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PubMed2001

Cytotoxicity of derivatives from dehydrocrotonin on V79 cells and Escherichia coli.

New derivatives from dehydrocrotonin (DHC, compound I), with the same anti-ulcerogenic properties but less toxicity were synthesised by reducing the cyclohexenone moiety of DHC with NaBH(4) (compound II), by reducing the cyclohexenone and lactone moieties with LiAlH(4) (compound III) and by transforming the lactone moiety into an amide (compound IV) using dimethylamine. The cytotoxicity of these derivatives from DHC was assayed on V79 fibroblast cell line. Three independent endpoints for cytotoxicity were evaluated; namely, the nucleic acid content (NAC), tetrazolium reduction (MTT) and neutral red uptake (NRU). IC(50) values of 540 and 350 microM were obtained for compound II in the NRU and NAC tests, respectively. Compound III was less toxic than the other DHC derivatives (IC(50)=1800 microM) on V79 cells based on NAC assay. Compound IV showed an IC(50) ranging from 350 to 600 microM based on the three endpoints evaluated. The three compounds were less toxic on V79 cells than DHC. DHC, compounds II, III and IV did not change the respiration rate of Escherichia coli on the acute toxicity assay.

Animals↗

PubMed1984

[Value of histochemical tetrazolium technics].

A short review is given about the value of the tetrazolium technique in histochemistry including some new aspects of the tetrazolium reduction. The different factors and properties determining the localization, pattern and colours of the formazans in the tissue slide are discussed. The current knowledge of the atypically coloured formazans caused by the nitro groups is presented.

Formazans↗

PubMed1990

Indium-111-antimyosin images compared with triphenyl tetrazolium chloride staining in a patient six days after myocardial infarction.

The results of indium-111 (111In) antimyosin imaging during life and the findings on postmortem imaging and triphenyl tetrazolium chloride (TTC) staining of the heart are reported from a patient who received 111In-antimyosin on the sixth day following myocardial infarction and died after imaging the next day. The planar images obtained during life showed abnormal 111In-antimyosin uptake in the posterior, lateral, and apical walls of the left ventricle. Autopsy revealed extensive infarction of the left ventricular lateral and posterior walls with cardiac rupture, which was the cause of sudden death. Direct imaging of the sliced specimen of heart revealed abnormal tracer uptake in the lateral and posterior walls of the left ventricle, which correlated closely with the area of necrosis outlined by TTC staining. Our results confirm the experimental findings that antimyosin antibody binds specifically to the acute irreversibly damaged myocardial cells. A high degree of tracer uptake can be seen even when 111In-antimyosin is injected six days postinfarction.

Aged↗

PubMedDate not supplied

Superoxide and bone resorption.

The reaction of superoxide with nitroblue tetrazolium produces an electron-dense diformazan precipitate which can be used to localize areas of superoxide production. Transmission electron microscopy was used to demonstrate that diformazan granules formed by the reaction of nitroblue tetrazolium with excess superoxide are electron dense, whereas monoformazan granules generated by hydrogen peroxide were not. On the basis of these observations, superoxide formed along the osteoclast-bone interface was localized by demonstrating the electron-dense diformazan granules between the osteoclastic membrane and the bone surface. The formation of this reaction product was inhibited by a superoxide scavenger, the deferoxamine mesylate-manganese complex (the "green" complex), confirming the specificity of the reaction product. The scavenger also inhibited bone resorption. High concentrations of superoxide generated in vitro at a neutral pH degraded osteocalcin into numerous peptide fragments, demonstrating the ability of superoxide to break peptide bonds. These studies localize superoxide production to the ruffled border space and suggest that superoxide generated at the osteoclast-bone interface is involved in bone matrix degradation.

Animals↗

PubMedDate not supplied

Rapid in vitro test for determination of anti-amoebic activity.

A rapid microplate assay for the detection of potential compounds active against Entamoeba histolytica is described. The assay is based on the metabolic reduction of a tetrazolium salt by E. histolytica trophozoites as an indicator of their viability which may be measured photometrically. The method was validated by determining the dose-response characteristics of standard amoebicides and correlating optical density and cell number; it provides a convenient means of selecting potentially novel anti-amoebic compounds for subsequent testing in vivo.

Amebicides↗

PubMed2000

Cytotoxicity assessment of antibiofouling compounds and by-products in marine bivalve cell cultures.

Short-term primary cell cultures were derived from adult marine bivalve tissues: the heart of oyster Crassostrea gigas and the gill of clam Ruditapes decussatus. These cultures were used as experimental in vitro models to assess the acute cytotoxicity of an organic molluscicide, Mexel-432, used in antibiofouling treatments in industrial cooling water systems. A microplate cell viability assay, based on the enzymatic reduction of tetrazolium dye (MTT) in living bivalve cells, was adapted to test the cytotoxicity of this compound: in both in vitro models, toxicity thresholds of Mexel-432 were compared to those determined in vivo with classic acute toxicity tests. The clam gill cell model was also used to assess the cytotoxicity of by-products of chlorination, a major strategy of biofouling control in the marine environment. The applications and limits of these new in vitro models for monitoring aquatic pollutants were discussed, in reference with the standardized Microtox test.

Animals↗

PubMed1977

Kinetics and mechanism of blue tetrazolium reaction with corticosteroids.

The kinetics of the reaction of blue tetrazolium with corticosteroids were investigated under pseudo-first-order conditions. The reaction rates for various corticosteroids were determined at various temperatures, and the enthalpy and entropy of activation for these compounds were determined. A mechanism is proposed in which an electron pair and a proton are transferred to blue tetrazolium from the anion formed by the action of tetramethylammonium hydroxide on the alpha-carbonyl moiety of the corticosteroid. The proposed mechanism is consistent with previous experimental results.

Adrenal Cortex Hormones↗

PubMed1984

Decreased activity of acetyl-CoA carboxylase during chemically induced neutrophilic differentiation of human promyelocytic leukemia cells.

In order to better understand the mechanism by which changes in the fatty acid composition of cellular lipids occur in leukemia cell lines induced to differentiate, the activity of the first enzyme of fatty acid biosynthesis, acetyl-CoA carboxylase (EC 6.4.1.2) was measured in HL-60 promyelocytic leukemia cells before, during and after treatment with compounds that induce these cells to mature to neutrophillike cells. After 24 h of exposure to dimethylsulfoxide, retinoic acid, or butyric acid, no morphological or biochemical (nitroblue tetrazolium reduction) evidence of differentiation occurred, but acetyl-CoA carboxylase activity decreased 44, 44.5, and 49% respectively, compared to untreated cells. After 7 days of culture in the presence of these agents, 79, 83, and 72% of cells acquired the ability to reduce nitroblue tetrazolium (versus 15% of control cells) and enzyme activity decreased 92.7, 99.7, and 98%, compared to control cultures, with the three compounds respectively. Thus, some of the reported changes in fatty acid composition of leukemia cells with differentiation may arise, in part, from the depression of the de novo fatty acid biosynthetic pathway and the loss of acetyl-CoA carboxylase activity may be a useful marker for neutrophilic differentiation in HL-60 cells.

Acetyl-CoA Carboxylase↗

PubMed1976

The quantification of formazans in tissue sections by microdensitometry. II. The use of BPST, a new tetrazolium salt.

This article describes the use of a microdensitometer for the measurement of BPST formazan in tissue sections. BPST is a new tetrazolium salt, 2-(2-benzothiazolyl)-3-(4-phthalhydrazidyl)-5-styryl-tetrazolium chloride, which produces a single, well-defined formazan, and is thus easily quantified. The formazan gives an excellent localization, since BPST was originally designed for ultrastructural work. Activities are expressed in absolute units as n moles hydrogen/mm3, and are thus directly comparable with standard biochemical data.

Animals↗

PubMed2000

In vitro cytotoxicity of various forms of cobalt for rat alveolar macrophages and type II pneumocytes.

It has been shown that cobalt (Co) and the mixture cobalt-tungsten carbide (CoWC) are cytotoxic for alveolar macrophages (AM) and alveolar type II cells (AT-II), but the exact mechanisms of toxicity are not entirely elucidated. In this study, we exposed primary cultures of AT-II and AM, in vitro, to different forms of Co (Co particles, CoWC particles, CoCl(2)) and assessed cell damage using the dimethylthiazol diphenyl tetrazolium bromide test. In some experiments, inserts were used to separate the particles from the cells. The results show that AT-II are twice as sensitive to the effects of 100 microg Co particles/well (1.88 cm(2)) than AM. For this latter cell type, the presence of WC almost doubled (at 25 microg Co/well) the toxic effects compared to pure Co, but this synergy between Co and WC only occurred if the particles were in close contact with the cells. Lactalbumin and, to a lesser degree, EDTA were able to reduce the toxicity of Co, CoWC, and CoCl(2) for AT-II and AM. CoCl(2) showed a similar toxicity for AT-II and AM. The use of Co-conditioned medium revealed that Co particles are "aged" after having been incubated for 24 h in an aqueous medium and are then no longer able to cause the same degree of cell damage as fresh Co particles (71 versus 15% viability for 100 microg Co/well). The time course of the toxicity of the different forms of Co for AT-II and AM showed different patterns in causing cell damage, suggesting different action mechanisms. Evaluation of cell damage by electron microscopy was consistent with biochemical indices. Overall, our results indicate that the Co ion does play a role in the toxicity of both Co particles and CoWC particles.

Animals↗

PubMed1982

Studies on the mechanism of toxicity of the mycotoxin, sporidesmin. I. Generation of superoxide radical by sporidesmin.

Sporidesmin (SDMS2), the mycotoxin responsible for 'facial eczema' in ruminants, contains a disulphide group which appears to be intimately involved in its toxic action. The reduced (dithiol) form of sporidesmin has been shown readily to undergo autoxidation in vitro in a reaction which generates superoxide radical (O2-). The autoxidation reaction, which takes place over a wide pH range, is strongly catalysed by trace amounts of copper, although the reaction was inhibited at high concentrations of this metal. Inhibition of the autooxidation of reduced sporidesmin (SDM(SH)2) was also observed in the presence of nickel, cobalt and manganese. Superoxide radical is also generated from SDMS2 itself in a cyclic reduction/autoxidation reaction with glutathione and other thiols; in view of the known toxicity of superoxide and its derivatives, it is suggested that oxygen-free-radicals may be involved in the initiation of the deleterious effects of the mycotoxin.

Chemical Phenomena↗

PubMed1993

Hexavalent chromium produces DNA strand breakage but not unscheduled DNA synthesis at sub-cytotoxic concentrations in hepatocytes.

Rat hepatocytes were used to investigate the possible induction of unscheduled DNA synthesis (UDS) and the extent of DNA strand breaks induced by sodium dichromate (a representative chromium(VI) compound) and chromium acetate hydroxide (chromium(III)) in vitro. Cytotoxicity, measured using tetrazolium salt (MTT) reduction assay, was found at a much higher dose of chromium(III), (> 50 microM), compared to that of chromium(VI), (> 2.5 microM), in cultured hepatocytes over 20 h treatment at 37 degrees C. Chromium(VI), but not chromium(III), stimulated minimal UDS in hepatocytes at sub-cytotoxic concentrations. A positive UDS response was only observed at cytotoxic concentration. DNA strand breaks in hepatocytes were induced by chromium(VI) following incubation at 37 degrees C for 1 h at doses of 10, 20 and 40 microM sodium dichromate. The subsequent ligation of such strand breaks in hepatocytes treated with 40 microM chromium(VI) for 1 h at 37 degrees C was demonstrated. The majority of strand breaks was repaired within 30 min following removal of the chromate. In conclusion, chromate-induced DNA strand breakage, possibly involving the formation of oxygen radicals and lack of significant UDS have some analogy to those produced by ionizing radiation.

Animals↗

PubMed2005

Protective effect of S-allylcysteine on 3-nitropropionic acid-induced lipid peroxidation and mitochondrial dysfunction in rat brain synaptosomes.

3-Nitropropionic acid is a neurotoxin that irreversibly inhibits succinate dehydrogenase, a relevant enzyme constituting the complex II of the respiratory chain during mitochondrial electron transport. 3-Nitropropionic acid is known to produce oxidative/nitrosative stress and evokes an experimental model of Huntington's disease. In this work we evaluated the effects of the antioxidant compound and major organosulfur garlic derivative, S-allylcysteine, on lipid peroxidation and mitochondrial dysfunction induced by 3-nitropropionic acid in synaptosomal fractions from rat brain. 3-Nitropropionic acid, at concentrations ranging 0.75-2.5 mM, produced enhanced levels of lipid peroxidation, while increasing concentrations of S-allylcysteine (0.1-2 mM) decreased the peroxidative action of 3-nitropropionic acid (1 mM) in synaptosomal fractions in a concentration-dependent manner. S-Allylcysteine (0.75 mM) also prevented the 3-nitropropionic acid (1mM)-induced mitochondrial dysfunction. These findings suggest that the protective actions that S-allylcysteine exert on the in vitro neurotoxicity induced by 3-nitropropionic acid are mediated by its antioxidant properties.

Animals↗

PubMed2004

Protective effects of S-nitrosoglutathione against neurotoxicity of 3-nitropropionic acid in rat.

Mitochondrial dysfunction and oxidative stress are often linked to various neurodegenerative disorders including ischemic stroke and Huntington's disease (HD). S-Nitrosoglutathione (GSNO) is an endogenous nitric oxide carrier recently identified as a potent antioxidant capable of neutralizing oxidative stress. In the present study, we explore the neuroprotective effects of GSNO against metabolic insults induced by 3-nitropropionic acid (3-NP), a mitochondrial complex II inhibitor commonly used as a pharmacological model for HD, in primary culture of fetal rat cortical and striatal neurons. Application of GSNO (1-5 microM) substantially reduced neuronal loss caused by 3-NP (1-5 mM) exposure based on MTT reduction, lactate dehydrogenase (LDH) release, and Hoechst staining assays. The protective effect of GSNO appeared to be more potent than N-acetyl-l-cysteine (NAC), a glutathione precursor, at the same concentrations. These results suggest that manipulation of GSNO metabolism may exert protective effects against mitochondrial dysfunction often observed in neurodegenerative disorders.

Analysis of Variance↗

PubMed1996

Verapamil reduces the size of reperfused ischemically injured myocardium in hypertrophied rat hearts as assessed by magnetic resonance imaging.

Contrast-enhanced magnetic resonance (MR) imaging was used to detect and quantify the extent of myocardial injury after a brief coronary occlusion and reperfusion in response to verapamil treatment in a rat model of left ventricular hypertrophy (LVH). Two groups of rats were prepared by banding the abdominal aorta for 7 to 8 weeks to produce LVH. Group 1 (n = 13) received oral verapamil for 3 days, whereas group 2 (n = 13) received no therapy. Before MR examination was performed, each rat was subjected to 25 min of coronary artery occlusion followed by 1 hour of reperfusion. T1-weighted spin echo images were acquired before and after 0.3 mmol/kg gadoteridol was injected. Three images were acquired at contiguous levels of the LV and used to estimate the size of the myocardial injury. The size of the infarcted region was demarcated at postmortem examination by using triphenyltetrazolium chloride dye (TTC). Before contrast medium was administered, no significant difference in signal intensity was seen between nonischemic and reperfused ischemically injured myocardium. After gadoteridol was injected, a hyperintense zone indicative of myocardial injury was observed in 8 of 13 rats treated with verapamil and in all untreated animals. The size of the injury was significantly larger in untreated hearts than in hearts treated with verapamil as defined on MR images (25% +/- 5% vs 18% +/- 5%, p < 0.05) and TTC staining (12% +/- 4% and 4% +/- 1%, p < 0.05). Good correlation (r = 0.91) was found between the two measurements. No significant difference in the size of jeopardy area was seen between the two groups as (defined by blue dye infusion). In conclusion, contrast-enhanced MR imaging is a suitable technique to evaluate the effects of therapies applied to reduce myocardial injury. Verapamil can cause reduction in the extent of ischemic injury after reperfusion of hypertrophied myocardium.

Animals↗

PubMed2002

The effects of ebselen on cisplatin and diethyldithiocarbamate (DDC) cytotoxicity in rat hippocampal astrocytes.

Ebselen is a seleno-organic compound with documented cytoprotective properties. Little work has been done, however, demonstrating ebselen's cytoprotective properties in neural cell lines. In order to examine the effects of this compound and its mechanism of action, astrocytes were exposed to two known neurotoxicants, cisplatin and diethyldithiocarbamate (DDC). Cells were pretreated with 30 microM ebselen and subsequently treated with either 150 microM DDC for 1 h or 250 and 500 microM cisplatin for 24 h. Results indicate significant increases in viability in cells pretreated with ebselen and exposed to cisplatin. Ebselen pretreatment did not significantly increase viability in cells exposed to DDC. Light and scanning electron microscopy studies confirm the viability studies. Gross morphological damage was seen in cells treated with cisplatin, however, cells pretreated with ebselen and then exposed to cisplatin, appeared similar to controls. No differences were noted in cells pretreated with ebselen and then exposed to DDC or cells treated with DDC alone. In order to examine the mechanism of protection of this compound, glutathione status was examined. Results show that ebselen does not significantly increase reduced or oxidized glutathione (GSH, GSSG). All cell groups treated with cisplatin showed an increase in GSH levels. Ebselen showed protection in glutathione depleted cells at the 250 microM cisplatin dose. DDC treatment showed no significant increase in either reduced or oxidized glutathione. We conclude that ebselen significantly protects against cisplatin, but not DDC toxicity. We further conclude that this protection is not related to changes in glutathione status in the rat hippocampal cell line as has been reported in other cell types.

Animals↗

PubMed2003

Synthesis, X-ray diffraction structures, spectroscopic properties, and in vitro antitumor activity of isomeric (1H-1,2,4-triazole)Ru(III) complexes.

Three ruthenium(III) complexes containing 1H-1,2,4-triazole (Htrz), viz., (H(2)trz)[cis-RuCl(4)(Htrz)(2)], 1, (H(2)trz)[trans-RuCl(4)(Htrz)(2)], 2, and (Ph(3)PCH(2)Ph)[trans-RuCl(4)(Htrz)(2)], 3, have been synthesized by reaction between RuCl(3) and excess of the triazole in 2.38 M HCl (1 and 2), while 3 was obtained by metathesis of 2 and [Ph(3)PCH(2)Ph]Cl in water. The products were characterized by IR, UV-vis, electrospray mass spectrometry, cyclic voltammetry, and X-ray crystallography (1 and 3). X-ray diffraction study revealed cis and trans arrangements of the triazole ligands in 1 and 3, correspondingly, and unprecedented monodentate coordination of the triazole through N2 and stabilization of its 4H tautomeric form, which is the disfavored one for the free triazole. The cytotoxicity of 1 and 2 has been assayed in three human carcinoma cell lines SW480, HT29 (colon carcinoma), and SK-BR-3 (mammary carcinoma). Both compounds exhibit antiproliferative activity in vitro. Time-dependent response of all three lines to 1 and 2 and a structure-activity relationship, i.e., higher activity of the trans-isomer 2 than that of cis-species 1, have been observed.

Antineoplastic Agents↗

PubMed1976

Evaluation of six short term tests for detecting organic chemical carcinogens and recommendations for their use.

Six short term tests for detecting carcinogenicity have been evaluated using 120 compounds, of which half were carcinogens and the rest non-carcinogens. The results obtained indicate that the Ames test and a "cell transformation" assay are both sufficiently sensitive to carcinogenicity, or the lack of it, in the compounds studied to enable them to be employed for detecting potential carcinogens. The consequences of using short term tests under various screening conditions have been explored. In order to have confidence in the results obtained for new or previously untested compounds it is important to use such tests in a carefully controlled manner.

Alkylating Agents↗