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PubMed1982

Inhibition of two mitochondrial enzymes by gold (III) halo complexes. Evidence for a binding mechanism.

Fumarase (EC 4.2.1.2) and mitochondrial L-malate dehydrogenase (EC 1.1.1.37) were both inhibited by NaAuCl4 and KAuBr4. The inhibition for both was measured as a function of gold complex concentration and aquation time, and the NaAuCl4 inhibition was also measured in the presence of 0.15 M NaCl. Regeneration of the enzyme activity after NaAuCl4 inhibition using L-cysteine, L-methionine and NaCN was also investigated. Sodium dodecyl sulfate (SDS) acrylamide gel electrophoresis and amino acid analysis was performed on the NaAuCl4 inhibited enzymes as well as on ribonuclease A (EC 3.1.26.2), lysozyme (EC 3.2.1.17) and liver alcohol dehydrogenase (EC 1.1.1.1). It was observed that the inhibition was proportional to the gold complex concentration but decreased markedly after aquation of the complex. In the presence of NaCl the initial rate of inactivation is essentially unaffected unless the complex has been aquated and then the initial rate is increased. Gel electrophoresis on gold complex-enzyme mixtures show polymerization for ribonuclease and lysozyme and amino acid analysis indicates that no oxidation has taken place. From these results, a binding mechanism is postulated for the inhibition of the dehydrogenases by direct displacement of a halide ligand, probably by two groups on the enzyme, at least one of which may be a sulfur containing acid.

Amino Acids↗
PubMed1993

Redox-linked ligand-independent cell surface triggering for extensive protein tyrosine phosphorylation.

Exposure of lymphocytes to 0.2-2 mM HgCl2, a thiol-reactive heavy metal, induced extensive tyrosine phosphorylation of multiple cellular proteins. The phosphorylation started as quickly as 5 s after exposure to HgCl2, and was irreversible. Another 3 thiol-reactive chemicals also displayed similar, though less marked, actions, whereas dithiothreitol, a reducing agent, antagonized the HgCl2 action. The demonstrated new action of HgCl2 indispensably required membrane-intact cells as a target. Whereas exposure of lymphocytes to > 0.2 mM HgCl2 caused rapid cell death, 0.01-0.1 mM HgCl2 affected the cells so as to accelerate their c-fos transcription. These results suggest a novel redox-linked mechanism of cell surface triggering of intracellular protein kinase activity, which is independent of receptor-ligand interactions.

4-Chloromercuribenzenesulfonate↗
PubMed1987

Coordination chemistry in biological media: reactions of antitumor Pt(II) and Au(III) complexes with cell culture media.

Reactions of cis-PtCl2(NH3)2 (1), Pt(1,2-diaminoethane)Cl2 (2), PtCl4(2-) (3), and AuCl4- (4) with intact cell culture media have been studied by spin-echo 500 MHz proton NMR spectroscopy. This has allowed us to observe reactions of components of the media at submillimolar concentrations. Upon the addition of 400 microM 1, 2, or 3 to the media, the S-methyl peak of methionine decreases in intensity and in each case a new peak appears which we have tentatively assigned to the S-CH3 of Pt(N,S-L-Met)2. In the spectra of the media with 2, an additional peak appears, assignable to the S-CH3 of Pt(1,2-diaminoethane)(N,S-L-Met). Upon the addition of Au(III) to the media, the S-CH3 peak of methionine also decreases in intensity and new peaks appear in the 2.6 to 2.8 ppm region, including a peak identified as the S(O)-CH3 peak of methionine sulfoxide. The other peaks are assignable to Au(I)-S(Met) species. Practical methods of following the reactions of metal complexes in cell culture media are becoming of wider significance with the increasing use of cell cultures for drug screening instead of animal tests.

Antineoplastic Agents↗
PubMed1984

A silver and gold technique for axons and axon-bundles in formalin-fixed central and peripheral nervous tissue.

We have modified the reduced silver procedure of Liesegang and added a gold treatment. The technique has been successfully and routinely used to impregnate both peripheral and central nervous tissues of mice of different ages, and central nervous tissue of man. It was applied on conventionally (formalin) fixed and cryostat-cut material. In the periphery, nerves, individual axons, and sensory and motor endings stained a dark purple. In the brain, both bundles of axons and individual fine axonal branches were stained. When counterstained by a Nissl method, an excellent overall image of CNS structure is obtained.

Age Factors↗
PubMed2004

Direct observation of covalent adducts with Cys34 of human serum albumin using mass spectrometry.

The interactions of the unpaired thiol residue (Cys34) of human serum albumin (HSA) with low-molecular-weight thiols and an Au(I)-based antiarthritic drug have been examined using electrospray ionization mass spectrometry. Early measurements of the amount of HSA containing Cys34 as the free thiol suggested that up to 30% of circulating HSA bound cysteine as a mixed disulfide. It has also been suggested that reaction of HSA with cysteine, occurs only on handling and storage of plasma. In our experiments, there were three components of HSA in freshly collected plasma from normal volunteers, HSA, HSA+cysteine, and HSA+glucose in the ratio approximately 50:25:25. We addressed this controversy by using iodoacetamide to block the free thiol of HSA in fresh plasma, preventing its reaction with plasma cysteine. When iodoacetamide was injected into a vacutaner tube as blood was collected, the HSA was modified by iodoacetamide, with 20-30% present as the mixed disulfide with cysteine (HSA+cys). These data provide strong evidence that 20-30% of HSA in normal plasma contains one bound cysteine. Reaction of HSA with [Au(S(2)O(3))(2)](3-) resulted in formation of the adducts HSA+Au(S(2)O(3)) and HSA+Au. Reaction of HSA with iodoacetamide prior to treatment with [Au(S(2)O(3))(2)](3-) blocked the formation of gold adducts.

Cysteine↗
PubMed2005

The effect of vitamin A on CCl4-induced hepatic injuries in rats: a histochemical, immunohistochemical and ultrastructural study.

In this study, we aimed to investigate the effect of vitamin A on the transformation of the Ito cells to fibrogenic form and suppression of the development of fibrosis. Carbon tetrachloride intoxication was performed on rats for 2, 8, 12 or 20 weeks and 5x10(4) IU vitamin A (as retinol palmitate) was injected subcutaneously once every 4 weeks. Ito cells were detected by gold chloride impregnation, as well as desmin and alpha-smooth muscle actin (alpha-SMA) immunohistochemistry. Additionally, all groups were examined ultrastructurally. The number of Ito cells that were labelled positively with gold impregnation decreased in the fibrotic groups; however, alpha-SMA and desmin immunopositive Ito cells increased. The samples from animals that were treated with vitamin A showed an increase in labelling with gold impregnation but a decrease in alpha-SMA immunopositivity. The data showed that vitamin A can prevent hepatic injury, by suppressing the transformation of Ito cells to fibrogenic form. We conclude that vitamin A has potential for the treatment of hepatic fibrotic diseases. Alpha-SMA immunohistochemistry was found to be more informative than desmin immunohistochemistry for monitoring liver fibrosis.

Actins↗
PubMed2004

Reductive activation of ricin and ricin A-chain immunotoxins by protein disulfide isomerase and thioredoxin reductase.

Intracellular activation of ricin and of the ricin A-chain (RTA) immunotoxins requires reduction of their intersubunit disulfide(s). This crucial event is likely to be catalyzed by disulfide oxidoreductases and precedes dislocation of the toxic subunit to the cytosol. We investigated the role of protein disulfide isomerase (EC 5.3.4.1, PDI), thioredoxin (Trx), and thioredoxin reductase (EC 1.8.1.9, TrxR) in the reduction of ricin and of a ricin A-chain immunotoxin by combining enzymatic assays, SDS-PAGE separation and immunoblotting. We found that, whereas PDI, Trx, and TrxR used separately were unable to directly reduce ricin and the immunotoxin, PDI and Trx in the presence of TrxR and NADPH could reduce both ricin and immunotoxin in vitro. PDI functioned only after pre-incubation with TrxR and the reductive activation of ricin was more efficient in the presence of glutathione. Similar results were obtained with microsomal membranes or crude cell extracts. Pre-incubation with the gold(I) compound auranofin, which irreversibly inactivates TrxR, resulted in a dose-dependent inhibition of ricin and immunotoxin reduction. Reductive activation of ricin and immunotoxin decreased or was abolished in microsomes depleted of TrxR and in cell extracts depleted of both PDI and Trx. Pre-incubation of U-937, Molt-3, Jurkat, and DU145 cells with auranofin significantly decreased ricin cytotoxicity with respect to mock-treated controls (P<0.05). Conversely, auranofin failed to protect cells from the toxicity of pre-reduced ricin which does not require intracellular reduction of disulfide between the two ricin subunits. We conclude that TrxR, by activating disulfide reductase activity of PDI, can ultimately lead to reduction/activation of ricin and immunotoxin in the cell.

Auranofin↗
PubMed2004

In vitro toxicity of palladium(II) and gold(III) porphyrins and their aqueous metal ion counterparts on Trypanosoma brucei brucei growth.

The trypanocidal effects of aqueous gold(III) and palladium(II) and their metalloporphyrin derivatives on Trypanosoma brucei brucei growth in culture have been studied using an Alamar Blue indicator assay. All the experiments were conducted in the dark. As previously described for mercury(II), cadmium(II) and lead(II) porphyrins [Chem.-Biol. Interact. 139 (2002) 177], the toxicity of the metalloporphyrin complex of palladium(II) to T. b. brucei parasites was much higher compared to the aqueous free palladium(II) and free base porphyrin. Palladium(II) porphyrin, free palladium(II), and the free base porphyrin were trypanocidal to T. b. brucei at concentrations >1.5 x 10(-6), >6.1 x 10(-6) and >1.9 x 10(-5) M, respectively. While gold(III) porphyrin was effective against the parasites at concentrations >4.8 x 10(-6) M, its aqueous gold(III) was toxic at concentrations as low as 2.0 x 10(-7) M due to the generation of free radicals in the presence of this metal ion which enhanced its toxicity to the T. b. brucei parasites. Although some cell division was observed in some of the cells treated with palladium(II) porphyrin, some dividing cells had no nucleus due to unequal division and delivery of the nuclei into the daughter cells. As a result, the rate of cell division decreased with time and cell death occurred within 24 h. Interestingly, trypanosomes treated with metalloporphyrin complexes displayed different morphological features from those cells treated with free base porphyrin or metal ions. Of all the porphyrins and free metal ions tested, only mercury(II) porphyrin and aqueous gold(III) ion were toxic to the trypanosomes in the 10(-7) M range. The chemotherapeutic potential of these observations is discussed.

Animals↗
PubMed2005

Open tubular capillary electrochromatography using capillaries coated with films of alkanethiol-self-assembled gold nanoparticle layers.

We have used alkanethiol self-assembly and dithiol layer-by-layer (LBL) self-assembly processes to prepare an Au nanoparticle (NP)-coated open tubular capillary electrochromatography (OTCEC) column for the separation of three neutral steroid drugs (testosterone, progesterone, and testosterone propionate). The CEC column was fabricated through LBL self-assembly of Au NPs on a 3-aminopropyltrimethoxysilane (APTMS)-modified fused-silica capillary and subsequent surface functionalization of the Au NPs through self-assembly of alkanethiols. We investigated the electrochromatographic properties of the resulting Au NP-coated CEC column using a "reversed phase" test mixture of three steroid drugs. We found that the key factors affecting the separation performance were the number of Au NP layers, the length of the carbon-atom chain of the alkanethiol self-assembled on the Au NPs, the percentage of organic modifier, and the pH of the running electrolyte. This study reveals that the self-assembly of alkanethiols and dithiols onto Au NPs provides stationary phases for CEC separation that are easy to prepare and whose retention behavior is highly controllable and reproducible. We believe that our findings will contribute to further studies of the application of nanotechnology to separation science.

Acetonitriles↗
PubMed2006

Cellular pharmacological properties of gold(III) porphyrin 1a, a potential anticancer drug lead.

The development of gold(III) complexes as potential anticancer drugs with higher cytotoxicity and fewer side effects than existing metal anticancer drugs has been actively pursued in recent years. In this study, we explored the cellular pharmacological properties of gold(III) porphyrin 1a, an anticancer drug lead we previously described. The cytotoxicity study of gold(III) porphyrin 1a by naphthol blue black (NBB) staining assay demonstrated that the higher cytotoxicity of gold(III) porphyrin 1a was not related to its photosensitizing activity. Serum dependent test revealed that serum proteins exhibited lesser effects on the activity of gold(III) porphyrin 1a. In addition, in vivo and in vitro binding assays showed that gold(III) porphyrin 1a acted on DNA noncovalently, which was differently from cisplatin. Flow cytometric study indicated that gold(III) porphyrin 1a inhibited cell growth partly through abrogating cell cycle at G(0)-G(1), and induced apoptosis in SUNE1 cells. The enhanced expression of p53, a cell cycle-controlling and apoptosis-related protein, further demonstrated that the cell cycle arrest and apoptosis induced by gold porphyrin 1a were p53 dependent. Our results highlighted the potential of gold(III) porphyrin 1a as an anticancer drug.

Animals↗
PubMed2004

Metal solubilization from metal-containing solid materials by cyanogenic Chromobacterium violaceum.

Different cyanogenic bacterial strains (Chromobacterium violaceum, Pseudomonas fluorescens, Bacillus megaterium) were cultivated under cyanide-forming conditions in the presence of metal-containing solids such as nickel powder or electronic scrap. All microorganisms were able to form water-soluble metal cyanides, however, with different efficiencies. C. violaceum was able to mobilize nickel as tetracyanonickelate [Ni(CN)4(2-)] from fine-grained nickel powder. Gold was microbially solubilized as dicyanaoaurate [Au(CN)2-] from electronic waste. Additionally, cyanide-complexed copper was detected during biological treatment of shredded printed circuit boards scrap. Regarding the formation of tetracyanonickelate, C. violaceum was more effective than P. fluorescens or B. megaterium. Besides a few previous reports on gold solubilization from gold-containing ores or native gold by C. violaceum, the findings demonstrate for the first time the microbial mobilization of metals other than gold from solid materials and represent a novel type of microbial metal mobilization based on the ability of certain microbes to form HCN. The results might have the potential for industrial applications (biorecovery, bioremediation) regarding the treatment of metal-containing solids since metal cyanides can easily be separated by chromatographic means and be recovered by sorption onto activated carbon.

Biodegradation, Environmental↗
PubMed2006

Copper(II)-rubeanic acid coprecipitation system for separation-preconcentration of trace metal ions in environmental samples for their flame atomic absorption spectrometric determinations.

A simple and facile preconcentration procedure based on the coprecipitation of trace heavy metal ions with copper(II)-rubeanic acid complex has been developed. The analytical parameters including pH, amounts of rubeanic acid, sample volume, etc. was investigated for the quantitative recoveries of Pb(II), Fe(III), Cd(II), Au(III), Pd(II) and Ni(II). No interferic effects were observed from the concomitant ions. The detection limits for analyte ions by 3 sigma were in the range of 0.14 microg/l for iron-3.4 microg/l for lead. The proposed coprecipitation method was successfully applied to water samples from Palas Lake-Kayseri, soil and sediment samples from Kayseri and Yozgat-Turkey.

Cadmium↗
PubMed2006

Synthesis and characterization of [Au(dppz)2]Cl3. DNA interaction studies and biological activity against Leishmania (L) mexicana.

[Au(dppz)(2)]Cl(3) was synthesized by the reaction of HAuCl(4) in excess of the dypirido[3,2-a: 2,3-c]phenazine (dppz) ligand. This complex was characterized by elemental analysis, fast atom bombardment (FAB) mass, NMR, UV-visible and IR spectroscopies. DNA-gold complex interactions were studied by spectroscopic titrations, viscosity measurements and electrophoretical assays. These studies showed that the gold complex interacts with DNA by intercalation mode. These observations, led us to carry out biological tests on cultures of promastigotes of Leishmania (L) mexicana. [Au(dppz)(2)]Cl(3) induced a dose dependent antiproliferative activity with minimal inhibitory concentration (MIC) of 3.4nM and lethal doses LD(26) of 17nM for 48h. These findings suggest that a very potent leishmanicidal activity could be associated to the cellular processes involving parasite DNA, constituting a new promising chemotherapeutic alternative in the search for definitive leishmaniasis cure.

Animals↗
PubMed2004

Ion-pair complex-based solvent extraction combined with chemiluminescence determination of chlorpromazine hydrochloride with luminol in reverse micelles.

A new chemiluminescence (CL) method is proposed for the determination of chlorpromazine hydrochloride, which is based on the dichloromethane solvent extraction of ion-pair complex of tetrachloroaurate(III) with chlorpromazine hydrochloride and luminol chemiluminescence detection in a reversed micellar medium formed by the cation surfactant cetyltrimethylammonium bromide in a dichloromethane-cyclohexane (1:1 V/V)-water (0.3 mol/L Na2CO3 buffer solution with the pH of 11.5). The ion-pair complex of tetrachloroaurate(III) with chlorpromazine hydrochloride produced an analytical chemiluminescence signal when it entered the reversed micellar water pool. In the optimum conditions, CL intensities are proportional to concentrations of the studied drug over the range 0.05 approximately 10 microg/mL with a detection limit (DL) of 6 ng/mL. The relative standard deviation (R.S.D.) is 2.6% for 1.25 microg/mL chlorpromazine hydrochloride (n = 11). R.S.D. (precision) of inter-day and intra-day is less than 6%, and accuracy of inter-day and intra-day is satisfactory. The method has been applied to the determination of studied drug in pharmaceutical preparations and biological fluids with satisfactory results.

Buffers↗
PubMed2002

Gold-facilitated in situ hybridization: a bright-field autometallographic alternative to fluorescence in situ hybridization for detection of Her-2/neu gene amplification.

Fluorescence in situ hybridization (FISH) represents an excellent method for profiling gene amplification in situ, but correlation with tissue morphology is difficult because of dark-field visualization. Validation of a bright-field assay for assessment of HER-2/neu gene amplification was investigated. Streptavidin-Nanogold was used to generate bright-field gene copy signals using GoldEnhance gold-based autometallography, catalyzed reported deposition, and a biotin-labeled probe. One hundred cases of invasive breast carcinoma were evaluated for which FISH gene copy results, and mRNA and oncoprotein gene expression, were known. Autometallographic signals were qualitatively evaluable without the use of oil immersion microscopy. Results correlated well with indirect and direct label FISH. Autometallographic gold-based in situ hybridization represents a promising bright-field assay for the assessment of HER-2/neu gene amplification.

Breast Neoplasms↗
PubMed1998

Inhibition of erythrocyte selenium-glutathione peroxidase by auranofin analogues and metabolites.

The effect of gold ligation on the inhibition of bovine erythrocyte selenium-glutathione peroxidase (GSH-Px) was examined. The anti-arthritic drug auranofin [2,3,4,6-tetra-O-acetyl-1-thio-beta-D-glucopyranosato-S)(triethylp hosphine) gold(I)] (Et3PAuSATg) and its analogue, Et3PAuCl, exhibited experimentally equivalent Ki values (11.6+/-0.8 and 10.8+/-0.5 microM, respectively), despite the greatly disparate affinities of their ligands for gold(I): 2,3,4,6-tetra-O-acetyl-1-thiolato-beta-D-glucopyranose (ATgS-) >> Cl-. This similarity reflects ligand exchange reactions that generate the glutathione complex Et3PAuSG from the excess glutathione (GSH, 1 mM) used in the assay. The Ki values for bis(glutathionato)gold(l) (Au(SG)2-) and gold(I) thioglucose (AuSTg) were also found to be equal (2.8+/-0.4 and 2.4+/-0.5 microM, respectively). This confirms the previous postulate of Chaudiere and Tappel (J Inorg Biochem 20: 313-325, 1984) that Au(SG)2- is generated from AuSTg in the presence of excess glutathione. Since auranofin metabolites accumulate in red blood cells, the inhibition of intracellular GSH-Px was examined by using intact erythrocytes. There was greater inhibition of the reaction when the cells were resuspended in isotonic buffer than in whole blood, because serum albumin in the latter competes for the auranofin and decreases the uptake by erythrocytes. After correction for the extent of gold uptake, the Ki values were determined to be the same as those observed for Au(SG)2- in the extracellular assay, indicating loss of both the Et3P and ATgS- ligands from auranofin. Thus, the inhibition of GSH-Px by gold complexes is dependent on their ligation, and the ultimate gold(I) compound that interacts with erythrocyte GSH-Px in intact red cells, Au(SG)2-, is radically different from the original auranofin molecule.

Animals↗
PubMed1999

A fiber-reinforced composite model of the viscoelastic behavior of the brainstem in shear.

Brainstem trauma occurs frequently in severe head injury, often resulting in fatal lesions due to importance of brainstem in crucial neural functions. Structurally, the brainstem is composed of bundles of axonal fibers distinctly oriented in a longitudinal direction surrounded by an extracellular matrix. We hypothesize that the oriented structure and architecture of the brainstem dictates this mechanical response and results in its selective vulnerability in rotational loading. In order to understand the relationship between the biologic architecture and the mechanical response and provide further insight into the high vulnerability of this region, a structural and mathematical model was created. A fiber-reinforced composite model composed of viscoelastic fibers surrounded by a viscoelastic matrix was used to relate the biological architecture of the brainstem to its anisotropic mechanical response. Relevant model parameters measured include the brainstem's composite complex moduli and relative fraction of matrix and fiber. The model predicted that the fiber component is three times stiffer and more viscous than the matrix. The fiber modulus predictions were compared with experimental tissue measurements. The optic nerve, a bundle of tightly packed longitudinally arranged myelinated fibers with little matrix, served as a surrogate for the brainstem fiber component. Model predictions agreed with experimental measures, offering a validation of the model. This approach provided an understanding of the relationship between the specific biologic architecture of the brainstem and the anisotropic mechanical response and allowed insight into reasons for the selective vulnerability of this region in rotational head injury.

Animals↗