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PubMed1996

Inhibition of NF-kappaB DNA binding by nitric oxide.

It has been suggested that the NF-kappaB transcription factor family may mediate expression of the gene encoding the cytokine-inducible form of nitric oxide synthase (iNOS). To establish if nitric oxide (NO) could in turn affect activity of NF-kappaB, the ability of NO-donor compounds to influence NF-kappaB DNA binding activity in vitro was investigated. NO-donor compounds sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) both inhibited the DNA binding activity of recombinant NF-kappaB p50 and p65 homodimers and of p50-p65 heterodimers. Inhibition of NF-kappaB p50 DNA binding by NO-donor compounds involved modification of the conserved redox-sensitive C62 residue, as a C62S p50 mutant was significantly more resistant to SNP-mediated inactivation. Non-reducing SDS-polyacrylamide gel electrophoresis demonstrated that SNP could inhibit p50 DNA binding by mechanisms other than the formation of intersubunit disulphide bonds involving p50 residue C62. Electrospray ionization mass spectrometry of a synthetic NF-kappaB p5O peptide containing the C62 residue suggested that NO gas can modify C62 by S-nitrosylation. This study indicates that NO-donors can directly inhibit the DNA binding activity of NF-kappaB family proteins, suggesting that cellular NO provides another control mechanism for modulating the expression of NF-kappaB-responsive genes.

Base Sequence↗
PubMed1992

A Rhizobium meliloti lipopolysaccharide mutant altered in competitiveness for nodulation of alfalfa.

A transposon Tn5-induced mutant of Rhizobium meliloti Rm2011, designated Rm6963, showed a rough colony morphology on rich and minimal media and an altered lipopolysaccharide (LPS). Major differences from the wild-type LPS were observed in (i) hexose and 2-keto-3-deoxyoctonate elution profiles of crude phenol extracts chromatographed in Sepharose CL-4B, (ii) silver-stained sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis patterns of crude and purified LPS fractions, and (iii) immunoreactivities otherwise present in purified LPS of the parental strain Rm2011. In addition, Rm6963 lost the ability to grow in Luria-Bertani medium containing the hydrophobic compounds sodium deoxycholate or SDS and showed a decrease in survival in TY medium supplemented with high calcium concentrations. The mutant also had altered symbiotic properties. Rm6963 formed nodules that fixed nitrogen but showed a delayed or even reduced ability to nodulate the primary root of alfalfa without showing changes in the position of nodule distribution profiles along the roots. Furthermore, 2 to 3 weeks after inoculation, plants nodulated by Rm6963 were smaller than control plants inoculated with wild-type bacteria in correlation with a transient decrease in nitrogen fixation. In most experiments, the plants recovered later by expressing a full nitrogen-fixing phenotype and developing an abnormally high number of small nodules in lateral roots after 1 month. Rm6963 was also deficient in the ability to compete for nodulation. In coinoculation experiments with equal bacterial numbers of both mutant and wild-type rhizobia, only the parent was recovered from the uppermost root nodules. A strain ratio of approximately 100 to 1 favoring the mutant was necessary to obtain an equal ratio (1:1) of nodule occupancy. These results show that alterations in Rm6963 which include LPS changes lead to an altered symbiotic phenotype during the association with alfalfa that affects the timing of nodule emergence, the progress of nitrogen fixation, and the strain competitiveness for nodulation.

Calcium↗
PubMed2003

[Cutaneous leishmaniasis].

Leishmaniasis is a vector-borne disease caused by an obligate intracellular protozoa, Leishmania, which resides in macrophages. The parasite is transmitted by an infected female sandfly. The incidence of cutaneous leishmaniasis approaches 2 million new cases per year with 90% of the cases occurring in the "Old World", while the "New World" accounts for the rest. Infection may be restricted to the skin with development of characteristic ulcers, or may affect the mucous membranes in its mucocutaneous form. The clinical diagnosis is verified by the presence of amastigotes in slit-skin smears. Therapeutic modalities include systemic treatments such as the pentavalent antimony compound sodium stibogluconate, liposomal formulations of amphotericin B, oral ketoconazole or itraconazole, as well as topical paromomycin sulphate, local heat, freezing with liquid nitrogen, or photodynamic therapy. An effective vaccine is not available.

Amphotericin B↗
PubMedDate not supplied

[Phenyl pyrazolones--novel oxidoreductase redox-mediators for degradation of xenobiotics].

An approach was developed to screening organic compounds for putative activity of redox mediators of oxidoreductases, including laccases and peroxidases, applicable for xenobiotic degradation. The study was carried out with a homogenous laccase preparation from the basidiomycete Trametes hirsuta and horse-radish root peroxidase. Compounds belonging to 1-phenyl-3-methylpyrazolones were selected. Spectroscopic and electrochemical investigation of two of the compounds, sodium 1-phenyl-2,3-dimethyl-4-aminopyrazolon 5n(4)-methanesulfonate (PPNa) and 1-(3'-sulfophenyl)-3-methylpyrazolone (SPP), was performed. Electrochemical oxidation of both PPNa and SPP gave rise to high-potential intermediates capable of oxidizing veratryl alcohol; a lignin-modeling compound. Kinetic indices of these compounds were determined in enzymatic reactions with the presence of laccase. It was shown that enzymatic oxidation of SPP by laccase produced high-potential intermediates capable of oxidizing veratryl alcohol to veratric acid. Veratryl alcohol did not oxidize during enzymatic oxidation of SPP by peroxidase. This points to a difference between the mechanisms of enzymatic oxidation of PPNa and SPP by laccase and peroxidase.

Basidiomycota↗
PubMed1996

Obstructive sialadenitis caused by intraparotid deposits of gold salts: a case report.

A case of obstructive sialadenitis caused by deposits of gold salt compound in the intraparotid lymphoid tissues in a woman with classic rheumatoid arthritis is presented. The patient had been treated with a parenteral gold salt compound (sodium aurothiomalate) for 10 years with chrysotherapy balance of 7525 mg. She presented with swelling of both parotid glands on eating, and computed tomography images showed accumulation of high density spots. Obstructive sialadenitis most probably was caused by local compression on the excretory ducts of the parotids. This clinical disorder should be classified as a case of mechanical, nontumoral, obstructive sialadenitis caused by gold salt compound.

Adult↗
PubMed2003

Role for c-Jun N-terminal kinase in beta-cell recovery from nitric oxide-mediated damage.

Treatment of rat islets with the cytokine IL-1 results in the inhibition of mitochondrial function and insulin secretion, events that are mediated by beta-cell expression of iNOS [inducible nitric oxide (NO) synthase] and production of NO. beta-Cells recover from the inhibitory actions of NO, produced following 24 h incubation with IL-1, on islet oxidative metabolism and insulin secretion if iNOS enzymatic activity is inhibited and the islets are cultured (in the presence of IL-1 and iNOS inhibitors) for a brief period of 8 h. Islet recovery from cytokine- and NO-mediated damage is an active process that requires new gene expression, and NO itself is one activator of this recovery process. In this study, the mechanism by which NO stimulates islet recovery has been examined. Incubation of rat islets or RINm5F cells with the NO donor compound, sodium (Z)-1(N,N-diethylamino) diazen-1-ium-1,2-diolate (DEA-NO) for 1 h results in a 60% inhibition of mitochondrial aconitase activity. beta-Cells completely recover aconitase activity if the cells are washed to remove the NO donor compound and incubated for an additional 5 h in the absence of DEA-NO. The recovery of mitochondrial aconitase activity correlates with a 4-fold increase in cyclic GMP accumulation and is prevented by the inhibition of guanylate cyclase. The recovery of aconitase activity also correlates with the activation of members of the MAPKs, p38, c-Jun N-terminal kinase (JNK) and ERK, and the activation p38 and JNK is attenuated by inhibition of guanylate cyclase. ERK and p38 do not appear to participate in the recovery process as selective inhibition of these kinases fails to prevent recovery of aconitase activity; however, transduction of beta-cells with a dominant negative mutant JNK prevents beta-cell recovery from NO-mediated damage. These findings support a role for guanylate cyclase and JNK in the recovery of beta-cells from NO-mediated damage.

Aconitate Hydratase↗
PubMed1993

Activation of human peripheral blood mononuclear cells by nitric oxide-generating compounds.

Recent work in this laboratory has identified immune-stimulatory properties of the oxidant hemin. In this study, we examined whether the nitrogen-based oxidant nitric oxide (NO) had inductive effects on human lymphocytes. We found that the NO-generating compounds sodium nitroprusside and S-nitroso-N-acetylpenicillamine rapidly enhanced the rate of glucose transport in resting human PBMC. In addition, NF-kappa B binding activity was induced by these agents as was the secretion of TNF-alpha. The data suggest that a cGMP-independent mechanism is involved as the cell permeant cGMP analogue, 8-Br-cGMP, had no effect in eliciting these inductive events. Activation of lymphocytes by these NO-generating compounds may be mediated through the protein tyrosine phosphorylation signal transduction pathway. We found that membrane-associated protein tyrosine phosphatase activity was enhanced in PBMC treated with sodium nitroprusside or S-nitroso-N-acetylpenicillamine and that the src family protein tyrosine kinase p56lck was activated in these cells. Inasmuch as p56lck activity is negatively controlled by tyrosine phosphorylation, its activation may be related to the enhancement of protein tyrosine phosphatase activity. 8-Br-cGMP had no effect on these enzymes. Taken together, these data suggest that NO may have immune-stimulatory properties and may signal through a hitherto undescribed cGMP-independent pathway.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1998

Effect of organic forms of selenium on delta-aminolevulinate dehydratase from liver, kidney, and brain of adult rats.

The inhibitory effect of various forms of organic selenium compounds and of diphenyl ditelluride (PhTe)2 on delta-aminolevulinate dehydratase (delta-ALA-D) from liver, kidney, and brain of rats was investigated because it has been reported that organocalcogens catalyze the oxidation of thiols. Diphenyl diselenide (PhSe)2, rho-chloro-diphenyl diselenide (rho ClPhSe)2, propyl-2-2-diphenyl diselenide, and propyl-2-methoxy-2-phenyl selenide inhibited delta-ALA-D and the IC50 ranged from 2 to 32 microM depending on the selenium compound and whether it was preincubated with the enzyme. (rho ClPhSe)2 was the most potent inhibitor of delta-ALA-D, and preincubation increased the inhibitory potency of all the tested compounds. Inorganic selenium compounds (sodium selenite, Na2SeO3 and selenium dioxide, SeO2) inhibited delta-ALA-D, and the potency of SeO2 was greater than that of (rho ClPhSe)2. Diphenyl ditelluride (PhTe)2 also inhibited delta-ALA-D but with relatively lower potency than that of organic and inorganic selenium compounds. The inhibitory effect of propyl-2-2-diphenyl diselenide and propyl-2-methoxy-2-phenyl selenide seems to be mediated by (PhSe)2 since the compounds decomposed rapidly to (PhSe)2 in aqueous medium. The inhibitory action of selenium forms on delta-ALA-D from liver, kidney, and brain was antagonized by sulfhydryl protecting agents (dithiotreitol and reduced glutathione). The effects of organic selenium compounds on delta-ALA-D were related to the stability of the Se-Se (or Se-C) bond because the compound methyl-diphenyl diselenide (which possesses the most stable Se-C-Se bond) did not inhibit the enzyme. The inhibitory action of (PhSe)2 was not related to the formation of oxyradicals in the medium since superoxide dismutase and catalase did not affect the inhibition of delta-ALA-D by (PhSe)2. delta-ALA-D from cucumber leaves was not inhibited by selenium or tellurium compounds which suggests that these compounds act directly on the B or beta-site of the animal enzyme. These results suggest that delta-ALA-D from liver, kidney, and brain is a potential molecular target for the toxic effect of organic forms of selenium and tellurium.

Animals↗
PubMed2004

The drug-binding pocket of the human multidrug resistance P-glycoprotein is accessible to the aqueous medium.

P-Glycoprotein (P-gp) is an ATP-dependent drug pump that transports a broad range of compounds out of the cell. Cross-linking studies have shown that the drug-binding pocket is at the interface between the transmembrane (TM) domains and can simultaneously bind two different drug substrates. Here, we determined whether cysteine residues within the drug-binding pocket were accessible to the aqueous medium. Cysteine mutants were tested for their reactivity with the charged thiol-reactive compounds sodium (2-sulfonatoethyl)methanethiosulfonate (MTSES) and [2-(trimethylammonium)ethyl)]methanethiosulfonate (MTSET). Residue Ile-306(TM5) is close to the verapamil-binding site. It was changed to cysteine, reacted with MTSES or MTSET, and assayed for verapamil-stimulated ATPase activity. Reaction of mutant I306C(TM5) with either compound reduced its affinity for verapamil. We confirmed that the reduced affinity for verapamil was indeed due to introduction of a charge at position 306 by demonstrating that similar effects were observed when Ile-306 was replaced with arginine or glutamic acid. Mutant I306R showed a 50-fold reduction in affinity for verapamil and very little change in the affinity for rhodamine B or colchicine. MTSES or MTSET modification also affected the cross-linking pattern between pairs of cysteines in the drug-binding pocket. For example, both MTSES and MTSET inhibited cross-linking between I306C(TM5) and I868C(TM10). Inhibition was enhanced by ATP hydrolysis. By contrast, cross-linking of cysteine residues located outside the drug-binding pocket (such as G300C(TM5)/F770C(TM8)) was not affected by MTSES or MTSET. These results indicate that the drug-binding pocket is accessible to water.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMedDate not supplied

A new form of inactive renin in rat brain. A latent renin.

A new inactive (latent) form of renin was found in rat brain extract. It is activated by sulfhydryl compounds such as dithiothreitol but not by proteases such as trypsin. The activated form of latent renin in crude brain extract was again inactivated by the disulfide compound sodium tetrathionate. Latent renin was separated, at least partially, from active renin by affinity chromatography on Affi-Gel Blue. In contrast to a marked (10-fold) increase of latent renin by dithiothreitol, the enzyme activity of active renin was increased by less than 50% by this sulfhydryl compound. Thus, the major part of the activating effect of dithiothreitol does not seem to be due to its effect on renin substrate. Latent renin showed affinity for pepstatin-Sepharose gel. These properties indicate that latent renin is different from inactive renin of the zymogen type, which is activated by protease or acid treatment but not by sulfhydryl compounds and does not show affinity to pepstatin. Latent renin has a molecular weight of 45,000 and is reduced to 34,000 upon activation by dithiothreitol. This observation suggests that latent renin may be a renin-inhibitor complex.

Animals↗
PubMed2003

Ethyl pyruvate provides durable protection against inflammation-induced intestinal epithelial barrier dysfunction.

Ethyl pyruvate (EP) has been shown to be an effective anti-inflammatory agent. Herein, we sought to test the following hypotheses: 1) the pharmacological effects of EP persist after cells have been exposed to the compound in vitro, even if the cultures are washed to minimize the amount of EP that is retained in the media; 2) the pharmacological effects of EP persist in vivo, even after waiting a prolonged period (i.e., 6 h) after the last dose of the compound; and 3) the in vivo pharmacological effects of EP are distinct from those of the closely related compound, sodium pyruvate. Incubation of Caco-2 human enterocyte-like monolayers with cytomix, a mixture of interleukin-1beta, interferon-gamma, and tumor necrosis factor, increased permeability to the fluorescent macromolecule, FITC-labeled Dextran (mol wt 4,000 Da). Co-incubation of the cells with 5 mM EP ameliorated cytomix-induced hyperpermeability and induction of iNOS mRNA expression. EP was associated with similar pharmacological effects when cells were pre-incubated with the compound for 24 h prior and then washed extensively prior to adding the cytokine cocktail. Injecting C57Bl/6 mice with lipopolysaccharide (LPS) resulted in gut barrier dysfunction and hepatocellular injury. Although equivalent doses of both EP and sodium pyruvate ameliorated these phenomena, EP was more efficacious than pyruvate. Pretreatment with EP ameliorated the deleterious effects of LPS, even when the duration between the last dose of EP and the endotoxic challenge was 6 h. We conclude that EP provides durable protection against some of the deleterious effects of LPS or pro-inflammatory cytokines.

Animals↗
PubMed1992

Subacute toxicity of pentavalent antimony compounds in rats.

A subacute toxicity study of pentavalent antimony (Sb) compounds, sodium stibogluconate (SSG) and meglumine antimoniate (MA) was carried out in rats. Three groups of 10 rats each were treated with saline (control group), 300 mg Sb kg-1 d-1 or 900 mg Sb kg-1 d-1 of SSG for 30 d. A parallel study of similar type was conducted for MA. Compared with controls, drug-treated rats showed an impairment of feeding habits and retardation of weight gain (P less than 0.01) during the treatment period. In both SSG- and MA-treated rats there was a dose-related reduction in haemoglobin concentration (P less than 0.001), and hematocrit (P less than 0.001). Red cell count was reduced in SSG-treated rats only. Both drugs, however, significantly raised the white cell count (P less than 0.05). These changes were more pronounced with SSG them with MA. There was no change in MCV, MCH and MCHC. SSG, 900 mg Sb kg-1 d-1, significantly raised AST (P less than 0.005), ALT (P less than 0.01) and alkaline phosphatase activity (P less than 0.01). SSG-treated rats also had raised BUN (P less than 0.01) and creatinine (P less than 0.001), but no significant change in bilirubin levels. MA significantly raised AST (P less than 0.01), ALT (P less than 0.01), BUN (P less than 0.001) and serum creatinine levels (P less than 0.001), but had no appreciable effect on bilirubin and alkaline phosphatase levels. Both SSG and MA decreased blood glucose levels (P less than 0.01) and induced proteinuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed2000

In situ monitoring of solid-state polymerization reactions in sodium chloroacetate and sodium bromoacetate by 23Na and 13C solid-state NMR spectroscopy

The thermally induced solidstate polymerization reactions in sodium chloroacetate and sodium bromoacetate, leading to poly(hydroxyacetic acid) (polyglycolide) and NaCl and NaBr, respectively, were studied by isothermal in situ solid-state NMR spectroscopy at 120, 130 and 140 degrees C with a time resolution of the order of 5 to 25 min. The nuclei probed were 23Na and 13C, allowing the parent compounds (sodium halogenoacetates) and both reaction products (polymer and alkali halide) to be monitored. For sodium chloroacetate, there is no evidence for the involvement of intermediate phases during the reaction whereas this cannot be excluded for sodium bromoacetate. The crystal structure of sodium bromoacetate was determined directly from powder diffraction data by the Monte Carlo method, and was found to be isostructural with sodium chloroacetate. The topochemical reaction mechanism proposed previously for sodium chloroacetate is thus also applicable for the polymerization reaction in sodium bromoacetate. The mechanistic and kinetic information obtained from our in situ solid-state NMR investigations is compared and contrasted with information obtained from other in situ probes of the polymerization reactions in these materials.

Journal Article↗
PubMed2004

Intra-arterial administration of sodium borocaptate (BSH)/lipiodol emulsion delivers B-10 to liver tumors highly selectively for boron neutron capture therapy: experimental studies in the rat liver model.

PURPOSE: Boron neutron capture therapy (BNCT) is particle radiotherapy with alpha ((4)He) particle and recoiled lithium nucleus ((7)Li) derived from a reaction of boron ((10)B) and thermal neutron. We investigated applying BNCT to malignant liver tumors. The purpose of the present study was to reveal the efficacy for administration of emulsion of a boron compound (sodium borocaptate; BSH) and lipiodol via a hepatic artery using a rat liver tumor model. METHODS AND MATERIALS: Rat liver tumors were developed by direct injection of Walker 256 cells into the liver parenchyma. BSH (75 mg/kg)/lipiodol (0.3 mL/kg) emulsion was administered via the hepatic artery. Boron concentrations in the tumors, liver, and blood were measured at 1, 6, and 12 h after administration. Neutron capture radiography (NCR) was taken to confirm the selective accumulation of (10)B in the liver tumors. RESULTS: Boron concentrations in the liver tumors and the tumor/liver (T/L) boron concentration ratio at 1, 6, and 12 h after administration of BSH/lipiodol emulsion (concentration: T/L ratio) were 479.2 ppm: 4.0, 197.3 ppm: 14.9, and 96.5 ppm: 6.6, respectively. Highly selective irradiation was clearly demonstrated by the NCR images. CONCLUSIONS: Intra-arterial administration of BSH/lipiodol emulsion is effective method for delivering high concentration of (10)B selectively to the liver tumors.

Animals↗
PubMed1992

[A study on reaction mechanism of sodium lauryl sulfate-hemoglobin (SLS-Hb), Part 1].

The cyanmethemoglobin (HiCN) method has been adopted as the international standard procedure for hemoglobin (Hb) determinations due to the accuracy and stability of result. However, the presence of potassium cyanide (KCN) and potassium ferricyanide (K3-Fe(CN)6) in the reagents has raised problems of laboratory and environmental pollution. In 1981, Oshiro and colleagues developed a cyanide free method of Hb determination that is based on a low toxicity compound Sodium Lauryl Sulfate (SLS). The SLS-Hb method provides stable SLS-Hb formation through the following steps. 1) Reaction of SLS to erythrocytic membrane (disruption of the erythrocytic membrane). 2) Conformation change of Hb by SLS. 3) Iron oxidation by oxygen (Fe2+----Fe2+). 4) Formation of stable SLS-Hb (coordination of SLS). The paper presents several findings on the reaction mechanism of the SLS-Hb method.

Blood Cell Count↗
PubMed2003

Characterization of N-methyl-D-aspartate-evoked taurine release in the developing and adult mouse hippocampus.

Taurine is an inhibitory amino acid acting as an osmoregulator and neuroromodulator in the brain, with neuroprotective properties. The ionotropic glutamate receptor agonist N-methyl-D-aspartate (NMDA) greatly potentiates taurine release from brain preparations in both normal and ischemic conditions, the effect being particularly marked in the developing hippocampus. We now characterized the regulation of NMDA-stimulated taurine release from hippocampal slices from adult (3-month-old) and developing (7-day-old) mouse using a superfusion system. The NMDA-stimulated taurine release was receptor-mediated in both adult and developing mouse hippocampus. In adults, only NO-generating compounds, sodium nitroprusside, S-nitroso-N-acetylpenicillamine and hydroxylamine reduced the release, as did also NO synthase inhibitors, 7-nitroindazole and nitroarginine, indicating that the release is mediated by the NO/cGMP pathway. On the other hand, the regulation of the NMDA-evoked taurine release proved to be somewhat complex in the immature hippocampus. It was not affected by the NOergic compounds, but enhanced by the protein kinase C activator 4 beta-phorbol 12-myristate 13-acetate and adenosine receptor A(1) agonists, N(6)-cyclohexyladenosine and R(-)N(6)-(2-phenylisopropyl)adenosine in a receptor-mediated manner. The activation of both ionotropic 2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors and metabotropic glutamate group I receptors also enhanced the evoked release. The NMDA-receptor-stimulated taurine release could be a part of the neuroprotective properties of taurine, being important particularly under cell-damaging conditions in the developing hippocampus and hence preventing excitotoxicity.

Animals↗
PubMed1976

Comparison of 99mTc-labeled phosphate and phosphonate agents for skeletal imaging.

The use of 99mTc-labeled phosphate and phosphonate compounds in place of 18F, 85Sr, and 87Sr for bone scintigraphy has become commonplace throughout the world in a relatively short time. The labeling of polyphosphate with 99mTc 4 years ago, followed rapidly by the introduction of 99mTc-labeled pyrophosphate for skeletal imaging, must therefore be regarded as a major contribution to the practice of diagnostic nuclear medicine. The markedly reduced patient radiation exposure and concomitant increase in photon detection efficiency derived from the more favorable physical decay characteristics of 99mTc led to increased sensitivity and resolution and in turn to improved diagnostic efficacy. The subsequent clinical use of the phosphonate complex 99mTc-HEDP represented a further modification of the same basic approach. Current clinical trials with 99mTc-labeled methylene diphosphonic acid (MDP), which appears to demonstrate enhanced biologic properties for scintigraphy of the osseous structures, is the latest example in this series of refinements. This article compares the technetium-labeled agents already in clinical use and, using animal data, contrasts them with several new multifunctional phosphonates and the novel inorganic compound sodium imidodiphosphate (IDP). In addition, an attempt is made to clarify the conflicting evidence in the nuclear medicine literature regarding the relationship between polyphosphate chain length and skeletal uptake.

Animals↗