Toxicology Mechanisms and Methods最新文献_第8页

Ameliorative effects of gallic acid, quercetin and limonene on urethane-induced genotoxicity and oxidative stress in Drosophila melanogaster 没食子酸、槲皮素和柠檬烯对氨基甲酸乙酯诱导的黑腹果蝇遗传毒性和氧化应激的改善作用

IF 3.2 4区医学

Toxicology Mechanisms and Methods Pub Date : 2017-01-18 DOI: 10.1080/15376516.2016.1278294

Isha Nagpal, S. Abraham

{"title":"Ameliorative effects of gallic acid, quercetin and limonene on urethane-induced genotoxicity and oxidative stress in Drosophila melanogaster","authors":"Isha Nagpal, S. Abraham","doi":"10.1080/15376516.2016.1278294","DOIUrl":"https://doi.org/10.1080/15376516.2016.1278294","url":null,"abstract":"Abstract The main objective of our present work was to ascertain the efficacy of Drosophila melanogaster model for assessing antigenotoxic and antioxidant effects of dietary phytochemicals gallic acid (GA), quercetin (QC) and limonene (Lim) against urethane (URE), a genotoxic environmental carcinogen. Oregon-K (ORK) adult male flies were fed GA, QC and Lim in combination with URE (20 mM) in 10% sucrose for 72 h. Third instar larvae were fed instant medium containing the above phytochemicals and URE for 24 h. Sex-linked recessive lethal (SLRL) test and assays for estimating glutathione content (GSH), glutathione S-transferase (GST), catalase (CAT), superoxide dismutase (SOD) and lipid peroxidation (MDA content) were performed. Adult feeding experiments demonstrated that co-treatment of flies with URE and the test phytochemicals has significantly decreased the frequencies of SLRL mutations in all the germ cell stages when compared to that with URE alone. Larval feeding experiments also showed a similar pattern. The above results correlate well with antioxidative potentials of the test agents where we observed the elevated enzymatic levels with a significant reduction in MDA level in Drosophila larvae. The results further suggest that the dietary phytochemicals have an antioxidant and antimutagenic property which can be assessed using D. melanogaster.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1278294","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41566153","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: 20

DNA damage and adduct formation in immune organs of developing chicks by polycyclic aromatic hydrocarbons 多环芳烃对发育雏鸡免疫器官DNA损伤及加合物形成的影响

IF 3.2 4区医学

Toxicology Mechanisms and Methods Pub Date : 2017-01-18 DOI: 10.1080/15376516.2016.1273432

A. Nisha, H. Hazilawati, M. L. Mohd Azmi, M. Noordin

{"title":"DNA damage and adduct formation in immune organs of developing chicks by polycyclic aromatic hydrocarbons","authors":"A. Nisha, H. Hazilawati, M. L. Mohd Azmi, M. Noordin","doi":"10.1080/15376516.2016.1273432","DOIUrl":"https://doi.org/10.1080/15376516.2016.1273432","url":null,"abstract":"Abstract Polycyclic aromatic hydrocarbons (PAHs) are persistent pollutants and chemically a class of structurally similar chemical compounds characterized by the presence of fused aromatic rings. This research was undertaken to find out immunotoxic effects produced by pyrene, phenanthrene and fluoranthene. These chemicals were injected into developing chicks at three dose levels (0.2, 2 and 20 mg per kg) through allantioc route to rule out possible mechanisms involved in immunotoxicity. DNA adduct produced by PAHs in immune organs were analyzed by DNA adduct enzyme-linked immunosorbent assay (ELISA) kit and DNA damage was assessed by comet assay. A significant increase in the DNA adduct levels was found in thymus and bursa in 2 mg and 20 mg dose levels of pyrene, fluoranthene and phenanthrene treated groups, whereas those in spleen simulated the value of controls. Comet assay indicated that PAHs especially pyrene, fluoranthene and phenanthrene were capable of inducing increased level of comet parameters in thymus at all the dose levels. Bursa of Fabricius and spleen also showed a gradual rise in comet parameters corresponding to all dose levels, but the increase was more marked as in thymus. Thus, it can be concluded that DNA adducts produced by PAHs lead to single-strand breaks and reduced DNA repair, which ultimately begin a carcinogenic process. Hence, this experiment can be considered as a strong evidence of genotoxic potential of PAHs like pyrene, phenanthrene and fluoranthene in developing chicks.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1273432","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43174271","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

Molecular interactions of dioxins and DLCs with the ketosteroid receptors: an in silico risk assessment approach 二恶英和dlc与酮类固醇受体的分子相互作用:一种计算机风险评估方法

IF 3.2 4区医学

Toxicology Mechanisms and Methods Pub Date : 2017-01-11 DOI: 10.1080/15376516.2016.1273423

M. F. Khan, M. Alam, G. Verma, W. Akhtar, M. Rizvi, Asif Ali, M. Akhter, M. Shaquiquzzaman

{"title":"Molecular interactions of dioxins and DLCs with the ketosteroid receptors: an in silico risk assessment approach","authors":"M. F. Khan, M. Alam, G. Verma, W. Akhtar, M. Rizvi, Asif Ali, M. Akhter, M. Shaquiquzzaman","doi":"10.1080/15376516.2016.1273423","DOIUrl":"https://doi.org/10.1080/15376516.2016.1273423","url":null,"abstract":"Abstract Dioxins and dioxin-like compounds (DLCs) are the ones with poor water solubility and low volatility, resistant to physical, chemical and biological processes, persistent in the environment even under extreme conditions. Due to lipophilic nature, they get adhered to the fatty material and concentrate through biomagnification and bioaccumulation, thereby easily getting incorporated into food chains, paving the way to endocrine disruption via modulation of various human receptors. This in turn leads to certain adverse health effects. In the present study, a total of 100 dioxins and DLCs were taken and their binding pattern was assessed with the ketosteroid receptors, i.e. androgen (hAR), glucocorticoid (hGR), progesterone (hPR) and mineralocorticoid (hMR) in comparison to the corresponding natural steroids and a known endocrine disrupting xenobiotic, Bisphenol A (BPA). Most of the DLCs, particularly those bearing hydroxyl (-OH) group showed considerable affinities with ketosteroid receptors. On comparing D scores of all the dioxins and DLCs against all four receptors, compound 8-hydroxy-3,4-dichlorodibenzofuran(8-OH-DCDF) exhibited least D score of -9.549 kcal mol−1 against hAR. 3,8-Dihydroxy-2-chlorodibenzofuran(3,8-DiOH-CDF), 4′-hydroxy-2,3,4,5-tetrachlorobiphenyl (4′-OH-TCB) and 4-hydroxy-2,2′,5′-trichlorobiphenyl(4-OH-TCB) also showed comparable molecular interactions with the ketosteroid receptors. These interactions mainly include H-bonding, π–π stacking, hydrophobic, polar and van der Waals’ interactions. In contrast, BPA and some natural ligands tested in this study showed lower binding affinities with these receptors than certain DLCs reported herein, i.e. certain DLCs might be more toxic than the proven toxic agent, BPA. Such studies play a pivotal role in the risk assessment of exposure to dioxins and DLCs on human health.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1273423","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47684545","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: 7

Oxcarbazepine-induced cytotoxicity and genotoxicity in human lymphocyte cultures with or without metabolic activation 奥卡西平在有或无代谢激活的人类淋巴细胞培养中诱导的细胞毒性和遗传毒性

IF 3.2 4区医学

Toxicology Mechanisms and Methods Pub Date : 2017-01-11 DOI: 10.1080/15376516.2016.1273430

Zülal Atlı Şekeroğlu, H. Kefeli̇oğlu, Seval Kontaş Yedier, V. Şekeroğlu, Berrin Delmecioğlu

{"title":"Oxcarbazepine-induced cytotoxicity and genotoxicity in human lymphocyte cultures with or without metabolic activation","authors":"Zülal Atlı Şekeroğlu, H. Kefeli̇oğlu, Seval Kontaş Yedier, V. Şekeroğlu, Berrin Delmecioğlu","doi":"10.1080/15376516.2016.1273430","DOIUrl":"https://doi.org/10.1080/15376516.2016.1273430","url":null,"abstract":"Abstract There has been considerable debate about the relationship between epilepsy and cancer. Oxcarbazepine (OXC) is used for treating certain types of seizures in patients with epilepsy. There have been no detailed investigations about genotoxicity of OXC and its metabolites. Therefore, the aim of this study is to investigate the cytotoxic and genotoxic effects of OXC and its metabolites on cultured human lymphocytes. The cytotoxicity and genotoxicity of OXC on human peripheral blood lymphocytes were examined in vitro by sister chromatid exchange (SCE), chromosomal aberration (CA) and micronucleus (MN) tests. Cultures were treated with 125, 250 and 500 μg/ml of OXC in the presence (3 h treatment) and absence (24 h and 48 h treatment) of a metabolic activator (S9 mix). Dimethyl sulfoxide (DMSO) was used as a solvent control. OXC showed cytotoxic activities due to significant decreases in mitotic index (MI), proliferation index (PI) and nuclear division index (NDI) in the absence of S9 mix when compared with solvent control. Metabolites of OXC also significantly reduced MI and PI in cultures with S9 mix. OXC significantly increased the CAs, aberrant cells, SCE and MN values in the presence and absence of S9 mix. Our results indicated that both OXC and its metabolites have cytotoxic, cytostatic and genotoxic potential on human peripheral blood lymphocyte cultures under the experimental conditions. Further studies are necessary to elucidate the relationship between cytotoxic, cytostatic and genotoxic effects, and to make a possible risk assessment in patients receiving therapy with this drug.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1273430","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49660070","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

Effects of pentachlorophenol and dichlorodiphenyltrichloroethane on secretion of interferon gamma (IFNγ) and tumor necrosis factor alpha (TNFα) from human immune cells 五氯酚和二氯二苯三氯乙烷对人免疫细胞分泌干扰素γ (IFNγ)和肿瘤坏死因子α (TNFα)的影响

IF 3.2 4区医学

Toxicology Mechanisms and Methods Pub Date : 2017-01-11 DOI: 10.1080/15376516.2016.1275906

Reda Massawe, Leon Drabo, M. Whalen

{"title":"Effects of pentachlorophenol and dichlorodiphenyltrichloroethane on secretion of interferon gamma (IFNγ) and tumor necrosis factor alpha (TNFα) from human immune cells","authors":"Reda Massawe, Leon Drabo, M. Whalen","doi":"10.1080/15376516.2016.1275906","DOIUrl":"https://doi.org/10.1080/15376516.2016.1275906","url":null,"abstract":"Abstract Pentachlorophenol (PCP) and dichlorodiphenyltrichloroethane (DDT) are pesticides that have been widely used and significantly contaminate the environment. Both are found in human blood and have been shown to alter the lytic and binding function of human natural killer (NK) cells. Interferon gamma (IFNγ) and tumor necrosis factor alpha (TNFα) are pro-inflammatory cytokines, which regulate immune responsiveness to pathogens and tumors. Their levels require very tight control to prevent loss of immune competence or excessive inflammation. Here, we examined the capacity of PCP and DDT to alter the secretion of these critical pro-inflammatory cytokines from increasingly reconstituted (more complex) preparations of human immune cells which included NK cells, monocyte-depleted (MD) peripheral blood mononuclear cells (PBMCs) (a preparation that is predominantly lymphocytes) and PBMCs (a preparation containing lymphocytes and monocytes). Results indicated that exposure to PCP decreased IFNγ secretion at the highest exposures (2.5 and 5 μM) and increased IFNγ secretion at lower concentrations. These effects were seen irrespective of the complexity of the cell preparation. PCP at 2.5 and 5 μM generally decreased TNFα secretion from NK cells, but had inconsistent effects in MD-PBMCs and PBMCs. Exposure of each of the immune cell preparations to DDT caused increase in IFNγ secretion. DDT (2.5 μM) increased TNFα secretion from MD-PBMCs after either 24 h or 48 h of exposure. The mechanism of PCP-induced increase in IFNγ secretion appears to involve the p38 mitogen activated protein kinase (MAPK) pathway, based on loss of PCP stimulated increase when this pathway was inhibited.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1275906","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47141548","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: 10

RETRACTED ARTICLE: Asiatic acid attenuates pre-neoplastic lesions, oxidative stress, biotransforming enzymes and histopathological alterations in 1,2-dimethylhydrazine-induced experimental rat colon carcinogenesis 文章摘要:在1,2-二甲基肼诱导的实验大鼠结肠癌中，亚洲酸可减轻肿瘤前病变、氧化应激、生物转化酶和组织病理学改变

IF 3.2 4区医学

Toxicology Mechanisms and Methods Pub Date : 2017-01-11 DOI: 10.1080/15376516.2016.1273422

Aktarul Islam Siddique, V. Mani, S. Arivalagan, N. Thomas, N. Namasivayam

{"title":"RETRACTED ARTICLE: Asiatic acid attenuates pre-neoplastic lesions, oxidative stress, biotransforming enzymes and histopathological alterations in 1,2-dimethylhydrazine-induced experimental rat colon carcinogenesis","authors":"Aktarul Islam Siddique, V. Mani, S. Arivalagan, N. Thomas, N. Namasivayam","doi":"10.1080/15376516.2016.1273422","DOIUrl":"https://doi.org/10.1080/15376516.2016.1273422","url":null,"abstract":"Abstract Statement of Retraction: Asiatic acid attenuates pre-neoplastic lesions, oxidative stress, biotransforming enzymes and histopathological alterations in 1,2-dimethylhydrazine-induced experimental rat colon carcinogenesis We, the Editors and Publishers of Toxicology Mechanisms and Methods have retracted the following article:  Aktarul Islam Siddique, Vijay Mani, Sivaranjani Arivalagan, Nisha Susan Thomas & Nalini Namasivayam (2017) Asiatic acid attenuates pre-neoplastic lesions, oxidative stress, biotransforming enzymes and histopathological alterations in 1,2-dimethylhydrazine-induced experimental rat colon carcinogenesis, Toxicology Mechanisms and Methods, 27:2, 136-150, DOI: 10.1080/15376516.2016.1273422 The article is being retracted due to image manipulation in Figures 3 and 9, as follows: Figure 3: Panel E is a subsection of Panel B; Figure 3: Panels C and D appear to contain clone stamps; Figure 9: Panels A and B are the same image, with the frame of reference shifted; Figure 9: Panels Ai and Bi are the same image, with the frame of reference shifted; Figure 9: Panels E and F contain an overlapping section (panel E lower right corner, panel F upper left corner); Figure 9: Panels Ei and Fi contain an overlapping section (panel Ei lower right corner, panel Fi upper left corner). These findings are not explained by the content of the article and the authors were not able to provide original data that would support the integrity of their research. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”. ","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1273422","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43096693","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

On the mechanism of genotoxicity of ethephon on embryonic fibroblast cells 乙烯利对胚胎成纤维细胞遗传毒性机制的研究

IF 3.2 4区医学

Toxicology Mechanisms and Methods Pub Date : 2017-01-08 DOI: 10.1080/15376516.2016.1273425

M. Hodjat, M. Baeeri, M. Rezvanfar, M. Rahimifard, M. Gholami, M. Abdollahi

{"title":"On the mechanism of genotoxicity of ethephon on embryonic fibroblast cells","authors":"M. Hodjat, M. Baeeri, M. Rezvanfar, M. Rahimifard, M. Gholami, M. Abdollahi","doi":"10.1080/15376516.2016.1273425","DOIUrl":"https://doi.org/10.1080/15376516.2016.1273425","url":null,"abstract":"Abstract Ethephon is one of the most widely used plant growth regulator in agriculture that its application has been increased in recent years. Many reports have raised concern over the safety of this organophosphorus compound. The aim of the current study was to assess the potential genotoxic effect of ethephon on murine embryonic fibroblast (MEF) cell line, using two genotoxicity endpoints: γH2AX expression and comet assay. γH2AX served as an early and sensitive biomarker of genotoxic damage. Oxidative stress biomarkers, including reactive oxygen species (ROS), lipid peroxidation (LPO) and total antioxidant capacity were also examined. The results showed a significant increase in cell proliferation, 24 h post-treatment with 10, 40,160 μg/ml ethephon, while at the higher concentrations cytotoxic effect was observed. The γH2AX expression and γH2AX foci count per cell were significantly increased at non-cytotoxic concentrations of ethephon, accompanied with increased DNA damage as illustrated by comet assay. LPO and ROS levels were elevated only at 160 μg/ml and higher doses. The results interestingly showed that low non-cytotoxic doses of ethephon promoted DNA damage inducing cell proliferation, raising the possibility of ethephon mutagenicity. The genotoxic effect of ethephon at low doses might not relate to oxidative damage and that increased in the level of ROS and LPO generation at higher doses could account for the cytotoxic effect of ethephon. Taken together, our study provides strong in vitro evidence on potential genotoxicity of ethephon at low doses. More precise studies are needed to clarify the mutagenic effect of chronic exposure to ethephon.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1273425","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45053601","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: 27

Involvement of the activation of Nrf2/HO-1, p38 MAPK signaling pathways and endoplasmic reticulum stress in furazolidone induced cytotoxicity and S phase arrest in human hepatocyte L02 cells: modulation of curcumin Nrf2/HO-1、p38 MAPK信号通路的激活和内质网应激参与呋喃唑酮诱导的人肝细胞L02细胞的细胞毒性和S期阻滞:姜黄素的调节

IF 3.2 4区医学

Toxicology Mechanisms and Methods Pub Date : 2017-01-08 DOI: 10.1080/15376516.2016.1273424

Chongshan Dai, L. Lei, Bin Li, Yang Lin, Xilong Xiao, Shusheng Tang

{"title":"Involvement of the activation of Nrf2/HO-1, p38 MAPK signaling pathways and endoplasmic reticulum stress in furazolidone induced cytotoxicity and S phase arrest in human hepatocyte L02 cells: modulation of curcumin","authors":"Chongshan Dai, L. Lei, Bin Li, Yang Lin, Xilong Xiao, Shusheng Tang","doi":"10.1080/15376516.2016.1273424","DOIUrl":"https://doi.org/10.1080/15376516.2016.1273424","url":null,"abstract":"Abstract Furazolidone (FZD) is extensively used as the antiprotozoal and antibacterial drug in clinic. The previous study has shown that curcumin pretreatment could improve FZD induced cytotoxicity by inhibiting oxidative stress and mitochondrial apoptotic pathway. The current study aimed to investigate the potential roles of endoplasmic reticulum (ER) stress, p38 mitogen-activated protein kinases (p38 MAPK) signaling pathway in curcumin against FZD cytotoxicity by using human hepatocyte L02 cells. The results showed that curcumin could markedly attenuate FZD induced cytotoxicity. Compared with FZD alone group, curcumin pretreatment significantly reduced the expression of phospho (p)-p38, cyclin D1, p-checkpoint kinase 1 (ChK1) and breast cancer associated gene 1 (BRCA1) protein, followed to attenuate S phase arrest. Meanwhile, curcumin pretreatment prevented FZD induced ER stress, evidenced by the inhibition of glucose-regulated protein 78 and DNA damage inducible gene 153/C/EBP-homologous protein (GADD153/CHOP) protein expression. Moreover, compared with the control, FZD exposure activated the protein and mRNA expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1), which were further activated by curcumin treatment. These results reveal that curcumin could prevent FZD induced cytotoxicity and S phase arrest, which may involve the activation of Nrf2/HO-1 pathway and the inhibition of p38 MAPK pathway and ER stress.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1273424","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42127344","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: 18

Effect of pregabalin on fear-based conditioned avoidance learning and spatial learning in a mouse model of scopolamine-induced amnesia 普瑞巴林对东莨菪碱致失忆症小鼠基于恐惧的条件回避学习和空间学习的影响

IF 3.2 4区医学

Toxicology Mechanisms and Methods Pub Date : 2017-01-08 DOI: 10.1080/15376516.2016.1273426

K. Sałat, A. Podkowa, N. Malikowska, J. Trajer

{"title":"Effect of pregabalin on fear-based conditioned avoidance learning and spatial learning in a mouse model of scopolamine-induced amnesia","authors":"K. Sałat, A. Podkowa, N. Malikowska, J. Trajer","doi":"10.1080/15376516.2016.1273426","DOIUrl":"https://doi.org/10.1080/15376516.2016.1273426","url":null,"abstract":"Abstract Objectives: Cognitive deficits are one of the frequent symptoms accompanying epilepsy or its treatment. Methods: In this study, the effect on cognition of intraperitoneally administered antiepileptic drug, pregabalin (10 mg/kg), was investigated in scopolamine-induced memory-impaired mice in the passive avoidance task and Morris water maze task. The effect of scopolamine and pregabalin on animals’ locomotor activity was also studied. Results: In the retention phase of the passive avoidance task, pregabalin reversed memory deficits induced by scopolamine (p < 0.05). During the acquisition phase of the Morris water maze pregabalin-treated memory-impaired mice performed the test with longer escape latencies than the vehicle-treated mice (significant at p < 0.05 on Day 5, and at p < 0.001 on Day 6). There were no differences in this parameter between the scopolamine-treated control group and pregabalin-treated memory-impaired mice, which indicated that pregabalin had no influence on spatial learning in this task. During the probe trial a significant difference (p < 0.05) was observed in terms of the mean number of target crossings between vehicle-treated mice and pregabalin-treated memory-impaired mice but there was no difference between the scopolamine-treated control group and mice treated with pregabalin + scopolamine. Pregabalin did not influence locomotor activity increased by scopolamine. Discussion: In passive avoidance task, pregabalin reversed learning deficits induced by scopolamine. In the Morris water maze, pregabalin did not influence spatial learning deficits induced by scopolamine. These results are relevant for epileptic patients treated with pregabalin and those who use it for other therapeutic indications (anxiety, pain).","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2017-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2016.1273426","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42880847","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

The effects of endoplasmic reticulum stress inducer thapsigargin on the toxicity of ZnO or TiO2 nanoparticles to human endothelial cells 内质网应激诱导剂thapsigargin对ZnO或TiO2纳米颗粒对人内皮细胞毒性的影响

IF 3.2 4区医学

Toxicology Mechanisms and Methods Pub Date : 2017-01-08 DOI: 10.1080/15376516.2016.1273429

Yuxiu Gu, Shanshan Cheng, Gui Chen, Yuexin Shen, Xiyue Li, Qin Jiang, Juan Li, Yi Cao

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引用次数: 41