients. Therefore, PQ-intoxicated patients should be supervised for up to several weeks, and kept in the hospital for a longer period of time. Clinical manifestations and laboratory findings are beneficial markers that act as useful predictors of PQ poisoning.
  • 机译 硫芥子气对精子和雄性育性毒性的细胞和分子机制
    摘要:Sulfur mustard (SM) is a toxic compound that can target human spermatozoa. SM induces a wide variety of pathological effects in human reproductive organs, including sexual hormone disturbance, testicular atrophy, impaired spermatogenesis, poor sperm quality, defects in embryo development, childhood physical abnormalities, and severe fertility problems. However, the molecular and cellular mechanisms of SM action on male reproductive health and human sperm function are unclear. Excessive production of reactive oxygen species and the resulting oxidative stress is likely a significant mechanism of SM action, and could be associated with sperm DNA damage, membrane lipid peroxidation, reduced membrane fluidity, mitochondrial deficiency, apoptosis, and poor sperm quality. In this review, we aim to discuss the cellular and molecular mechanisms of SM action on sperm and reproductive health, the significance of OS, and the mechanisms through which SM enhances the infertility rate among SM-exposed individuals.
  • 机译 ZnO薄膜结晶度对体外生物相容性的影响
    摘要:This study evaluated the cytocompatibility of single- and poly-crystalline ZnO thin films using extract and direct contact methods. Exposure to poly-crystalline ZnO extract resulted in reduced cell viability, on average 82%/70% as measured by MTS/LDH assays, respectively. Direct exposure to both single- and poly-crystalline ZnO thin films resulted in reduced cell viability, which was attributed to anoikis due to inhibition of cell adhesion to the substrate by zinc. Intracellular zinc imaging suggests that single crystalline ZnO thin films do not result in a significant change in intracellular zinc concentrations. Overall, the results suggest that single-crystalline ZnO thin films have better short-term (24 h) cytocompatibility and support their potential to serve as a biocompatible sensor material.
  • 机译 沙利度胺型致畸性:同源物的结构-活性关系
    摘要:Unravelling the molecular basis of thalidomide embryotoxicity, which is remarkably species–specific, is challenging in view of its low toxicity in the mature animal. Employing data derived solely from proven sensitive primate species or susceptible strains of rabbit, the structure–activity relationship of over 50 compounds which are, arguably, congeners of thalidomide has been reviewed. The molecular requirement for ‘thalidomide-type’ teratogenicity was highly structure dependent. Both the phthalimide and glutarimide groups were essential for embryopathic activity, although minor substitutions in either or both rings could be tolerated without a loss of toxicity. An α-linkage between the two cyclic structures was essential; a β-link resulted in a complete loss of embryopathic activity. Crucially, this α-configuration provided a centre of asymmetry enabling the existence of stereoisomers. The thalidomide molecule is not a static entity and under physiological conditions it undergoes a number of intra- and inter-molecular reactions. Besides irreversible hydrolysis, its keto–enol tautomerism, base-assisted proton transfer and glutarimide ring rotation lead to rapid interconversion of the thalidomide enantiomers. These enantiomers form equilibria between themselves and also between both homochiral and heterochiral dimers. It is proposed that the more energetically favourable and stable heterochiral dimer of thalidomide is an active agent that possesses the structural features of the paired nucleotides of the double-stranded DNA. Its capacity to enter into hydrogen bonding interactions affects DNA expression in a chaotic manner without causing permanent mutations. This disruption may well be concentrated at nucleotide sites known to be involved in specific promoter regions of the genome.
  • 机译 阿霉素对体外精原细胞,睾丸间质细胞和支持细胞的微RNA信号的干扰
    摘要:We have previously shown that in addition to its widely recognised cardiotoxicity, the chemotherapeutic doxorubicin (DOX) is able to induce transcriptional, microRNA (miRNA) and DNA methylation changes in the mouse testis. These changes perturb pathways involved in stress/cell death and survival and testicular function and lead to germ cell loss and reproductive organ damage. Here, we further investigated the differential miRNA expression induced by DOX in mouse spermatogonial (GC1), Leydig (TM3) and Sertoli (TM4) cell lines in vitro. We began by performing cell cycle analysis of the three mouse testicular cell lines to evaluate their sensitivity to DOX and thus select suitable doses for miRNA profiling. In keeping with our in vivo data, the spermatogonial cell line was the most sensitive, and the Sertoli cell line the most resistant to DOX-induced cell cycle arrest. We then further demonstrated that each cell line has a distinct miRNA profile, which is perturbed upon treatment with DOX. Pathway analysis identified changes in the miRNA-mediated regulation of specialised signalling at germ–Sertoli and Sertoli–Sertoli cell junctions following treatment with DOX. Amongst the most significant disease categories associated with DOX-induced miRNA expression were organismal injury and abnormalities, and reproductive system disease. This suggests that miRNAs play significant roles in both normal testicular function and DOX-induced testicular toxicity. Comparison of our in vitro and in vivo data highlights that in vitro cell models can provide valuable mechanistic information, which may also help facilitate the development of biomarkers of testicular toxicity and high-throughput in vitro screening methods to identify potential testicular toxicants.
  • 机译 用于纳米毒性测试的3D人肺芯片模型
    摘要:The prevalent application of nanoparticles (NPs) has drawn intense concerns about their impact on the environment and human health. Inhalation of NPs is the major route of NP exposure and has led to adverse effects on the lung. It is of great concern to evaluate the potential hazards of nanoparticles for human health during pulmonary exposure. Here, we proposed a novel 3D human lung-on-a-chip model to recreate the organ-level structure and functions of the human lung that allow to us evaluate the pulmonary toxicity of nanoparticles. The lung-on-a-chip consists of three parallel channels for the co-culture of human vascular endothelial cells and human alveolar epithelial cells sandwiching a layer of Matrigel membrane, which recapitulate the key features of the alveolar capillary barrier in the human lung. Cell–cell interaction, cell–matrix interaction and vascular mechanical cues work synergistically to promote the barrier function of the lung-on-a-chip model. TiO2 nanoparticles and ZnO nanoparticles were applied on the lung-on-a-chip to assay their nanotoxicity on both epithelial cells and endothelial cells. Junction protein expression, increased permeability to macromolecules, dose dependent cytotoxicity, ROS production and apoptosis were assayed and compared on the chip. This lung-on-a-chip model indicated its versatile application in human pulmonary health and safety assessment for nanoparticles, environment, food and drugs.
  • 机译 磺胺基非离子表面活性剂的溶血和细胞毒理学:疏水性药物的脂质体载体
    摘要:Biocompatible surfactants are of diverse pharmaceutical interest due to their ability to self-assemble into nano-particulate systems which can be used for single-step drug loading, based upon the hydrophobic–hydrophobic interaction between a hydrophobic drug and the lipophilic part of a surfactant molecule. However, surfactants are associated with cytotoxicity and hemolysis due to their amphiphilic interaction with cellular membranes. This study reports a novel membrane-compatible surfactant, synthesized from sulfanilamide and its self-micellization into niosomes. The surfactant was synthesized in a single step reaction via the introduction of an alkyl chain in the sulfanilamide moiety by conjugation with deconyl chloride. The synthesized surfactant (S-SDC) was characterized by 1H and 13C NMR, mass spectrometry and single crystal XRD. The S-SDC niosomes were explored for drug delivery with clarithromycin as a model drug. The biocompatibility of the surfactant was investigated through hemolysis and cytotoxicity. The surfactant presented a very low critical micellar concentration (CMC) of 0.04 mM and entrapped 65% of the drug which was released in a sustained manner, over 12 h, at acidic and physiological pH. The vesicles were spherical in shape with 234 ± 3.61 nm mean diameter and a narrow size distribution. Niosomes were hemocompatible and nontoxic to cellular membrane. The results suggested the sulfanilamide based surfactant can be applied as a novel and cell membrane compatible niosomal drug delivery vehicle.
  • 机译 表皮屏障的缺陷引起线虫中PEG修饰的氧化石墨烯的毒性和移位
    摘要:The developmental basis for the epidermal barrier against the translocation of nanomaterials is still largely unclear in organisms. We here investigated the effect of deficits in the epidermal barrier on the translocation and toxicity of PEG modified graphene oxide (GO-PEG) in Caenorhabditis elegans. In wild-type or NR222 nematodes, GO-PEG exposure did not cause toxicity and affect the expression of epidermal-development related genes. However, GO-PEG exposure resulted in toxicity in mlt-7(RNAi) nematodes with deficit in the function of epidermal barrier. Epidermal RNAi knockdown of mlt-7 allowed GO-PEG accumulation and translocation into targeted organs through the epidermal barrier. Epidermal-development related proteins of BLI-1 and IFB-1 were identified as targets for MLT-7 in the regulation of GO-PEG toxicity and accounted for MLT-7 function in maintaining the epidermal barrier. AAK-2, a catalytic α subunit of AMP-activated protein kinase, was identified as another target for MLT-7 in the regulation of GO-PEG toxicity. AAK-2 functioned synergistically with BLI-1 or IFB-1 in the regulation of GO-PEG toxicity. Our data provide the molecular basis for the role of epidermal barrier against the toxicity and translocation of nanomaterials in organisms.
  • 机译 蜂蜜辅助燃烧法对煅烧过程对CdO-ZnO纳米复合材料抗菌性能的影响
    摘要:This work reports on honey as a combustion agent of CdO : ZnO nanocomposites and the effects of further annealing (100 °C, 200 °C, 300 °C and 400 °C) on their structural, optical, morphological, elemental, electrical and antimicrobial properties are investigated. X-ray diffraction spectra confirm the cubic and hexagonal structure of CdO : ZnO nanocomposites at 400 °C. When the calcination temperature was increased, the crystallinity, absorbance, bandgap, luminescence intensity, morphological dispersion and mean particle size were also increased. HR-TEM imaging confirmed spherical particles with an average particle size of ∼49 nm. The electrical conductivity of the CdO : ZnO nanoparticles was investigated. The antimicrobial activity of CdO : ZnO nanocomposites was tested for various bacterial and fungal organisms using a zone inhibition method.

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