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71.
The aim of the present study was to evaluate the potential toxicity and general mechanisms involved in single walled carbon nanotubes (SWCNTs)-induced cytotoxicity using human embryonic kidney cell line (HEK293) cells. Carbon nanotubes (coded as CNT) used in this study were synthesized by the chemical vapor deposition method. To elucidate the possible mechanisms underlying SWCNT-induced cytotoxicity, cell viability, cell membrane damage (lactate dehydrogenase activity (LDH) assay), reduced glutathione (GSH), interleukin-8 (IL-8) and lipid peroxidation products levels were quantitatively assessed following SWCNT exposure for 48 hr using HEK293 cells. Exposure of cells to SWCNT at 3–300 μg/ml produced significant reduction in cell viability in a concentration-dependent manner. The IC50 value of SWCNT was found to be 87.58 μg/ml. Exposure of HEK cells to SWCNT at 10–100 μg/ml resulted in concentration-dependent cell membrane damage, increased production of IL-8, elevated levels of thiobarbituric acid reactive substances like malondialdehyde and decreased intracellular GSH levels. In summary, exposure to SWCNT resulted in a concentration-dependent cytotoxicity in cultured HEK293 cells that was associated with increased oxidative stress. 相似文献
72.
Chromate uptake, reduction, cytotoxicity and mutagenicity were studied with human red blood cells, Chinese hamster ovary (CHO) cells and/or Salmonella typhimurium mutant cells. All cell types rapidly took up chromates whereas chromium(III) salts were excluded under the experimental conditions. Red blood cells reduced and accumulated chromium from chromate. At concentrations above 0.1 mM, chromate inactivated the red cell chromate carrier. Chromate above 0.01 mM inhibited CHO cell proliferation irrespective of the cations present. Chromate and two chromium(III) complexes were mutagenic with Salmonella mutants in the Ames’ assay. A model for chromate metabolism and genotoxicity is proposed. 相似文献
73.
The effects of NiCl2 were studied in two human cell lines, HeLa and diploid embryonic fibroblasts as well as in V79 Chinese hamster cells and in L‐A mouse fibroblasts. NiCl2 produces a dose‐dependent depression of proliferation, mitotic rate, and viability, accompanied by an increasing release of lactic dehydrogenase and stimulation of lactic acid production. The plating efficiency is reduced, as are DNA and protein synthesis and, to a lesser degree, RNA synthesis. The cytotoxicity of NiCl2 is comparable in degree to those of PbCl2 and MnCl2, but is weaker than those of HgCl2 and CdCl2. However, the different sensitivities of different cell lines must also be considered. NiCl2 effects are more severe in serum‐free medium than in medium containing serum or serum albumin indicating that serum constituents, notably albumin, bind the metal effectively and inhibit cellular uptake; this confirms earlier reports on the serum binding and slow uptake of NiCl2. Synchronized cells are most sensitive in the Gl and early S phases of the cell cycle. In the Painter test the depression of DNA synthesis persists following cessation of exposure to NiCI2. These findings contribute an explanation for the known genotoxic effects of nickel. 相似文献
74.
David N. Skilleter 《毒物与环境化学》2013,95(3):213-228
The carcinogenicity of beryllium to several animal species is well established and evidence exists which strongly suggests that this is the case in human exposure. In this review several biochemical properties of the metallocarcinogen are considered including, the causation of cell transformation, and infidelity of DNA synthesis, inhibition of cell division and enzyme induction, and interference with regulatory mechanisms controlling gene expression. These effects are discussed in relation to beryllium chemistry, cellular accumulation mechanisms and distribution to subcellular organdies and molecular targets. It is suggested that the ultimate location and interactions of the metal ion in cell nuclei and its selective inhibition of certain protein phosphorylation reactions in particular are the biochemical effects potentially most relevant to induction of beryllium carcinogenesis. 相似文献
75.
Andrea Hartwig Ursula Kasten Kwabena Boakye‐Dankwa Regina Schlepegrell Detmar Beyersmann 《毒物与环境化学》2013,95(4):205-215
Literature data concerning the genotoxicity of cobalt salts have been conflicting. To establish appropriate incubation conditions, we conducted a series of uptake studies, before genotoxicity was determined by DNA strand break induction in HeLa cells and mutagenicity in V79 Chinese hamster cells. Co(II) is taken up by HeLa cells in a concentration‐dependent manner and is accumulated inside the cell. The uptake is preceded by a fast association step to the outer membrane, with no saturation up to 24 h. DNA strand breaks as determined by nucleoid sedimentation are induced at concentrations as low as 50μMCoCl2. The induction is time‐dependent, showing the highest number of breaks after 4h incubation with no further increase up to 24h. CoCl2 is mutagenic at the HPRT‐locus, enhancing the spontaneous mutation frequency 4.2‐fold at 100μ?. Besides direct interactions with DNA, the mutagenicity of CoCl2 could also be due to a decrease in the Fidelity of DNA polymerisation. 相似文献
76.
Detmar Beyersmann 《毒物与环境化学》2013,95(1-4):61-67
The biochemical speciation of chromium compounds in mammalian cells is discussed with respect to uptake, metabolism, DNA binding and damaging. Whereas soluble hexavalent chromium is taken up rapidly and accumulated intracellularly after its reduction, compounds of trivalent chromium penetrate biomembranes about three orders of magnitude slower. Cr(VI) after its uptake is metabolised by electron donating compounds via Cr(V) to Cr(III) compounds. Chromium from various Cr(III) compounds, but not chromate, binds to chromatin in isolated cell nuclei. The DNA‐protein crosslinks and DNA strand breaks observed in rat liver and kidney after chromate administration are also found in vitro, when Cr(III) compounds (but not chromate) interacts with isolated nuclei. In the Chinese Hamster cell HGPRT mutation assay, three out of four tested Cr(III) complexes were found to be mutagenic. In a direct DNA strand break assay with supercoiled bacteriophage PM 2 DNA, neither chromate nor the four Cr(III) compounds tested caused nicks. However, the combined action of chromate plus glutathione as well as the isolated complex of pentavalent chromium, Na4Cr(glutathione)4, did cause DNA breaks. Reactive oxygen species are inferred to be the ultimate DNA nicking agents in this assay. In conclusion there appear to be two mechanisms of chromate genotoxicity; one with direct DNA damage caused by Cr(V) species and one via DNA‐protein crosslinks formed with Cr(III), the final reduction state of chromate. 相似文献
77.
Bacterial systems have not had success predicting metal carcinogenicity. Hypotheses explaining this failure are examined. Using a broad genetic endpoint, λ prophage induction, under sub‐toxic growing conditions, genotoxicity is seen for compounds of chromium, manganese, lead, molybdenum and tungsten. Copper, manganese, arsenic and molybdenum compounds enhanced UV mutagenesis in E. coli WP2. The toxicity of metal compounds to cultured mammalian cells correlates well with rat oral LD50 values. Whereas insolubility can present problems in bacterial studies, concentrations of metal compounds toxic to mammalian cells can be determined even in the presence of precipitate, and sometimes [Pb(NO3)2, BaCl2 and BeCl2] occurs only in its presence. PbS and MnS, which are insoluble, are much more toxic than the more soluble compounds Pb(NO3)2 and MnCl2. These results demonstrate the importance of cellular phagocytosis of insoluble metal compounds as a factor in studying the toxicity and genotoxicity of metal compounds. 相似文献
78.
通过构建填料型微生物燃料电池(MFC),首次对以喹啉为燃料时的MFC阳极表面的微生物群落进行了分析.PCR-DGGE的试验结果表明,随着燃料的改变,微生物群落也发生改变.当以喹啉和葡萄糖的混合溶液稳定地作为燃料时,由于受到喹啉毒性的抑制,微生物多样性降低,优势菌也发生明显的改变.与葡萄糖共基质相比,以单一喹啉为燃料时的阳极微生物优势菌落发生明显改变.新增加一类菌,这类菌与Pseudomonas sp. DIC5RS 的同源性为100%,推测该菌在单一喹啉为MFC燃料时喹啉的降解过程中起到关键作用. 相似文献
79.
大气颗粒物对肺免疫系统有潜在毒性作用,打破免疫系统平衡,大气颗粒物成分中危害首当其冲的是大气细颗粒物(PM_(2.5)),为研究大气细颗粒物引起的机体T淋巴细胞中Th1/Th2免疫失衡方向。本研究通过免疫组化实验方法检测暴露后小鼠肺组织中T淋巴细胞的表达,进一步采用流式细胞术检测大气细颗粒物气管滴注后小鼠肺脏淋巴细胞中Th1/Th2比例。暴露组小鼠肺组织免疫组化研究结果提示浸润细胞区有大量的CD4~+T细胞,中高剂量暴露组小鼠肺组织中淋巴细胞亚群Th1/Th2比例向Th1偏移。大气细颗粒物影响免疫失衡,使T淋巴细胞向Th1漂移。 相似文献
80.
为了研究环境污染物四氯联苯对移植的原始生殖细胞增殖性迁移的影响,将发育至14期的供体鸡胚原始生殖细胞用PKH26荧光染料标记,然后移植到经过四氯联苯处理的受体鸡胚生殖新月区域,继续孵化,检测其迁移和增殖情况.结果表明,和对照组相比,四氯联苯可明显降低移植原始生殖细胞在血液和性腺中的数量;四氯联苯对外源性原始生殖细胞迁移有明显影响,但雌二醇对外源性原始生殖细胞的增殖性迁移无明显影响,揭示四氯联苯可能影响的是受体性腺的诱引物质,且这种影响是非雌激素样的作用. 相似文献