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The alloys used in orthodontics are subject in the moist environment of the oral cavity to various corrosion processes. If the products of the corrosion are introduced into a biological system they may cause changes. In the present investigation the corrosion rate of 23 different orthodontic wires (preformed arch wires and straight wires) made from 5 different alloys were examined in a nutrient medium by ICP-AES analysis, and the influence of the corrosion products on the cytotoxicity of a fibroblast culture was investigated using Mosmann's MTT test. The nickel-titanium wires Nitinol, Sentalloy and Original Chinese Wire and the beta-titanium alloy TMA had no effect on the rate of cell proliferation. Nor did stainless steel wires inhibit growth significantly, with the exception of Australian Wire and Wildcat Wire. The manganese-steel alloys Noninium h and Mezanium caused significant reductions in growth rate, which were attributed to the manganese ions released by the corrosion. The most severe growth inhibition was caused by the Co-Cr-Ni alloy Elgiloy, and this reaction is independent of the 4 levels of resilience. The degree of growth inhibition depended upon the concentration of corrosive cobalt and nickel ions in the eluate. In spite of the differences observed, all the orthodontic wires examined are graded under ISO-standard 10993-5 as "non-cytotoxic". The degree of toxicity was found to be determined essentially by the corrosion rate of the alloy and the cytotoxic characteristics of the resulting trace elements.
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PMID:In vitro investigation into the biological assessment of orthodontic wires. 980 Apr 40

We used steady-state susceptibility contrast MRI to evaluate the regional cerebral blood volume (rCBV) response to hypocapnia in anesthetised rats. The rCBV was determined in the dorsoparietal neocortex, the corpus striatum, the cerebellum, as well as blood volume in extracerebral tissue (group 1). In addition, we used laser-Doppler flow (LDF) measurements in the left dorsoparietal neocortex (group 2), to correlate changes in CBV and in cerebral blood flow. Baseline values, expressed as a percentage of blood volume in each voxel, were higher in the brain regions than in extracerebral tissue. Hypocapnia (P(a)CO(2) approximately 25 mmHg) resulted in a significant decrease in CBV in the cerebellum (-17 +/- 9%), in the corpus striatum (-15 +/- 6%) and in the neocortex (-12 +/- 7%), compared to the normocapnic CBV values (group 1). These changes were in good agreement with the values obtained using alternative techniques. No significant changes in blood volume were found in extracerebral tissue. The CBV changes were reversed during the recovery period. In the left dorsoparietal neocortex, the reduction in LDF (group 2) induced by hypocapnia (-21 +/- 8%) was in accordance with the values predicted by the Poiseuille's law. We conclude that rCBV changes during CO(2) manipulation can be accurately measured by susceptibility contrast MRI. Abbreviations used: ANOVA analysis of variance CBF cerebral blood flow CBV cerebral blood volume CPMG Carr-Purcell-Meiboom-Gill FiO(2) fractional inspired oxygen ICP intracranial pressure LDF laser-Doppler flow MABP mean arterial blood pressure MRI magnetic resonance imaging MTT mean transit time PaCO(2) arterial partial pressure of carbon dioxide PaO(2) arterial partial pressure of oxygen PET positron emission tomography rCBV regional cerebral blood volume SPECT single-photon emission computed tomography
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PMID:Regional cerebral blood volume response to hypocapnia using susceptibility contrast MRI. 1111 61

Iron overload augments diseases of the liver and microorganism infection as well as deregulates the immune system. In vitro analysis of the effects of iron loading and its chelation involves determining the amount of iron constituting overload, which metal sources and cell lines to use and reliable assay methods. The uptake of 500 microM FeSO4 or FeEDTA by CEMss, U937 or leukocytes was confirmed by inductively coupled plasma-atomic emission spectroscopy (ICP-AES). Excess iron increased CEMss viability (assessed by MTT, XTT, Trypan- and Alamar Blue) by an average of 18% (P = 0.034). Flow cytometry indicated dye-viable cells to be undergoing apotosis/necrosis while still confirming an increase (9%, P < 0.001) in excess iron-induced viability. The iron chelator desferioxamine (DFO) when added in addition to Fe, reversed the effects of excess iron (and vice versa) and had detrimental effects when used on its own (33% inhibition of viability as measured by dyes and 10.85%; P = 0.0427 assessed by flow cytometry). The 4 dyes demonstrated different levels of sensitivity in detecting the influence of iron or DFO but gave a related, qualitative picture while flow cytometry and ICP-AES data was more quantitative.
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PMID:Comparing qualitative and quantitative spectroscopic techniques for the detection of the effect of direct iron loading of mammalian cell cultures. 1248 27

Arsenic is an environmental toxicant and a human carcinogen. The kidney, a known target organ of arsenic toxicity, is critical for both in vivo arsenic biotransformation and elimination. This study investigates the potential of an immortalized human proximal tubular epithelial cell line, HK-2, to serve as a representative model for low level exposures of the human kidney to arsenic. Subcytotoxic concentrations of arsenite (< or = 10 micromol/L) and arsenate (< 100 micromol/L) were determined by leakage of LDH from cells exposed for 24 h. Threshold concentrations of arsenite (between 1 and 10 micromol/L) and arsenate (between 10 and 25 micromol/L) were found to affect MTT processing by mitochondria. Biotransformation of subcytotoxic arsenite or arsenate was determined using HPLC-ICP-MS to detect metabolites in cell culture media and cell lysates. Following 24 h, analysis of media revealed that arsenite was minimally oxidized to arsenate and arsenate was reduced to arsenite. Only arsenite was detected in cell lysates. Pentavalent methylated arsenicals were not detected in media or lysates following exposure to either inorganic arsenical. The activities of key arsenic biotransformation enzymes--MMAV reductase and AsIII methyltransferase--were evaluated to determine whether HK-2 cells could reduce and methylate arsenicals. When compared to the activities of these enzymes in other animal tissues, the specific activities of HK-2 cells were indicative of a robust capacity to metabolize arsenic. It appears this human renal cell line is capable of biotransforming inorganic arsenic compounds, primarily reducing arsenate to arsenite. In addition, even at low concentrations, the mitochondria are a primary target for toxicity.
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PMID:Toxicity and metabolism of subcytotoxic inorganic arsenic in human renal proximal tubule epithelial cells (HK-2). 1468 17

In this study, the general toxicity tests including acute toxicity test, haemolysis test, MTT assay of Ti-Fe-Mo-Mn-Nb-Zr alloys were carried out. The morphology of these cells was also observed under phase-contrast microscope. By using X-ray photoelectron spectroscopy(XPS), the kind and mol% of element in surface film were studied. The kind and concentration of element in dipping fluid were investigated by ICP atomic emission spectrometry. The results showed the primary component is TiO2 in surface film. The dipping fluid of Ti-Fe-Mo-Mn-Nb-Zr alloys contains Fe 0.2-1.07 mg/l and Mn 0.16-0.5 mg/l; such dental materials are beneficial to health. No cytotoxic effect was disclosed by in vitro and in vivo tests. The level of cytotoxicity was grade 0 and 1; the haemolysis degree was 0.558%-0.642%, i.e. less than 5%. The cells growing in the extract showed normal morphology. These data indicate that Ti-Fe-Mo-Mn-Nb-Zr alloy, as a dental material, has good biocompatibility.
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PMID:[Evaluation on biocompatibility of Ti-Fe-Mo-Mn-Nb-Zr alloy]. 1514 39

Chronic arsenic exposure increases risk for the development of diabetes, vascular disease, and cancers of the skin, lung, kidney, and bladder. This study investigates the effects of arsenite [As(III)] on human urothelial cells (UROtsa). As(III) toxicity was determined by exposing confluent UROtsa cells to As(III) (0.5-200 microM). Depleting cellular glutathione levels with buthionine sulfoximine (BSO) potentiated the toxicity of As(III). Cell viability was assessed with the (4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. UROtsa cell ability to biotransform As(III) was determined by dosing cells with environmentally relevant concentrations of As(III) followed by HPLC/ICP-MS analysis of cell media and lysate. Both pentavalent and trivalent monomethylated products were detected. Although cytotoxicity was observed at high doses of As(III) (approximately 100 microM) in UROtsa cells, perturbations of a variety of molecular processes occurred at much lower doses. Exposure to low-level As(III) (0.5-25 microM) causes an accumulation of ubiquitin (Ub)-conjugated proteins. This effect is enhanced when cellular glutathione levels have been reduced with BSO treatment. Because As(III) has many effects on UROtsa cells, a greater understanding of how As(III) is affecting cellular proteins in a target tissue will lead to a better understanding of the mechanism of toxicity and pathogenesis for low-level As(III).
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PMID:Effects of arsenite on UROtsa cells: low-level arsenite causes accumulation of ubiquitinated proteins that is enhanced by reduction in cellular glutathione levels. 1527 21

Effects of Ce on the short-term biocompatibility of Ti-Fe-Mo-Mn-Nb-Zr alloy designed for implant materials were studied by acute toxicity test, hemolytic test, and MTT assay. The elements and their concentration in surface films and extraction media of Ti alloys were investigated with XPS and ICP, respectively. The primary compositions of the surface films of Ti alloys with 0.3% Ce and without Ce were TiO2 and Nb2O5. There were 0.2 mg/l Fe and 0.16 mg/l Mn in the extraction medium of Ti alloy without Ce, while 0.27 mg/l Fe and 0.87 mg/l Mn in the extraction medium of Ti alloy with 0.3% Ce. The concentrations of Fe and Mn in the medium were too low to have any significant effects on human health. There was no sign of cytotoxicity in these tests. The cytotoxicity levels of Ti alloys without Ce and with 0.3% Ce were graded 0 and 1, respectively. The hemolytic degrees of Ti alloys without Ce and with 0.3% Ce were 0.558% and 0.67%, respectively. The cells being incubated in the extraction medium were normal. These phenomena indicated that Ce was innocuous within the concentration range of this study. In addition, the hemolytic ratio and toxicity level of Ti alloy with 0.3% Ce were a little higher than that of Ti alloy without Ce. This meant that Ce would slightly increase the toxicity of Ti alloy.
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PMID:Effects of Ce on the short-term biocompatibility of Ti-Fe-Mo-Mn-Nb-Zr alloy for dental materials. 1534 36

Cadmium is a widely distributed industrial and environmental pollutant. Principle target organs are soft tissues such as the liver, where cadmium accumulates with a biological half-life of approximately 20-30 years causing a variety of toxic responses. In HepG2, CdCl(2) exposure for short periods (from 1 to 24h) induces differential expression of stress proteins, including MT and hsp70. However, less is known about the stress response during a prolonged exposure to this metal. MTT assay showed a low cytotoxicity of CdCl(2) (0.1, 0.5, 1, 2, 5, 10microM), over a period of 72h. Cadmium uptake by ICP-AES technique and the corresponding expression of stress proteins (MT, hsp70) during the same prolonged time were also analysed. Results show that Cd was continuously and increasingly accumulated, at the highest of the concentrations tested. Metallothionein expression was up-regulated with a saturation curve at 48 as well as 72h after CdCl(2) exposure. High levels of MT probably confer an acquired tolerance to the stress and protection against cell injury as demonstrated by low cytotoxicity values. On the contrary, the unchanged pattern of hsp70 expression suggests that this protective mechanism, unlike other members of the family, is less involved during CdCl(2) prolonged exposure.
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PMID:Metallothionein and hsp70 expression in HepG2 cells after prolonged cadmium exposure. 1705 95

Seven new mixed ammine/propylamine platinum(II) complexes with carboxylates (a-g) have been synthesized and characterized by elemental analysis, conductivity, IR, UV, and (1)H NMR spectra techniques. The cytotoxicity of these complexes was tested by MTT assay. The levels of total platinum bound to DNA were measured by ICP-MS. The results indicate that the complexes (a-g) have better cytotoxicity against EJ and HL-60 than other carcinoma cell lines. The cytotoxicity increases in the sequence: g<f<e<d<b<c<a against tested carcinoma cell lines. The cytotoxicity of complexes (a-c) is equal to that of cisplatin against HL-60. The cytotoxicity of complex a is also equal to that of cisplatin against EJ. However, the complexes (a-g) are significantly less potent than cisplatin against BGC-823, HCT-8 and MCF-7. The total DNA-platination levels increase in the sequence: cisplatin<g<e<f<d<b<c<a under the same experimental conditions. It suggests that there is no correlation between total DNA-platination levels in HL-60 cells and cytotoxicity of ammine/propylamine platinum complexes. When leaving groups are aromatic carboxylates, the complexes have better cytotoxicity, and moreover, the substituent in benzene ring also influences cytotoxicity.
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PMID:Synthesis, cytotoxicity and DNA-binding levels of ammine/propylamine platinum(II) complexes with carboxylates. 1708 87

Seven new tri-functional mononuclear platinum(II) complexes (a-g) have been synthesized and characterized by elemental analysis, conductivity, thermal analysis, IR, UV and (1)H NMR spectral techniques. The cytotoxicity of these complexes was tested by MTT and SRB assays. The cell cycle analysis and the levels of total platinum bound to DNA were measured by flow cytometry and ICP-MS. The results indicate that the complexes (a-g) have selectivity against tested carcinoma cell lines; they have weaker cytotoxicity against HCT-8 and MCF-7. Complexes a, b, d and g also exert weaker cytotoxicity against BGC-823 and complexes a, b, e and f have better cytotoxicity against EJ, but their cytotoxicity is weaker than that of cisplatin. Complexes c, e and f, confer substantially greater cytotoxicity against HL-60 with an IC(50) value of 7.68+/-0.23, 3.87+/-0.19 and 2.41+/-0.18 microM, respectively, moreover, cytotoxicity of complex f is equal to that of cisplatin. Complexes c, e and f cause significant G(2)/M arrest and a concomitant decrease of cell population in G(1) and S phases. The total DNA-platination levels of them are higher than that of cisplatin under the same experimental conditions. It suggests that there is no correlation between total DNA-platination levels in HL-60 cells and cytotoxicity of complexes. When leaving groups are aromatic carboxylates, the complexes have better cytotoxicity, moreover, the substituent in benzene ring also influences cytotoxicity. In addition, when leaving groups are dicarboxylates, dicarboxylates coordinating with platinum through oxygen atoms form different chelate cycle and cycle size also affects their cytotoxicity.
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PMID:Synthesis, cytotoxicity and DNA binding levels of tri-functional mononuclear platinum(II) complexes. 1758 65


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