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排序方式: 共有501条查询结果,搜索用时 31 毫秒
81.
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
82.
The present study was carried out to evaluate the question of whether or not royal jelly affects N-acetylation and metabolism of 2-aminofluorene (2-AF) in the human liver tumor cell line (J 5). N-acetylation and metabolism of 2-AF in intact J5 cells was determined by using high performance liquid chromatography for the amounts of acetylated and nonacetylated 2-AF and profile of 2-AF metabolism. The results indicated that royal jelly displayed a dose-dependent inhibition of N-acetylation of 2-AF in J5 cells. Royal jelly also decreased the profile of 2-AF metabolites in J5 cells. This report is the first demonstration which showed that royal jelly affects N-acetylation of 2-AF in human liver tumor cells (J5). 相似文献
83.
The environmental impact of nanotechnology has caused a great concern. Many in vitro studies showed that many types of nanoparticles were cytotoxic. However, whether these nanoparticles caused cell membrane damage was not well studied. F2-isoprostanes are specific products of arachidonic acid peroxidation by nonenzymatic reactive oxygen species and are considered as reliable biomarkers of oxidative stress and lipid peroxidation. In this article, we investigated the cytotoxicity of different nanoparticles and the degree of cellular membrane damage by using F2-isoprostanes as biomarkers after exposure to nanoparticles. The human lung epithelial cell line A549 was exposed to four silica and metal oxide nanoparticles: SiO2 (15 nm), CeO2 (20 nm), Fe2O3 (30 nm), and ZnO (70 nm). The levels of F2-isoprostanes were determined by using high-performance liquid chromatography/mass spectrometry. The F2-isoprostanes’ peak was identified by retention time and molecular ion m/z at 353. Oasis HLB cartridge was used to extract F2-isoprostanes from cell medium. The results showed that SiO2, CeO2, and ZnO nanoparticles increased F2-isoprostanes levels significantly in A549 cells. Fe2O3 nanoparticle also increased F2-isoprostanes level, but was not significant. This implied that SiO2, CeO2, ZnO, and Fe2O3 nanoparticles can cause cell membrane damage due to the lipid peroxidation. To the best of our knowledge, this is the first report on the investigation of effects of cellular exposure to metal oxide and silica nanoparticles on the cellular F2-isoprostanes levels. 相似文献
84.
Lead (Pb) is a heavy metal, known to induce oxidative stress and produce damage to the antioxidant defence system ultimately leading to cell death. Antioxidants such as epigallocatechin 3-gallate (EGCG), a green tea polyphenol, was shown to play a protective role during Pb-exposure. In this study, human SH-SY5Y neuroblastoma cells were exposed to different concentrations (0.01–10?µM) of Pb for 48?h to determine effects on the viability of cells. It was observed that IC50 was at 5?µM and at this concentration the cells exhibited a significant increase in caspase-3 activity, an indicator of apoptosis at least by 10-fold and the decrease of 59.4% in glutathione (GSH) content. The total cellular prostaglandin-E2 (PGE2) level was found to be elevated at least 10-fold upon Pb exposure. However, the effects of Pb on cells pre-incubated with 50?µM EGCG followed by 5?µM Pb showed 40% inhibition in cell viability, 17.3% decrease in caspase-3 activity, 23% increase in GSH content, and 11.4% fall in PGE2 levels when compared with cells exposed to Pb only. Data suggest that EGCG exerted a significant protection to cell viability in preventing cell death and elevation in levels of GSH in cells exposed to Pb. However, EGCG did not elicit any significant effect on release of PGE2 indicating the nature of EGCG as an effective anti-apoptotic, antioxidant, and anti-inflammatory agent. 相似文献
85.
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
86.
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
87.
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
88.
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
89.
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
90.
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