Toxicology Mechanisms and Methods最新文献

筛选
英文 中文
The effects of di 2-ethyl hexyl phthalate (DEHP) on cellular lipid accumulation in HepG2 cells and its potential mechanisms in the molecular level 邻苯二甲酸二乙酯(DEHP)对HepG2细胞脂质积累的影响及其在分子水平上的潜在机制
IF 3.2 4区 医学
Toxicology Mechanisms and Methods Pub Date : 2017-02-01 DOI: 10.1080/15376516.2016.1273427
Wang Zhang, Xin-yue Shen, Wen-wen Zhang, Hao-Yun Chen, Wei-ping Xu, Wei Wei
{"title":"The effects of di 2-ethyl hexyl phthalate (DEHP) on cellular lipid accumulation in HepG2 cells and its potential mechanisms in the molecular level","authors":"Wang Zhang, Xin-yue Shen, Wen-wen Zhang, Hao-Yun Chen, Wei-ping Xu, Wei Wei","doi":"10.1080/15376516.2016.1273427","DOIUrl":"https://doi.org/10.1080/15376516.2016.1273427","url":null,"abstract":"Abstract Diethylhexyl phthalate (DEHP) is suspected to be an inevitable factor related to metabolic disease. Our previous study demonstrated that excess DEHP could exacerbate non-alcoholic fatty liver disease (NAFLD) in SD rats. Addressing the terra incognita in DEHP-induced metabolic dysfunction, this study used HepG2 cells to investigate the potential mechanisms involved in DEHP-induced toxicity in vitro. The cells were established lipid overload model with oleic acid and BSA, then exposed to different concentrations (5, 10, 25, 50, 100 μmol/l DEHP) of DEHP for further analysis. The Oil Red O staining results showed that DEHP could promote lipid accumulation in cells. The level of superoxide dismutase (SOD) and malondialdehyde (MDA) changed suggested the balance of oxidative stress was disrupted. Additionally, western blot analysis showed that DEHP could promote the expression of peroxisome proliferator-activated receptor α (PPARα) and sterol regulatory element-binding protein 1c (SREBP-1c). By quantifying the expressions of the two proteins, it is of interest to determine that DEHP could promote lipid accumulation in hepatocytes via activating the SREBP-1c and PPARα-signaling pathway.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1273427","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41546962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 54
Toxicity and oxidative stress induced by T-2 toxin in cultured mouse Leydig cells T-2毒素对小鼠间质细胞的毒性及氧化应激作用
IF 3.2 4区 医学
Toxicology Mechanisms and Methods Pub Date : 2017-02-01 DOI: 10.1080/15376516.2016.1258747
Yong Fa Zhang, Jian Ying Yang, Yong Li, W. Zhou
{"title":"Toxicity and oxidative stress induced by T-2 toxin in cultured mouse Leydig cells","authors":"Yong Fa Zhang, Jian Ying Yang, Yong Li, W. Zhou","doi":"10.1080/15376516.2016.1258747","DOIUrl":"https://doi.org/10.1080/15376516.2016.1258747","url":null,"abstract":"Abstract To explore the toxic mechanism of T-2 toxin on Leydig cells of mice, we would investigate the toxicity and oxidative stress induced by T-2 toxin in the cells. Leydig cells were isolated and cultured with control or T-2 toxin (10−7 M, 10−8 M, or 10−9 M) for 24 h, then cells and supernatants were harvested to examine cell viability, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities, expression of messenger RNA (mRNA) related to oxidative stress, malondialdehyde (MDA) content and DNA damage. The cell viability was evaluated in mouse Leydig cells by MTT assay, MDA content and SOD, GSH-Px and CAT activities were measured by routine kits, expression of mRNA related to oxidative stress were examined by quantitative real-time polymerase chain reaction (PCR), and DNA damage was investigated by comet assay. Leydig cells treated with T-2 toxin showed significant reductions in cell viability, SOD, GSH-Px and CAT activities, and expression of mRNA related to oxidative stress, and remarkable increases in MDA content and levels of DNA damage. This study proves that T-2 toxin is toxic to Leydig cells of mice. Furthermore, oxidative stress plays an important role in the above-mentioned negative effects of T-2 toxin.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1258747","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41593403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 24
Construction and comparison of yeast whole-cell biosensors regulated by two RAD54 promoters capable of detecting genotoxic compounds 两种RAD54启动子调控的酵母全细胞生物传感器的构建及比较
IF 3.2 4区 医学
Toxicology Mechanisms and Methods Pub Date : 2017-02-01 DOI: 10.1080/15376516.2016.1266540
Yongjie Tian, Yixin Lu, Xiuju Xu, Chao Wang, Tianqi Zhou, Xiangming Li
{"title":"Construction and comparison of yeast whole-cell biosensors regulated by two RAD54 promoters capable of detecting genotoxic compounds","authors":"Yongjie Tian, Yixin Lu, Xiuju Xu, Chao Wang, Tianqi Zhou, Xiangming Li","doi":"10.1080/15376516.2016.1266540","DOIUrl":"https://doi.org/10.1080/15376516.2016.1266540","url":null,"abstract":"Abstract Two yeast enhanced green fluorescence protein (yEGFP) yeast reporter vectors, pR1558-yEGFP and pR406-yEGFP, which are regulated by two RAD54 promoters containing 406-bp and 1558-bp DNA sequences, respectively, were constructed using molecular biological techniques and transformed into yeast for the screening of genotoxins. The constructed biosensors were named W303-1A/R1558-yEGFP and W303-1A/R406-yEGFP. To quantify biosensor performance, both transformed yeast cells were exposed to multiple doses of genotoxins including methylmethane sulfonate (MMS; a DNA alkylating agent), 4-nitroquinoline-N-oxide (4-NQO; a DNA cleavage agent), 5-fluorouracil (5-Fu; an inhibitor of polymerases and topoisomerases) and colchicine and canavanine (affecting other biochemical activities). The yeast bioassay performance was analyzed using fluorescence-activated cell sorting (FACS) and Multi-Mode Reader in a 96-well black microplate. The observed W303-1A/R1558-yEGFP dose-effect relationship was more obvious and the maximum inductions were 5.96-fold (MMS), 2.19-fold (4-NQO) and 2.71-fold (5-Fu); the corresponding values for W303-1A/R406-yEGFP were 2.53-, 1.50- and 1.91-fold, respectively. It is suggested that it is best to select the entire RAD54 promoter when constructing recombinant yeast cells for screening mutagens.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1266540","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48526929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 12
The effect of ingested sulfite on active avoidance in normal and sulfite oxidase-deficient aged rats 摄入亚硫酸盐对正常和亚硫酸氧化酶缺乏老年大鼠主动回避的影响
IF 3.2 4区 医学
Toxicology Mechanisms and Methods Pub Date : 2017-02-01 DOI: 10.1080/15376516.2016.1253812
O. Ozsoy, Sinem Aras, Ayse Ozkan, H. Parlak, B. Gemici, N. Uysal, M. Aslan, P. Yargiçoğlu,, A. Agar
{"title":"The effect of ingested sulfite on active avoidance in normal and sulfite oxidase-deficient aged rats","authors":"O. Ozsoy, Sinem Aras, Ayse Ozkan, H. Parlak, B. Gemici, N. Uysal, M. Aslan, P. Yargiçoğlu,, A. Agar","doi":"10.1080/15376516.2016.1253812","DOIUrl":"https://doi.org/10.1080/15376516.2016.1253812","url":null,"abstract":"Abstract The aim of this study was to investigate the possible toxic effects of sulfite on neurons by measuring active avoidance learning in normal and sulfite oxidase (SOX)-deficient aged rats. Twenty-four months of age Wistar rats were divided into four groups: control (C), sulfite-treated group (S), SOX-deficient group (D) and SOX-deficient + sulfite-treated group (DS). SOX deficiency was established by feeding rats with a low molybdenum (Mo) diet and adding 200 ppm tungsten (W) to their drinking water. Sulfite in the form of sodium metabisulfite (25 mg/kg) was given by gavage for six weeks. Active avoidance responses were determined by using an automated shuttle box. Hepatic SOX activity was measured to confirm SOX deficiency. The hippocampus was used for determining the activity of cyclooxygenase (COX) and caspase-3 enzymes and the level of prostaglandin E2 (PGE2) and nitrate/nitrite. SOX-deficient rats had an approximately 10-fold decrease in hepatic SOX activity compared with normal rats. Sulfite did not induce impairment of active avoidance learning in SOX-deficient rats and in normal rats compared with their control groups. Sulfite had no effect on the activity of COX and caspase-3 in the hippocampus. Treatment with sulfite did not significantly increase the level of PGE2 and nitrate/nitrite in the hippocampus.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1253812","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46699232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Early assessment of proarrhythmic risk of drugs using the in vitro data and single-cell-based in silico models: proof of concept 使用体外数据和基于单细胞的计算机模型对药物致心律失常风险的早期评估:概念验证
IF 3.2 4区 医学
Toxicology Mechanisms and Methods Pub Date : 2017-02-01 DOI: 10.1080/15376516.2016.1256460
Mitra Abbasi, B. Small, N. Patel, M. Jamei, S. Polak
{"title":"Early assessment of proarrhythmic risk of drugs using the in vitro data and single-cell-based in silico models: proof of concept","authors":"Mitra Abbasi, B. Small, N. Patel, M. Jamei, S. Polak","doi":"10.1080/15376516.2016.1256460","DOIUrl":"https://doi.org/10.1080/15376516.2016.1256460","url":null,"abstract":"Abstract Background and purpose: To determine the predictive performance of in silico models using drug-specific preclinical cardiac electrophysiology data to investigate drug-induced arrhythmia risk (e.g. Torsade de pointes (TdP)) in virtual human subjects. Experimental approach: To assess drug proarrhythmic risk, we used a set of in vitro electrophysiological measurements describing ion channel inhibition triggered by the investigated drugs. The Cardiac Safety Simulator version 2.0 (CSS; Simcyp, Sheffield, UK) platform was used to simulate human left ventricular cardiac myocyte action potential models. Results: This study shows the impact of drug concentration changes on particular ionic currents by using available experimental data. The simulation results display safety threshold according to drug concentration threshold and log (threshold concentration/ effective therapeutic plasma concentration (ETPC)). Conclusion and implications: We reproduced the underlying biophysical characteristics of cardiac cells resulted in effects of drugs associated with cardiac arrhythmias (action potential duration (APD) and QT prolongation and TdP) which were observed in published 3D simulations, yet with much less computational burden.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1256460","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44764515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 16
Protective effects of lemongrass essential oil against benzo(a)pyrene-induced oxidative stress and DNA damage in human embryonic lung fibroblast cells 柠檬草精油对苯并芘诱导的人胚胎肺成纤维细胞氧化应激和DNA损伤的保护作用
IF 3.2 4区 医学
Toxicology Mechanisms and Methods Pub Date : 2017-02-01 DOI: 10.1080/15376516.2016.1266541
Jiao Jiang, Henggui Xu, Hetong Wang, Yining Zhang, P. Ya, Chun Yang, Fasheng Li
{"title":"Protective effects of lemongrass essential oil against benzo(a)pyrene-induced oxidative stress and DNA damage in human embryonic lung fibroblast cells","authors":"Jiao Jiang, Henggui Xu, Hetong Wang, Yining Zhang, P. Ya, Chun Yang, Fasheng Li","doi":"10.1080/15376516.2016.1266541","DOIUrl":"https://doi.org/10.1080/15376516.2016.1266541","url":null,"abstract":"Abstract Benzo(a)pyrene (BaP) was a well-known environmental pollutant, numerous studies had implicated BaP as a causative agent in human cancer, particularly lung cancer. The lemongrass essential oil (LEO) possessed various pharmacological activities, especially the anti-oxidative stress and cancer prevention. In the current study, human embryonic lung fibroblast (HELF) cells were treated with 25 mM BaP in the absence or presence of 0.5%, 1% or 2.5% LEO and the cell viability and levels of oxidative stress (OS) and DNA damage in the cells were then measured. Nineteen chemical constituents were identified in LEO, with citral being the main component, representing about 68.78%. LEO was able to protect the HELF cells against BaP-induced loss in cell viability, achieving a maximum of 95.58% cell viability at the 0.5% concentration. Treatment of HELF cells with BaP alone significantly increased the level of Malondialdehyde (MDA) and decreased superoxide dismutase (SOD) and catalase (CAT). However, these effects were suppressed when the cells were also treated with LEO, leading to enhanced levels of SOD and CAT activities (2.9- and 2-fold, respectively, compared with BaP treatment only) and reduced the level of MDA in the cells (43% reduction in malondialdehyde level). At the same time, LEO also reduced the level of DNA damage, as shown by a reduced level of 8-hydroxy-deoxyguanosine (8-OHdG). Taken together, the results showed that LEO offered protection against BaP-induced OS and DNA damage, suggesting that LEO could be a promising agent for lung cancer chemoprevention.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1266541","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47173805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 15
Evaluation of oxidative stress induction in rats following exposure to silver nanorods 银纳米棒暴露后大鼠氧化应激诱导的评价
IF 3.2 4区 医学
Toxicology Mechanisms and Methods Pub Date : 2017-01-25 DOI: 10.1080/15376516.2016.1274351
Harikiran Lingabathula, N. Yellu
{"title":"Evaluation of oxidative stress induction in rats following exposure to silver nanorods","authors":"Harikiran Lingabathula, N. Yellu","doi":"10.1080/15376516.2016.1274351","DOIUrl":"https://doi.org/10.1080/15376516.2016.1274351","url":null,"abstract":"Abstract The study investigated the oxidative stress induction by the 10 and 25 nm silver nanorods (SNRs) following intra-tracheal instillation in rats after 1 day, 1 week, 1 month and 3 months post instillation periods at 1 and 5 mg/kg b.w. doses. The blood was withdrawn by retro orbital plexus method after exposure periods and different oxidative stress markers were estimated. The results showed that the both sizes of SNRs induced increased levels of malondialdehyde (MDA) and depleted glutathione (GSH) levels after 1 day and 1 week post exposure periods. The 10 and 25 nm SNRs at both doses displayed that significantly reduced levels of superoxide dismutase (SOD) and catalase following 1 day and 1 week post exposure periods. Also, the results have shown that decrease in total antioxidant capacity (TAC) of both sizes of SNRs significantly following 1 day and 1 week post exposure periods, indicating the oxidative stress induction by SNRs. In spite, there were no significant changes in oxidative stress markers following 1 month and 3 months post exposure periods may be due to recovery. The increased levels of MDA and decreased levels of GSH, SOD, catalase and TAC activity are strongly associated to ROS production and lipid peroxidation, suggesting the induction of oxidative stress in rats. The 10 nm SNRs at 5 mg/kg b.w. dose exposures in rats have shown greater changes in all oxidative stress parameters, indicating the greater induction of oxidative stress when compared with the 25 nm SNRs, representing the size–dose-dependent induction of oxidative stress of SNRs.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1274351","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45656506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 5
C2-ceramide influences alveolar epithelial barrier function by downregulating Zo-1, occludin and claudin-4 expression C2神经酰胺通过下调Zo-1、occludin和claudin-4的表达影响肺泡上皮屏障功能
IF 3.2 4区 医学
Toxicology Mechanisms and Methods Pub Date : 2017-01-24 DOI: 10.1080/15376516.2017.1278812
Jin Yang, Ying Wang, Hui Liu, Ji-rui Bi, Youjin Lu
{"title":"C2-ceramide influences alveolar epithelial barrier function by downregulating Zo-1, occludin and claudin-4 expression","authors":"Jin Yang, Ying Wang, Hui Liu, Ji-rui Bi, Youjin Lu","doi":"10.1080/15376516.2017.1278812","DOIUrl":"https://doi.org/10.1080/15376516.2017.1278812","url":null,"abstract":"Abstract Noncardiogenic lung edema is a key factor affecting the prognosis of acute lung injury (ALI). Previous studies have been focused on regulatory roles of ceramide on lung vascular endothelial barrier functions and had already identified ceramide as mediator involved in the formation of lung edema. However, the effects of ceramide on lung epithelial barrier were still unknown. This study aimed to investigate the effects of ceramide on the barrier function of alveolar epithelial cells. Primary mouse alveolar type II epithelial cells (AECII) were grown on Transwell polyester membranes to construct monolayer, and stimulated with different concentrations of ceramide. Transepithelial resistance (TER) was measured to assess the epithelial cell permeability. Western blotting and real-time quantitative polymerase chain reaction were used to detect the mRNA and protein levels of tight junction, respectively. After incubation with different concentrations of c2-ceramide, TER of AECII monolayer decreased significantly in a dose-dependent manner. Moreover, expressions of ZO-1, occludin and claudin-4 were significantly reduced by c2-ceramide in the study. This study demonstrated that ceramide could increase alveolar epithelial cell monolayer permeability by downregulation of tight junction proteins. Therefore, modulation of ceramide expression may serve as a new therapeutic approach to treat acute lung injury.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2017.1278812","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44308750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 22
Epigallocatechin-3-gallate attenuates acrylamide-induced apoptosis and astrogliosis in rat cerebral cortex 表没食子儿茶素-3-没食子酸酯减轻丙烯酰胺诱导的大鼠大脑皮层细胞凋亡和星形胶质细胞形成
IF 3.2 4区 医学
Toxicology Mechanisms and Methods Pub Date : 2017-01-22 DOI: 10.1080/15376516.2017.1279251
Yin He, Dehong Tan, B. Bai, Zhaoxia Wu, Shu-juan Ji
{"title":"Epigallocatechin-3-gallate attenuates acrylamide-induced apoptosis and astrogliosis in rat cerebral cortex","authors":"Yin He, Dehong Tan, B. Bai, Zhaoxia Wu, Shu-juan Ji","doi":"10.1080/15376516.2017.1279251","DOIUrl":"https://doi.org/10.1080/15376516.2017.1279251","url":null,"abstract":"Abstract The potent neurotoxic agent acrylamide (ACR) is formed during Maillard reaction in food processing. Epigallocatechin-3-gallate (EGCG), a major bioactive component of green tea, is an antioxidant, but its effects on ACR-induced neurotoxicity are unclear. Here, we investigated the neuroprotective effects of EGCG against ACR-induced apoptosis and astrogliosis in the cerebral cortex. Rats were pretreated with EGCG for 4 d and then co-administered ACR for 14 d. Immunohistochemical analysis of glial fibrillary acidic protein and 8-hydroxy-2′-deoxyguanosine indicated that EGCG attenuated astrogliosis and DNA damage in ACR-treated rats. Analysis of DNA fragmentation and protein expression of Bax, Bcl-2, caspase 3, and cytochrome c revealed that EGCG inhibited ACR-induced apoptosis. Furthermore, EGCG inhibited oxidative stress by enhancing the activity of antioxidant enzymes and glutathione levels and reducing the formation of reactive oxygen species and lipid peroxidation. Taken together, our data demonstrate that EGCG inhibits ACR-induced apoptosis and astrogliosis in the cerebral cortex.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2017.1279251","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48322620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 34
A comparison of neuroprotective efficacy of two novel reactivators of acetylcholinesterase called K920 and K923 with the oxime K203 and trimedoxime in tabun-poisoned rats 两种新型乙酰胆碱酯酶再激活剂K920和K923和肟K203和曲马多肟对塔本中毒大鼠神经保护作用的比较
IF 3.2 4区 医学
Toxicology Mechanisms and Methods Pub Date : 2017-01-22 DOI: 10.1080/15376516.2016.1275907
J. Kassa, J. Misík, J. Hatlapatková, J. Zdarova Karasova
{"title":"A comparison of neuroprotective efficacy of two novel reactivators of acetylcholinesterase called K920 and K923 with the oxime K203 and trimedoxime in tabun-poisoned rats","authors":"J. Kassa, J. Misík, J. Hatlapatková, J. Zdarova Karasova","doi":"10.1080/15376516.2016.1275907","DOIUrl":"https://doi.org/10.1080/15376516.2016.1275907","url":null,"abstract":"Abstract The ability of two newly developed bispyridinium oximes (K920, K923) to reduce tabun-induced acute neurotoxic signs and symptoms was compared with the oxime K203 and trimedoxime using a functional observational battery (FOB). The neuroprotective effects of the oximes studied combined with atropine on rats poisoned with tabun at a sublethal dose (130 μg/kg i.m.; 80% of LD50 value) were evaluated. Tabun-induced neurotoxicity was monitored by FOB at 2 h after tabun administration. The results indicate that all tested oximes combined with atropine enable tabun-poisoned rats to survive till the end of experiment while one non-treated tabun-poisoned rat died within 2 h. Both newly developed oximes (K920, K923) combined with atropine were able to markedly decrease tabun-induced neurotoxicity in the case of sublethal poisoning although they did not eliminate all tabun-induced acute neurotoxic signs and symptoms. Their ability to decrease tabun-induced acute neurotoxicity did not prevail the neuroprotective efficacy of trimedoxime and the oxime K203. Therefore, the newly developed oximes are not suitable for the replacement of currently available oximes (especially trimedoxime) in the treatment of acute tabun poisonings.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1275907","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49350635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信