Amperometric titration of organic compounds with sodium nitrite. 3. Indirect determination of aldehydes by dimedone.
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Aldehydes↗
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Amperometric titration of organic compounds with sodium nitrite. 2. Determination of aminophenols.
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Chemistry, Pharmaceutical↗
Gas chromatographic analysis of coyote and magpie tissues for residues of compound 1080 (sodium fluoroacetate).
Tissues of coyotes and magpies administered known dosages of 1080 were analyzed for residues by an analytical method specifying gas chromatography and electron capture detection. The repeatability of the method was determined for the replicate analyses of coyote muscle tissue samples aged under different storage conditions. The average coefficient of variation (CV) was 6% for quadruplicate determinations of 1080 in fresh tissues, 12-14% for samples stored at - 10 degrees C for 30-60 days, and 24% for samples aged for 7 days at ambient temperatures. The larger CV value obtained for stored samples is attributed more to greater sample variability than to less precision of the analytical method. Residues of 1080 appear to be relatively stable in tissues; there was essentially no change in the concentration of 1080 in samples stored up to 28 days at ambient temperature. Residue levels in the muscle, heart, kidney, and intestine were comparable, slightly lower in the liver, and much higher in the stomach. The concentration of 1080 in the muscle tissue was related to the administered dosages. Correlation analyses of dosages and residue levels in coyote muscle tissue showed a correlation coefficient of 0.99 for 1080 administered by gavage, and 0.88 for 1080 administered by bait. A correlation coefficient of 0.99 was observed between dosages and mean residues in the breast muscle tissues of magpies. The average CV value was 3.5% for duplicate analyses of 1 g samples of magpie tissues.
Animals↗
Modified gas-liquid chromatographic method for determination of compound 1080 (sodium fluoroacetate).
A method capable of determining 0.1 ppm 1080 (sodium fluoroacetate) in 1 g animal tissue was developed. It involves extraction of 1080 from the sample with acetone-water, and then evaporation of the acetone followed by extraction of 1080 as fluoroacetic acid from water with ethyl acetate. Ethyl acetate is removed by volatilization from fluoroacetic acid which is retained as the triethanolammonium fluoroacetate salt. Fluoroacetic acid is subsequently derivatized with alpha-bromo-2,3,4,5,6-pentafluorotoluene and quantitated by gas-liquid chromatography with an electron capture detector. The method is rapid and requires no special apparatus or equipment and no more than 12 mL of any one solvent. Recoveries of 1080 from tissue samples fortified with 0.1-100 ppm averaged about 85%.
Animals↗
Action of T-2 toxin on gastrointestinal transit in mice: protective effect of an argillaceous compound.
Using sodium [51Cr]chromate as radiolabeled marker, gastrointestinal transit of a milk test meal was determined in mice receiving for 4 days T-2 toxin (1 mg/kg per day per os) alone or with a clay, smectite (2 g/kg per day), given according to four different procedures. Gastric emptying and small intestinal transit were significantly accelerated after the 1st T-2 administration and during the 4 days of treatment. When smectite was given together with the toxin with or without pretreatment by smectite alone for 2 days, the T-2 induced disturbances in gastrointestinal transit remained unchanged. A pretreatment by smectite for 4 days abolished the T-2 induced acceleration of gastric emptying but not of small intestinal transit. When T-2 was incubated with smectite for 24 h before oral administration, gastric emptying and small intestinal transit were not significantly accelerated.
Animals↗
Antigenotoxic properties of selenium: studies in the wing spot test in Drosophila.
The genotoxic activity of three selenium compounds (sodium selenite, sodium selenate, and selenious acid) and the antigenotoxic effects of sodium selenite in combination with the chromium compound potassium dichromate were studied using the wing spot test of Drosophila melanogaster. This assay is based on the principle that the loss of heterozygosity of suitable recessive markers, multiple wing hairs (mwh) and flare-3 (flr[3]), can lead to the formation of mutant clones of larval cells, which are then expressed as spots on the wings of the adult flies. Pretreatment and chronic cotreatment was comparatively used for the antigenotoxicity study. From the results obtained, it was evident that all selenium compounds are unable to increase the frequency of any of the three categories of spots recorded (small, large, and twin spots). Nevertheless, the antigenotoxic effects of sodium selenite were clearly demonstrated, in both cotreatment and pretreatment, by a complete suppression of those clones induced by potassium dichromate. Therefore, the D. melanogaster wing spot test was revealed to be a good assay, not only for evaluating genotoxic activity but also for detecting antigenotoxic effects in vivo.
Animals↗
Stable water-oil emulsions from the new insoluble surfactant sodium 5-(1-dodecylaminocarbonyl) picolinate.
The new compound sodium 5-(1-dodecylaminocarbonyl) picolinate (NaDPA) has been prepared and found to have the unusual surfactant property of forming stable water-oil (w/o) emulsions in the presence of water and a variety of organic liquids. A study of droplet size (diameters=0.1-1.0 mm) as a function of the amount of surfactant used shows that a near constant coverage of surfactant molecules exists at the water-oil interface and that the interface is made up of multiple layers. The structure of NaDPA, with its multiple hydrogen-bonding possibilities, probably contributes to the observed stability of the emulsions. The emulsions are made up of droplets that are stable for months and can be filled with dyes, buffers, and solutions of high ionic strength.
Journal Article↗
Epigenetic targets in hematopoietic malignancies.
Frequent genetic alterations in hematopoietic neoplasias (chromosomal translocations, point mutations, etc.) have provided biologic targets for the development of effective novel therapies. A rapidly increasing body of knowledge provides evidence also for multiple epigenetic alterations in these disorders, which can complement or even precede genetic aberrations. Gene inactivation ('silencing') of tumor suppressor and growth inhibitory genes (e.g. the cyclin-dependent kinase inhibitors p16, p15, p21) is frequently mediated by DNA methylation of gene promoters. The acetylation state of histones (functionally linked to the DNA methylation state by the methylcytosine binding protein 2, recruiting histone deacetylases) provides a second major epigenetic silencing mechanism. Therapeutic reversal strategies are being developed for acute leukemias, myelodysplastic syndromes and malignant lymphomas. Since the discovery of the DNA methyltransferase (Dnmt) inhibitory activity of two azanucleosides (5-azacytidine, 5-aza-2'-deoxycytidine/decitabine) even at doses with minimal nonhematologic toxicity, both have been clinically studied in several myeloid neoplasias, particularly in elderly patients unable to tolerate aggressive treatment. Further development of agents counteracting aberrant methylation is directed at more targeted approaches, for example, antisense molecules against Dnmts. Histone deacetylases (HDACs) can be inhibited by numerous compounds (sodium phenylbutyrate, valproic acid, novel compounds such as depsipeptide), which have entered the clinical arena in similar indications as Dnmt inhibitors. Impressive effects of HDAC inhibition in acute promyelocytic leukemia models (PML/RARA expression) translate the finding of HDAC recruitment by this chimeric transcription factor to its target genes. The recent discovery of recruitment by PML/RARA also of Dnmt activity to the retinoic acid receptor-beta promoter makes it an interesting candidate for Dnmt inhibitors. Studies combining a 're-expressor' strategy with inhibitors of Dnmts and HDACs are underway. Thus, resensitization to biological agents such as retinoids, colony-stimulating factors and other differentiation inducers may be envisioned.
DNA Methylation↗
Periodic ab initio calculation of nuclear quadrupole parameters as an assignment tool in solid-state NMR spectroscopy: applications to 23Na NMR spectra of crystalline materials.
Periodic ab initio HF calculations using the CRYSTAL code have been used to calculate (23)Na NMR quadrupole parameters for a wide range of crystalline sodium compounds including Na(3)OCl. An approach is developed that can be used routinely as an alternative to point-charge modelling schemes for the assignment of distinct lines in (23)Na NMR spectra to specific crystallographic sodium sites. The calculations are based on standard 3-21 G and 6-21 G molecular basis sets and in each case the same modified basis set for sodium is used for all compounds. The general approach is extendable to other quadrupolar nuclei. For the 3-21 G calculations a 1:1 linear correlation between experimental and calculated values of C(Q)((23)Na) is obtained. The 6-21 G calculations, including the addition of d-polarisation functions, give better accuracy in the calculation of eta((23)Na). The sensitivity of eta((23)Na) to hydrogen atom location is shown to be useful in testing the reported hydrogen-bonded structure of Na(2)HPO(4).
Algorithms↗
Determination of diclofenac sodium and related compounds in raw materials and formulations.
A liquid chromatographic method has been developed for determination of drug and related compounds in diclofenac sodium raw material, slow-release, and enteric coated tablets. The method specifies a 5 microns octadecylsilane bonded phase column, a mobile phase of tetrahydrofuran-acetonitrile-buffer, pH 5 (1 + 4 + 8.3), and detection at 229 nm. The method resolves 10 known related compounds with limits of quantitation of 0.2% or less. Seventeen drug raw material samples were evaluated. Total impurity levels ranged from 0.1 to 0.9%. The method has also been used for determination of drug content in raw materials and formulations. Mean assay levels in drug raw materials ranged between 98.3% and 101.8%.
Chromatography, Liquid↗
Immunological effects of arsenic compounds on mouse spleen cells in vitro.
Immunological effects of arsenic compounds on mouse spleen cells in vitro were examined. Three kinds of arsenic compounds: sodium arsenite, sodium arsenate and dimethyl arsenic acid, at high doses, suppressed the plaque-forming cell response to sheep erythrocytes and the proliferative response to mitogens, whereas at low doses they enhanced both responses. And each of arsenic compounds differs in strengths at which the modulation effects on both responses were exerted. The strength was comparable to general toxicity of arsenic compounds.
Animals↗
Contact sensitivity to arsenical compounds. Clinical and experimental studies.
Two arsenic compounds (sodium arsenate and sodium arsenite) were included in our standard patch test series and 2 of 379 tested dermatitis patients reacted. They had not experienced any exposure to arsenicals and showed concomitant reactions to nickel and cobalt. In the guinea pig maximization test (GPMT) the compounds were found to be Grade-I-allergens. There are some convincing case reports in the literature on contact sensitivity to arsenicals and the discrepancy between these reports and the results from the GPMT should be further evaluated by clinical studies on workers with arsenical dermatitis.
Animals↗
Inhibition by selenium compounds of catecholamine secretion due to inhibition of Ca2+ influx in cultured bovine adrenal chromaffin cells.
Selenium is an essential trace metal element, whereas large doses of selenium exert adverse effects to the human body. We examined the effects of selenium compounds, sodium selenite (Na2SeO3) and sodium selenate (Na2SeO4), on catecholamine secretion from cultured bovine adrenal chromaffin cells. Treatment of chromaffin cells with sodium selenite for 72, 48, and 24 h caused decreases in protein and catecholamine contents, in association with cell damage, at concentrations over 30, 300, and 300 microM, respectively. The cells treated with subtoxic conditions (<100 microM, 48 h) of sodium selenite were used for further experiments. Sodium selenite treatment for 48 h inhibited carbachol (CCh)-induced catecholamine secretion in a concentration-dependent and non-competitive manner, while it did not affect high K+- and veratridine-induced catecholamine secretion. Sodium selenite (100 microM) did not affect CCh- and veratridine-induced 22Na+ influx, while the compound inhibited 45Ca2+ influx induced only by CCh, but not high K+ and veratridine. Sodium selenate even at higher concentrations (1000 microM) did not affect any stimulus-induced catecholamine secretion and 45Ca2+ influx. Thus, sodium selenite may specifically exert adverse effects, such as inhibition of physiological stimulus-induced catecholamine secretion from adrenal chromaffin cells due to inhibition of Ca2+ influx.
Adrenal Medulla↗
Comparative effects of selenite and selenite on the glutathione-related enzymes activity in pig blood platelets.
The effects of inorganic selenium (Se) compounds (sodium selenite and selenate) on the activities of glutathione-related enzymes (glutathione peroxidase, glutathione-S-transferase [GST] and glutathione reductase [GR]) in pig blood platelets were investigated in vitro. GST activity in blood platelets treated with 10(-4)M of selenite was reduced to 50%, whereas no decrease GST activity was observed after the treatment of platelets with the same dose of selenate. In platelets incubated with physiological doses (10(-7) and 10(-6)M) of Se compounds, the activity of glutathione peroxidase (GSH-Px) was enhanced (about 20%). GR activity after the exposure of platelets to tested Se compounds was unaffected.
Animals↗
Effect of detergents on pathogenicity plasmids of escherichias.
The study dealth with effects of cationic detergents miramistin (alkylamidopropyldimethylbenzylammonium chloride), catamine AB (alkyldimethylbenzylammonium chloride) and the anionic compound sodium dodecyl sulphate (SDS) on the elimination from E. coli cells of plasmids determining the Hly, Ent and, indirectly, Col, F, and R markers of pathogenicity as well as their transfer upon conjugation. At subbacteriostatic concentrations, miramistin and catamine AB were found to suppress the transfer of Hly, Ent, F, and R plasmids during conjugation when applied to the donor, recipient or added to the conjugation medium without, however, eliminating plasmids. This is due to the disruption by detergents of F, J pili and other surface cell structures resulting in diminished ability to conjugate. Anionic SDS eliminated F and R plasmids without affecting Hly, Ent and Col.
Benzalkonium Compounds↗
Influence of phosphate compounds on certain fungi and their preservative effects on fresh cherry fruit (Prunus cerasus, L.).
Studies were conducted to ascertain the retarding effects of four phosphate compounds (sodium hexametaphosphate, sodium tripolyphosphate, sodium tetraphosphate, and tetrasodium pyrophosphate) on molding of fresh cherries (Prunus cerasus, L.). In vitro studies on their antimycotic effects against the most common fungal spoilers, Penicillium expansum, Rhizopus nigricans, and Botrytis sp., were also carried out. Sodium tetraphosphate appeared to be the most effective compound in preserving cherries and also had the greatest antimycotic effects in the in vitro studies. A 10% concentration, when applied as a dip, inhibited fungal growth on fresh cherries for up to 30 days of storage at 1.1 C (34 F) and a relative humidity of 94%, whereas untreated controls showed fungal growth at 14 days. Following in order of effectiveness were sodium hexametaphosphate, sodium tripolyphosphate, and tetrasodium pyrophosphate.
Antifungal Agents↗
Inorganic and dimethylated arsenic species induce cellular p53.
Arsenic compounds are known for their ability both to cause and to treat human cancers, although the molecular mechanisms underlying these actions are incompletely understood. The simplest explanation is that arsenic causes DNA damage that leads to mutations. However, the majority of scientific evidence indicates that arsenic is not a genotoxin or DNA-damaging agent. DNA damage typically leads to cellular responses designed to minimize the replication of damaged DNA, such as the induction of p53, and p53 induction has therefore been used as an indicator of DNA damage. Because this approach can be applied to human cells and does not rely on a specific, heritable mutation occurring at a particular site, it seemed possible that this method could detect DNA damage that was undetectable using other techniques. To examine the genotoxic potential of arsenic compounds, therefore, seven of these compounds (sodium arsenite, sodium arsenate, methyloxoarsine, iododimethylarsine, disodium methyl arsonate, dimethylarsinic acid, and arsenic trioxide) were tested for their ability to increase the cellular level of p53 as measured by ELISA. Of this group, arsenic trioxide was the strongest inducer of cellular p53, while dimethylarsinic acid, iododimethylarsine, and sodium arsenite also caused p53 induction in a dose- and time-dependent manner. Sodium arsenate, as well as the two monomethyl compounds tested, methyloxoarsine and disodium methyl arsonate, did not cause detectable increases in cellular p53. Our results indicate, therefore, that cells respond to several of these arsenic compounds as they do to chemicals that damage DNA, suggesting that exposure of cells to these compounds does in fact cause DNA damage. Such damage could then result in mutations and the observed development of cancer.
Animals↗
[Studies on chemical constituents of the gall of Python molurus bivittatus Schlegel].
Two constituents were isolated from the gall of Python molurus bivittus Schlegel, one is sodium taurodeoxycholate (I). The other is a new compound--sodium tauropythocholate (II). Its structure was elucidated as 3 alpha, 12 alpha, 16 alpha-trihydroxy-5-cholan-24-oic acid N-[2-sulfoethyl] amide by IR, 1HNMR, 13CNMR, MS 13C-1H COSY, and chemical reaction.
Animals↗