Spontaneous alloying of zinc atoms into gold clusters and formation of compound clusters.
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Journal Article↗
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Inhibition of avian myeloblastosis virus reverse transcriptase by aurochloric acid.
We investigated the inhibitory effects of aurochloric acid (AuCl4H) on reverse transcriptase (RT) derived from avian myeloblastosis virus and DNA polymerase alpha (pol. alpha) purified from HeLa S3 cells. The activities of RT, pol. alpha and E. coli DNA polymerase I (pol. I) with dTTP as the substrate were inhibited 50% at AuCl4H concentrations of 18 microM, 43 microM and 230 microM, respectively. AuCl4H inhibited RT activity competitively with respect to the substrate, dTTP, and uncompetitively with the template/primer, (rA)n(dT)12-18. In assays with dGTP as the substrate, 50% inhibitions of RT, pol. alpha and pol. I activities were observed at AuCl4H concentrations of 100 microM, 450 microM and 580 microM, respectively. AuCl4H inhibited RT activity uncompetitively with respect to the substrate, dGTP, and noncompetitively with the template/primer, (rC)n(dG)12-18. AuCl4H at concentrations causing more than 50% inhibition of RT activity had little inhibitory effect on the colony-forming ability of HeLa cells or their syntheses of DNA, RNA and protein.
Avian Myeloblastosis Virus↗
Acute poisoning with gold cyanide.
A case of deliberate ingestion of an electroplating solution containing gold cyanide is described. Despite the use of an antidote, and supportive treatment for cyanide poisoning, the patient died after 13 hours. Sublethal cyanide and high red blood cell gold levels suggest acute gold toxicity as the most likely cause of death. Evidence for this is discussed and recommendations are made for the treatment of cyanide poisoning.
Acute Disease↗
Immunohistochemical and ultrastructural study of Langerhans's cells in squamous cell carcinoma of the cervix.
OBJECTIVE: To study Langerhans's cells (LCs) in cervical squamous cell carcinoma. STUDY DESIGN: The study was carried out in the Shatby University Hospital, Alexandria, Egypt. Thirty cases with squamous cell carcinoma, 10 cases with cervical intra-epithelial neoplasia (CIN) and 10 cases with normal exocervix were recruited. Sections from the exocervix were stained with gold chloride, immunostaining with S-100 protein antiserum, adenosine triphosphatase ATPase and electron microscopy. Statistical evaluation was done using the t-test. RESULTS: Gold chloride staining revealed significantly increased number of LCs in all cases of CIN compared to normal controls and with increasing grade of CIN (p < 0.001). No relationship between LCs number and the grade of carcinoma. Least branched LCs were predominant in the normal tissue while in neoplasia, these cells were of the most branched type, indicating a hyperactivity. S-100 protein positive LCs were almost absent in normal controls while their number were almost lower than the corresponding cases of CIN and invasive carcinoma after gold chloride or ATPase stainings. Signs of hyperactivity were evident in LCs of neoplastic cases after electron microscopy. CONCLUSIONS: Proliferation and increased number of LCs in CIN is an immune response, while such reaction is suppressed by invasive carcinoma.
Adenosine Triphosphatases↗
Unusual cutaneous reaction after a gold chloride patch test.
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Dermatitis, Contact↗
Occupational dermatitis from gold plating.
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Adult↗
Rôle of ear piercing in metal allergic contact dermatitis.
To evaluate the effect of ear piercing on sensitization to gold and other metals, diagnostic patch testing with 18 metals was performed. 377 patients (65 men and 312 women, ranging in age from 15 to 78 years; mean 34.2, S.D +/- 15.1 years) were patch tested; 107 had pierced earlobes. Metals were applied on the back for 2 days, and the results read with the ICDRG scoring system 3 days after application. Reactions of + to +3 were regarded as positive. There were significantly more patients reacting to gold chloride (p < 0.001), mercuric chloride and nickel sulfate (p < 0.05) in patients with pierced ears than in those without. Statistical issues included: (i) a significant number of patients with pierced ears referred because of earring dermatitis; (ii) those with pierced ears represented a different age group from those without; (iii) a significant number of patients without eczema in the non-pierced ear group. However, our data suggests that ear piercing is a risk factor not only for nickel but also for gold sensitization. Gold was the second most frequent metal allergen after nickel in the pierced group.
Adolescent↗
Patch test materials for mercury allergic contact dermatitis.
The objective of this study was to define adequate patch test materials to evaluate mercury allergic contact dermatitis. We applied 0.1% and 0.05% mercuric chloride, and 0.5% and 0.2% mercury in petrolatum to systemic eczematous contact-type dermatitis (baboon syndrome), and gold-dermatitis patients. All baboon-syndrome patients reacted not only to mercuric chloride but also to metallic mercury. In gold-dermatitis patients, significantly more patients reacted to mercuric chloride than to metallic mercury (21 of 35, 60%, versus 2 of 19, 10.5%, p < 0.0005). We speculated that sensitization to mercury may be of 2 types: one a reaction to ionized mercury only, the other to both ionized mercury and non-ionized mercury. The possibility that the phenomenon is caused by differences in bioavailability or percutaneous penetration between ionized and non-ionized mercury cannot be ruled out, but could be explored by penetration measurement. For the evaluation of mercury hypersensitivity, it may be more reliable to apply both ionized and non-ionized mercury, rather than only mercuric chloride or ammoniated mercury.
Adult↗
Gold--a controversial sensitizer. European Environmental and Contact Dermatitis Research Group.
Until recently, gold allergy was considered to be extremely rare. Gold has been used and worshipped for thousands of years without any obvious complaints of skin problems, either in those participating in mining and other ways of prospecting, or in those wearing jewellery. When studies on contact allergy to gold sodium thiosulfate were published at the beginning of the 1990s, the allergic nature of the reported positive patch test reactions to gold was questioned. The major argument for such questioning was the lack of demonstrable clinical relevance in most positive reactors. A major reason for the questioning may have been confusion in differentiating between contact allergy and allergic contact dermatitis. To arrive at a diagnosis of allergic contact dermatitis, 3 steps have, in principle, to be fulfilled: (i) establishment of contact allergy; (ii) demonstration of present exposure; (iii) assessment of clinical relevance, i.e., causing or aggravating a contact dermatitis. In this paper, these steps are discussed with regard to gold. With our present knowledge of contact allergy-allergic contact dermatitis, we do not recommend including gold sodium thiosulfate in the standard series. It should be applied for scientific purposes and when allergic contact dermatitis from gold is suspected.
Dermatitis, Allergic Contact↗
Multiple inhibitory effects of Au(CN)(2-) ions on cystic fibrosis transmembrane conductance regulator Cl(-) channel currents.
Lyotropic pseudohalide anions are potentially useful as high affinity probes of Cl(-) channel pores. However, the interaction between these pseudohalides and the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel have not been described in detail. Here we show that Au(CN)(2-) ions applied to the intracellular face of membrane patches from stably transfected baby hamster kidney cells inhibit CFTR channel currents by at least two mechanisms, which can be distinguished at the single channel level or by inhibiting channel closure using 2 mM pyrophosphate. Low concentrations (< 10 microM) of Au(CN)(2-) significantly reduced CFTR channel open probability. This effect was apparently voltage insensitive, independent of extracellular Cl(-) concentration, and lost following exposure to pyrophosphate. Higher concentrations of intracellular Au(CN)(2-) caused an apparent reduction in unitary current amplitude, presumably due to a kinetically fast blocking reaction. This effect, isolated following exposure to pyrophosphate, was strongly voltage dependent (apparent K(d) 61.6 microM at -100 mV and 913 microM at +60 mV). Both the affinity and voltage dependence of block were highly sensitive to extracellular Cl(-) concentration. We propose that Au(CN)(2-) has at least two inhibitory effects on CFTR currents: a high affinity effect on channel gating due to action on a cytoplasmically accessible aspect of the channel and a lower affinity block within the open channel pore. These results offer important caveats for the use of lyotropic pseudohalide anions such as Au(CN)(2-) as specific high affinity probes of Cl(-) channel pores.
Animals↗
Molecular determinants of Au(CN)(2)(-) binding and permeability within the cystic fibrosis transmembrane conductance regulator Cl(-) channel pore.
Lyotropic anions with low free energy of hydration show both high permeability and tight binding in the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel pore. However, the molecular bases of anion selectivity and anion binding within the CFTR pore are not well defined and the relationship between binding and selectivity is unclear. We have studied the effects of point mutations throughout the sixth transmembrane (TM6) region of CFTR on channel block by, and permeability of, the highly lyotropic Au(CN)(2)(-) anion, using patch clamp recording from transiently transfected baby hamster kidney cells. Channel block by 100 microM Au(CN)(2)(-), a measure of intrapore anion binding affinity, was significantly weakened in the CFTR mutants K335A, F337S, T338A and I344A, significantly strengthened in S341A and R352Q and unaltered in K329A. Relative Au(CN)(2)(-) permeability was significantly increased in T338A and S341A, significantly decreased in F337S and unaffected in all other mutants studied. These results are used to define a model of the pore containing multiple anion binding sites but a more localised anion selectivity region. The central part of TM6 (F337-S341) appears to be the main determinant of both anion binding and anion selectivity. However, comparison of the effects of individual mutations on binding and selectivity suggest that these two aspects of the permeation mechanism are not strongly interdependent.
Animals↗
Coupled movement of permeant and blocking ions in the CFTR chloride channel pore.
The cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel pore is blocked in a voltage-dependent manner by a broad range of anionic substances added to the cytoplasmic side of the membrane. Here we investigate the origin of the voltage dependence of block by intracellular Au(CN)2-, a highly permeant lyotropic anion which also acts as a high-affinity blocker of Cl- permeation. Not only the affinity, but also the voltage dependence of block by intracellular Au(CN)2- ions is strongly dependent on extracellular Cl- concentration; following replacement of most extracellular Cl- by glucose or by impermeant anions, block by Au(CN)2- shows greatly weakened voltage dependence. This suggests that coupled movement of Au(CN)2- and Cl- ions within the pore contributes to the voltage dependence of block. This explanation requires that interactions between different anions take place within the pore, implying simultaneous binding of multiple anions to intrapore sites. Other anions are able to substitute for extracellular Cl- and interact with intracellular Au(CN)2- ions. Analysis of the effects of different extracellular anions on the apparent affinity and voltage dependence of block by intracellular Au(CN)2- ions suggests that extracellular anions do not need to permeate through the channel in order to destabilize Au(CN)2- binding within the pore, implying that this destabilizing effect results from binding to an externally accessible site in the permeation pathway. We propose that multiple anions can bind simultaneously within the CFTR channel pore, and that repulsive interactions between bound anions speeds anion exit from the pore.
Animals↗
Molecular determinants and role of an anion binding site in the external mouth of the CFTR chloride channel pore.
Chloride permeation through the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel is blocked by highly lyotropic permeant anions which bind tightly within the pore. Here we show that several different substitutions of a positively charged amino acid residue, arginine R334, in the putative outer mouth of the CFTR pore, greatly reduce the block caused by lyotropic Au(CN)2- ions applied to the intracellular side of the channel. Fixed positive charge at this site appears to play a role in Au(CN)2- binding, as judged by multiple substitutions of differently charged amino acid side chains and also by the pH dependence of block conferred by the R334H mutant. However, non-charge-dependent effects also appear to contribute to Au(CN)2- binding. Mutation of R334 also disrupts the apparent electrostatic interaction between intracellular Au(CN)2- ions and extracellular permeant anions, an interaction which normally acts to relieve channel block. All six mutations studied at R334 significantly weakened this interaction, suggesting that arginine possesses a unique ability to coordinate ion-ion interactions at this site in the pore. Our results suggest that lyotropic anions bind tightly to a site in the outer mouth of the CFTR pore that involves interaction with a fixed positive charge. Binding to this site is also involved in coordination of multiple permeant anions within the pore, suggesting that anion binding in the outer mouth of the pore is an important aspect in the normal anion permeation mechanism.
Animals↗
Pulmonary intravascular macrophages: their contribution to the mononuclear phagocyte system in 13 species.
The organ uptake of intravenously injected particles was examined in 13 species. All animals were injected intravenously with 198Au colloid and magnetic iron oxide particles. Vascular clearance kinetics of 198Au colloid was similar in all species. Pulmonary uptake of 198Au colloid ranged from 17 to 60% in sheep, calves, pigs, and cats but was <1.1% in monkeys, hyraxes, rabbits, guinea pigs, rats, mice, and chickens. For iron oxide particles, pulmonary uptake ranged from 80 to 99% in sheep, calves, pigs, goats, and cats and 15 to 18% in hamsters, hyraxes, and monkeys and was <10% in rabbits, chicken, mice, rats, and guinea pigs. In all species, the bulk of the remainder of particle uptake was in the liver. Pulmonary intravascular macrophages are the cellular site of lung uptake in calves, cats, pigs, goats, and sheep, whereas monocytes and neutrophils predominate in other species. Kupffer cells were the site of uptake in the liver. Our data show marked species differences in the fate of circulating particles; ruminants, pigs, and cats have extensive pulmonary localization due to phagocytosis by pulmonary intravascular macrophages.
Animals↗
Muscle-fiber compartmentalization in cat splenius muscles.
Splenius is a structurally complex muscle that is supplied by nerves from four cervical segments. We have examined the architectural organization of extrafusal fibers in splenius by microdissecting muscles stained "en bloc" with gold chloride. We also analyzed the distribution of motor units supplied from different cervical segments using the glycogen-depletion technique. Microdissections show that the fiber architecture of splenius is different in medial and lateral muscle parts. In medial splenius, muscle fascicles run uninterrupted from the muscle origin to insertion, while in lateral splenius, separate compartments of muscle fascicles are linked in series by two tendinous inscriptions. In muscle fascicles longer than 2.0 cm, many extrafusal fibers do not run the whole length of the fascicle. Instead, these fibers end intramuscularly by tapering to a fine strand that is closely adherent to adjacent extrafusal fibers. Less than 1% of extrafusal fibers in splenius exceeds 3.0 cm in length. Experiments using glycogen depletion showed that nerves from different spinal segments innervate different muscle regions. Nerves from C1 supply muscle fibers in a small rostromedial zone. Nerves from C2-C4 have motor domains that extend from the medial to the lateral muscle edge and are arranged in series. In lateral splenius, the motor domains are separated by tendinous inscriptions. In medial splenius, where no inscriptions are present, the motor domains of adjacent segmental nerves have overlapping boundaries due to the extensive interdigitation of motor units supplied from different segmental nerves. A single muscle fascicle in medial splenius is commonly composed of two sets of fibers supplied by adjacent segments that are distributed at opposite ends of the fascicle and interdigitate in midregions of the fascicle. The in-series compartmentalization of splenius has important implications for its motor control. To secure effective muscle shortening or tension development, central mechanisms may be required to coordinate the recruitment of in-series motor units. The presence of many short fibers with intramuscular insertions leads us to question how contractile forces are developed and transmitted in splenius and other mammalian muscles that are composed of short, in-series fibers.
Animals↗
GoldIII porphyrin 1a induced apoptosis by mitochondrial death pathways related to reactive oxygen species.
Apoptosis is a tightly controlled multistep mechanism of cell death, and mitochondria are considered to play a central role in this process. Mitochondria initiate two distinct apoptosis pathways, one caspase-dependent and the other caspase-independent. In addition, mitochondrial production of reactive oxygen species (ROS) seems to play a role in cell death. Most chemotherapeutic agents induce apoptosis through at least one of these pathways. The post-initiation mechanisms of gold(III) porphyrin 1a were investigated in this study. HONE1 cells exposed to gold(III) porphyrin 1a underwent apoptosis after 24 hours. Functional proteomic studies revealed the alteration of several cytoplasmic protein expressions in HONE1 cells after treatment with the drug. These proteins include enzymes participating in energy production and proteins involved in cellular redox balance. There was a quick attenuation of mitochondrial membrane potential (DeltaPsi(m)) with the alterations of Bcl-2 family proteins, the release of cytochrome c, and apoptosis-inducing factor (AIF) following gold(III) porphyrin 1a treatment. Cytochrome c in turn activated caspase-9 and caspase-3. Cotreatment with caspase inhibitor (zVAD-fmk) showed that the activated caspases worked in conjunction with AIF-initiated apoptosis pathways. Further study showed that ROS played a part in gold(III) porphyrin 1a-induced apoptosis by regulating DeltaPsi(m). In summary, gold(III) porphyrin 1a induced apoptosis through both caspase-dependent and caspase-independent mitochondrial pathways, and intracellular oxidation affected gold(III) porphyrin 1a-induced apoptosis. These results support a role for gold(III) porphyrin 1a as a promising anticancer drug lead and as a possible novel therapeutic agent directed toward the mitochondria.
Apoptosis↗
Gold chloride-mercuric bromide impregnation.
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Bromides↗
Intrinsic innervation of the uterus in guinea pig and rat.
The pattern of distribution of cholinergic and adrenergic nerves in the uterus of albino rats and guinea pigs was examined histochemically. In the albino rat, the uterus was found well-innervated by both adrenergic and cholinergic nerves with a clear regional variation. Dense innervation was demonstrated at the tubal and cervical ends of the uterus and in the cervix. Cholinergic nerves supplying the glands were more numerous than the adrenergic nerves which were relatively few. In the guinea-pigs, the uterus was richly innervated by adrenergic nerves with a clear regional variation. No cholinesterase-positive nerves or nerve cells were demonstrated.
Adrenergic Fibers↗