Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: KEGG:D01170 (ZnO)
13,684 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two experiments were conducted to evaluate the effect of the addition of high levels of Cu (as CuSO4), Fe (as FeSO4) or Zn (as ZnO) to swine starter and grower diets on performance and vitamin E and Se status. The stability of natural tocopherols in mixed feeds was evaluated during storage. Addition of 1,000 ppm Fe or 1,000 ppm Zn had no effect on rate or efficiency of weight gain in either experiment. In Exp. 1, the addition of 250 ppm Cu improved daily gain and efficiency of feed utilization (P less than .05) during the first 3 wk of the experiment. Copper had no effect on pig performance during the rest of Exp. 1 or in Exp. 2. Serum lactate dehydrogenase or glutathione peroxidase activity was not affected (P greater than .1) by any of the mineral additions. Serum tocopherols were not affected by the mineral treatments in Exp. 1. In Exp. 2, addition of 250 ppm Cu decreased (P less than .01) serum tocopherol levels throughout the 8-wk experiment. The alpha-tocopherol levels of the starter diet decreased (P less than .05) during storage. Addition of 250 ppm Cu (P less than .01) or 1,000 ppm Fe (P less than .05) or 1,000 ppm Zn (P less than .05) increased the destruction of alpha-tocopherol in the starter diet. Alpha- and gamma-tocopherol levels of the starter diet decreased to near zero in 22 d in the presence of 250 ppm Cu. In the grower diet, the addition of 250 ppm Cu (P less than .01) or 1,000 ppm Fe (P less than .05) increased the destruction of tocopherols.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of excess dietary copper, iron or zinc on the tocopherol and selenium status of growing pigs. 240 63

Ultrafine metal oxide particles (diameters less than 0.1 microns) and sulfur dioxide are important products of coal combustion. Interaction of these products in the effluent stream results in formation of ultrafine particles with adsorbed sulfur compounds, including sulfuric acid. The toxicity of ultrafine zinc oxide particles with adsorbed sulfuric acid was evaluated by comparing pulmonary lavage fluid from guinea pigs exposed for 1, 2, 3, 4, or 5 consecutive daily 3-h periods to ultrafine zinc oxide generated in the presence of sulfur dioxide (ZnO + SO2) to pulmonary lavage fluid from guinea pigs exposed to an equivalent concentration of ultrafine ZnO. Two groups of guinea pigs exposed either to SO2 or to particle-free furnace gas served as additional controls. Cells, protein, and activities of lactate dehydrogenase, acid phosphatase, and alkaline phosphatase were increased in lavage fluid obtained from guinea pigs exposed to ZnO + SO2 as compared to guinea pigs exposed to ZnO. These results demonstrate the potential importance of ultrafine metal oxides as carries of sulfuric acid derived from fossil fuel combustion.
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PMID:Changes in pulmonary lavage fluid of guinea pigs exposed to ultrafine zinc oxide with adsorbed sulfuric acid. 292 80

A system is described for assessing the toxicity of freshly mixed restorative materials in vitro by measuring changes in the levels of beta-galactosidase and lactic dehydrogenase in both cultured cells and supernatants. The toxic effects of a zinc phosphate and silicate cement, a composite, and zinc oxide/eugenol were studied on two cell types, macrophages and fibroblasts, after 24 h exposure. Zinc oxide/eugenol, Silicap, and zinc phosphate were toxic to macrophages, in that order; Concise appeared to be nontoxic. Only zinc oxide/eugenol exerted significant effects on fibroblasts. Interposing dentine powder between the test cells and the material ameliorated the effects of all materials, possibly by the absorption of toxic components.
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PMID:A comparison of the in vitro cytotoxicity of four restorative materials assessed by changes in enzyme levels in two cell types. 621 26

Along with existing and emerging use of nanoscale materials, growing concerns have arisen about their unintentional health and environmental impact. The objective of the ongoing study was to assess the toxicity profile of metal oxide nanoparticles proposed for use in industrial production methodology. Metal oxide nanoparticles used in this study included TiO2, ZnO, Fe3O4, Al2O3, and CrO3 with particle sizes ranging from 30 to 45 nm. Cellular morphology, mitochondrial function, membrane leakage of lactate dehydrogenase (LDH), permeability of plasma membrane, and apoptosis were assessed under controlled and exposed conditions (2 to 72 h of exposure). The microscopic studies demonstrated that nanoparticle-exposed Neuro-2A cells (especially ZnO) at doses >100 microg/mL became abnormal in size, displaying cellular shrinkage, and detachment from the surface of flasks. Mitochondrial function decreased significantly in the cells exposed to ZnO at 50 to 100 microg/mL. However, Fe3O4, Al2O3, and TiO2 had no measurable effect on the cells until the concentrations reached greater than 200 microg/mL. LDH leakage significantly increased in the cells exposed to ZnO (50 to 100 microg/mL), while other nanoparticles tested displayed LDH leakage only at higher doses (>200 microg/mL). Flow cytometer tests showed that apoptosis took place in cells exposed to ZnO nanoparticles. More cells became necrotic as the concentrations increased.
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PMID:Toxicity of metal oxide nanoparticles in mammalian cells. 1711 1

Previous studies have reported little correlation between the relative toxicity of particle types when comparing lung toxicity rankings following in vivo instillation versus in vitro cell culture exposures. This study was designed to assess the capacity of in vitro screening studies to predict in vivo pulmonary toxicity of several fine or nanoscale particle types in rats. In the in vivo component of the study, rats were exposed by intratracheal instillation to 1 or 5 mg/kg of the following particle types: (1) carbonyl iron (CI), (2) crystalline silica (CS) (Min-U-Sil 5, alpha-quartz), (3) precipitated amorphous silica (AS), (4) nano-sized zinc oxide (NZO), or (5) fine-sized zinc oxide (FZO). Depending on particle type and solution state, these particles range in size from 90 to 500 nm in size. Following exposures, the lungs of exposed rats were lavaged and inflammation (neutrophil recruitment) and cytotoxicity end points (bronchoalveolar lavage [BAL] fluid lactate dehydrogenase [LDH] values) were measured at 24 h, 1 week, 1 and 3 months postexposure. For the in vitro component of the study, three different culture conditions were utilized. Cultures of (1) rat L2 lung epithelial cells, (2) primary alveolar macrophages (AMs) (collected via BAL from unexposed rats), as well as (3) AM-L2 lung epithelial cell cocultures were incubated with the particle types listed above, and the culture fluids were evaluated for cytotoxicity end points (LDH, 1-(4,5-dimethylthiazol-2-yl)-3,5-diphenylformazan [MTT]) as well as inflammatory cytokines (macrophage inflammatory 2 protein [MIP-2], tumor necrosis factor alpha [TNF-alpha], and interleukin-6 [IL-6]) at one (i.e., cytokines) or several (cytotoxicity) time periods. Results of in vivo pulmonary toxicity studies demonstrated that instilled CI particles produced little toxicity. CS particles produced sustained inflammation and cytotoxicity. AS particles produced reversible and transient inflammatory responses. NZO or FZO particles produced potent but reversible inflammation which was resolved by 1 month postinstillation exposure. Results of in vitro pulmonary cytotoxicity studies demonstrated a variety of responses to the different particle types, primarily at high doses. With respect to the LDH results, L2 cells were the most sensitive and exposures to nano- or fine-sized ZnO for 4 or 24 h were more cytotoxic than exposures to CS or AS particles. Macrophages essentially were resistant and epithelial macrophage cocultures generally reflected the epithelial results at 4 and 24 h incubation, but not at 48 h incubation. MTT results were also interesting but, except for nano- and fine-sized ZnO, did not correlate well with LDH results. Results of in vitro pulmonary inflammation studies demonstrated that L2 cells did not produce MIP-2 cytokines, but CS- or AS-exposed AMs and, to a lesser degree, cocultures secreted these chemotactic factors into the culture media. Measurements of TNF-alpha in the culture media by particle-exposed cells demonstrated little activity. In addition, IL-6 secretion was measured in CS, AS, and nano-sized ZnO-exposed cocultures. When considering the range of toxicity end points to five different particle types, the comparisons of in vivo and in vitro measurements demonstrated little correlation, particularly when considering many of the variables assessed in this study-such as cell types to be utilized, culture conditions and time course of exposure, as well as measured end points. It seems clear that in vitro cellular systems will need to be further developed, standardized, and validated (relative to in vivo effects) in order to provide useful screening data on the relative toxicity of inhaled particle types.
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PMID:Assessing toxicity of fine and nanoparticles: comparing in vitro measurements to in vivo pulmonary toxicity profiles. 1730 Oct 66

The present study demonstrated that the zinc concentration in bovine milk and blood plasma is significantly affected by the intake of saturated fat supplements. Sixteen Holstein cows were used in a 4 x 4 Latin square design with 4 periods of 12 d, and 4 dietary treatments were conducted. A total mixed ration based on corn silage, grass-clover silages, and pelleted sugar beet pulp was used on all treatments. A high de novo milk fat diet was formulated by adding rapeseed meal and molasses in the total mixed ration [39 mg of Zn/kg of dry matter (DM)], and a low de novo diet by adding saturated fat, fat-rich rapeseed cake, and corn (34 mg of Zn/kg of DM). Dietary Zn levels were increased by addition of ZnO to 83 and 80 mg of Zn/kg of DM. Treatments did not affect daily DM intake, or yield of energy-corrected milk, milk fat, or milk protein. The high de novo diet significantly increased milk fat percentage and milk content of fatty acids with chain length from C6 to C16, and decreased content of C18 and C18:1. Treatments did not influence milk free fatty acids at 4 degrees C at 0 or 28 h after milking. The average diameter of milk fat globules was significantly greater in milk from cows offered low de novo diets. Furthermore, the low de novo diet significantly increased the concentration of nonesterified fatty acids and d-beta-hydroxybutyrate in blood plasma, the latter was also increased in milk. Treatments did not affect the enzyme activity of lactate dehydrogenase and N-acetyl-beta-d-glucosaminidase in milk or the activity of isocitrate dehydrogenase and malate dehydrogenase in blood plasma. The low de novo diet significantly increased plasma Zn and milk Zn content, whereas dietary Zn level did not in itself influence these parameters. This indicates that the transfer of fat from diet to milk might facilitate transfer of Zn from diet to milk.
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PMID:Transfer of dietary zinc and fat to milk--evaluation of milk fat quality, milk fat precursors, and mastitis indicators. 1834 47

With the increasing use of nanomaterials incorporated into consumer products, there is a need for developing approaches to establish "quantitative structure-activity relationships" (QSARs). These relationships could be used to predict various biological responses after exposure to nanomaterials for the purposes of risk analysis. This risk analysis is applicable to manufacturers of nanomaterials in an effort to determine potential hazards. Because metal oxide materials are some of the most widely applicable and studied nanoparticle types for incorporation into cosmetics, food packaging, and paints and coatings, we focused on comparing different approaches for establishing QSARs for this class of materials. Metal oxide nanoparticles are believed, by some, to cause alterations in cellular function due to their size and/or surface area. Others have said that these nanomaterials, because of the oxidized state of the metal, do not induce stress in biological tests systems. This controversy highlights the need to systematically develop structure-activity relationships (i.e., the relationship between physicochemical features to the cellular responses) and tools for predicting potential biological effects after a metal oxide nanomaterial exposure. Here, we attempt to identify a set of properties of two specific metal oxide nanomaterials-TiO(2) and ZnO-that could be used to characterize and predict the induced cellular membrane damage of immortalized human lung epithelial cells. We adopt a mathematical modeling approach that uses the engineered nanomaterial size characterized as a dry nanopowder and the nanomaterial behavior in ultrapure water, phosphate buffer, and cell culture media to predict nanomaterial-induced cellular membrane damage (via lactate dehydrogenase release). Results of these studies provide insights on how engineered nanomaterial features influence cellular responses and thereby outline possible approaches for developing and applying predictive computational models for biological responses caused by exposure to nanomaterials.
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PMID:Comparative study of predictive computational models for nanoparticle-induced cytotoxicity. 2056 Dec 63

Although nanozinc oxide (nano-ZnO) is applied widely in photocatalysts and gas sensors and in biological fields, it can cause serious oxidative stress and DNA damage to mammalian cells. Our aim in this study was to reduce the cytotoxicity of nano-ZnO by coating it with a TiO(2) layer. We used a sol-gel method to synthesize core (nano-ZnO)/shell (TiO(2)) nanoparticles (NPs) with various degrees of coating. Transmission electron microscopy and Raman spectroscopy confirmed that TiO(2) was coated on the nano-ZnO. Moreover, a decrease in the intensity of the pre-edge signal in Ti K-edge X-ray absorption near edge structure spectra revealed that the core/shell NPs had more Ti-O coordination than pure TiO(2) particles; in addition, the Zn K-edge extended X-ray absorption fine structure spectra revealed that after the ZnO NPs had been coated with TiO(2), the coordination number of the ZnO shell increased to 3.3 but that of the ZnZn shell decreased to 6.2, providing further evidence for the ZnO/TiO(2) core/shell structure. To ensure that the core/shell structures did indeed decrease the toxicity of nano-ZnO, we tested the effects of equal amounts of physical mixtures of ZnO and TiO(2) NPs for comparison, employing methyl tetrazolium (MTT), interleukin-8 (IL-8), lactate dehydrogenase (LDH), and 2',7'-dichlorofluorescin diacetate (DCFH-DA) to assess the particle-induced cytotoxicity, inflammatory response, membrane damage, and intercellular reactive oxygen species (ROS). From X-ray diffraction patterns, we identified the TiO(2) shell as having an amorphous phase, which, unfortunately, exhibited slight cytotoxicity toward the human lung epithelial cell line (A549). Nevertheless, our core/shell nanostructures exhibited less oxidative stress toward A549 cells than did their corresponding ZnO/TiO(2) physical mixtures. In addition, a greater coating of TiO(2) decreased the toxicity of the ZnO NPs. It appears that the ZnO/TiO(2) core/shell structure moderated the toxicity of nano-ZnO by curtailing the release of zinc ions and decreasing the contact area of the ZnO cores.
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PMID:Titanium oxide shell coatings decrease the cytotoxicity of ZnO nanoparticles. 2134 4

Extensive use of engineered nanoparticle (ENP)-based consumer products and their release into the environment have raised a global concern pertaining to their adverse effects on human and environmental health. The safe production and use of ENPs requires improvement in our understanding of environmental impact and possible ecotoxicity. This study explores the toxicity mechanism of ZnO and TiO(2) ENPs in a gram-negative bacterium, Escherichia coli. Internalization and uniform distribution of characterized bare ENPs in the nano range without agglomeration was observed in E. coli by electron microscopy and flow cytometry. Our data showed a statistically significant concentration-dependent decrease in E. coli cell viability by both conventional plate count method and flow cytometric live-dead discrimination assay. Significant (p<0.05) DNA damage in E. coli cells was also observed after ENP treatment. Glutathione depletion with a concomitant increase in hydroperoxide ions, malondialdehyde levels, reactive oxygen species, and lactate dehydrogenase activity demonstrates that ZnO and TiO(2) ENPs induce oxidative stress leading to genotoxicity and cytotoxicity in E. coli. Our study substantiates the need for reassessment of the safety/toxicity of metal oxide ENPs.
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PMID:Engineered ZnO and TiO(2) nanoparticles induce oxidative stress and DNA damage leading to reduced viability of Escherichia coli. 2192 Apr 32

The toxicological effects of zinc oxide nanoparticles (ZnO-NPs) are attracting increasing concern as the field of nanotechnology progresses. Although the literature suggests that toxicity of ZnO-NPs may be related to their dissolution, the mechanism for ZnO-NP perturbation of cytosolic zinc concentration ([Zn(2+)](c)) homeostasis remains obscure. Using FluoZin-3 and RhodZin-3, this study investigated changes in both [Zn(2+)](c) and mitochondrial free Zn(2+) concentration ([Zn(2+)](m)) under conditions of ZnO-NP treatment in vivo and in vitro. In human leukemia Jurkat cells and human lung carcinoma H1355 cells, ZnO-NP treatment resulted in an elevation of both [Zn(2+)](c) and [Zn(2+)](m). In H1355 cells, ZnO-NP treatment induced depolarization of mitochondrial membrane potential, as well as caspase-3 activation and lactic dehydrogenase (LDH) release. In our in vivo experiments, when rats were exposed to ZnO-NPs, higher [Zn(2+)](c) and [Zn(2+)](m) were recorded in both broncho-alveolar lavage (BAL) cells and white blood cells isolated from ZnO-NP-exposed rats, compared with high efficiency particulate air-filter-protected controls LDH levels were also elevated in the BAL of ZnO-NP-exposed rats compared with controls. A mechanical toxicological pathway for ZnO-NP toxicity is suggested by these results: an elevation in [Zn(2+)](c) resulting from ZnO-NP dissolution in the intracellular endosome; cytosolic Zn(2+) sequestration by mitochondria; and elevated [Zn(2+)](m) leading to mitochondrial dysfunction, caspase activation, and cell apoptosis. We conclude that exposure to ZnO-NPs interferes with the homeostasis of [Zn(2+)](c,) and that elevated [Zn(2+)](c) results in cell apoptosis.
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PMID:Zinc oxide nanoparticles interfere with zinc ion homeostasis to cause cytotoxicity. 2211 99


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