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PubMed1990

Embryotoxic effects of sodium arsenite and sodium arsenate on mouse embryos in culture.

Embryotoxic effects of two inorganic arsenic compounds, sodium arsenite (Asi) and sodium arsenate (Asa), on the development of mouse embryos during early organogenesis were studied using the whole embryo culture technique. Embryos with three to five somites exposed to 1-40 microM Asi or to 10-400 microM Asa were cultured for 48 hours and their development was compared with that of control embryos. Asi proved to be teratogenic between 3 and 4 microM and embryolethal at higher concentrations; Asa had similar activity but at concentrations ten times higher than for Asi. Both compounds produced a growth retardation and a similar pattern of defects. Growth retardation was indicated by a statistically significant reduction in crown-rump length, head length, and yolk sac diameter. Abnormal embryos were characterized by hypoplasia of the prosencephalon with open neural tube, hydropericardium, somite abnormalities, and failure of development of limb buds and sensory placodes. These results confirm that both Asa and Asi are embryotoxic compounds and that the Asi activity occurs at concentrations ten times lower than for Asa. Our results suggest that in humans both of these compounds may be involved in part of "unaccountable" early abortions and malformations claimed to be due to the toxicity of heavy metals.

Animals↗
PubMed1999

Lattice dynamics and Debye-Waller factors of some compounds with the sodium chloride structure.

The lattice dynamics of 19 compounds with the sodium chloride structure have been investigated using shell models. The models are compared with existing experimentally measured phonon-dispersion curves and refined using a multidimensional downhill simplex method. Debye-Waller factors for these compounds are calculated over the temperature range from 1 to 1000 K where appropriate and the results are fitted analytically using polynomial regression. The results are compared with experimentally measured room-temperature Debye-Waller factors and for most of the compounds the agreement is found to be better than 10%. At lower temperatures, it is expected that these results would be more accurate, since the harmonic approximation, which is crucial to the calculation of the Debye-Waller factors, works better. In choosing the models for particular applications, it is recommended that the model with the smallest standard error sigma is used for fitting the experimentally measured phonon-dispersion curves, or the model that shows best agreement with reliable experimental measurements of more relevant physical quantities, such as Debye-Waller factors in crystallography.

Journal Article↗
PubMed1997

Effects of quaternary ammonium compounds with 0.1% sodium hydroxide on swine vesicular disease virus.

The effects of quaternary ammonium compounds (QACs) with sodium hydroxide on swine vesicular disease virus (SVDV), an enterovirus were studied. Didecyldimethylammonium chloride (DDAC) with 0.1% NaOH showed a stronger effect against SVDV than other QACs with 0.1% NaOH. The effect of DDAC with 0.1% NaOH was strong at 40 degrees C. DDAC was effective against SVDV at pH values around 11.0, but not in the distilled water control. The effect of DDAC with 0.1% NaOH was already observed at 1 min after mixing of the DDAC with SVDV. Observation under an electron microscopy revealed that the probable mechanism of inactivation of DDAC with 0.1% NaOH is as follows: The virus particles were partially destroyed by 0.1% NaOH. DDAC gathered these affected particles and formed a micelle, then SVDV lost its infectivity. From these results, QACs with 0.1% NaOH are considered to be very effective against SVDV representing enteroviruses.

Animals↗
PubMed1990

Responses of the colonic epithelium to auranofin: evidence for involvement of enteric nerves.

Auranofin, the orally effective gold compound, stimulated the canine colonic epithelium in vitro. It increased short circuit currents across both the innervated mucosal and functionally "nerve-free" epithelial preparation, when added to either the luminal or serosal solutions. Serosal responses were inhibited by tetrodotoxin (TTX). A hydrophilic gold compound, sodium aurothiosulphate produced similar effects but only on serosal addition. Gold compounds can thus alter colonic transport activating enteric nerves and releasing a neurotransmitter. Thus gold induced diarrhea could have a significant neural component.

Animals↗
PubMed1988

Sodium aurothiomalate inhibits T cell responses to interleukin-2.

We studied the effects of the gold compound sodium aurothiomalate (SATM) on the responses of murine CTLL2 cells, and human T cells to Interleukin-2 (IL-2). SATM inhibited tritiated thymidine (3HTdR) incorporation by CTLL2 cells stimulated with human recombinant IL-2. Human T cells were cultured with phytohemagglutinin (PHA) in separate experiments and IL-2 receptor expression measured by using immunofluorescent anti-Tac serum; SATM inhibited IL-2 receptor expression. Furthermore, SATM when added concurrently with PHA, and IL-2 inhibited 3HTdR incorporation by human T cells in 5 day cultures. The kinetics of inhibition were further studied by adding PHA to T cells for 48 hours followed by the addition of SATM and IL-2; SATM inhibited 3HTdR incorporation even though receptor expression had occurred. These results suggest that SATM inhibits the stimulatory effects of IL-2 on T cells partly by interfering with IL-2 receptor expression, and partly by other mechanisms of action. These effects of SATM may explain some of the conflicting data in the literature on T cell responses to IL-2 in rheumatoid arthritis (RA), and suggest a possible mechanism of action for the drug in the treatment of RA.

Female↗
PubMed1981

Biotransformation of the pesticide sodium arsenate.

Biotransformation is an important parameter in assessing the environmental impact and fate of pesticides since metabolites produced may be either more or less toxic than the parent compound. Sodium arsenate (+5 inorganic), the wood preservative and insecticide, may be converted to both inorganic (+3) and organic compounds (-3) by microorganisms in soil, sediment and water bodies. Biotransformation of sodium arsenate was studied in pure cultures of 5 bacterial species using a mineral salt and limited carbon source medium. Arsenate concentrations were 10 microgram/ml and 100 microgram/ml of arsenic respectively. The rate of biodegradation of the parent compound was described by a first order composite exponential equation of the form Ct = C1e-k1t+C2e-k2t. Rates of production of metabolites (arsenite, monomethylarsine, dimethylarsine and trimethylarsine) were described by a first order exponential equation of the form Ct = Co (1-e-kt).

Arsenates↗
PubMed1983

The bacterial mutagenicity of three naturally occurring indoles after reaction with nitrous acid.

Three naturally occurring indoles were evaluated for potential nitrosatability using the Nitrosation Assay Procedure (NAP test) as recommended by the World Health Organisation. All three indoles i.e. tryptophan, tryptamine and 5-hydroxy-tryptamine were nitrosated to products which were directly mutagenic for S. typhimurium TA1537. In addition, the products of nitrosation of tryptamine and 5-hydroxytryptamine were also mutagenic for strains TA1538, TA98 and TA1535 without the need for metabolic activation. The sensitivities of the frameshift-detecting strains TA1537, TA1538 and TA98 were of particular interest, since nitroso compounds are characteristically base-substitution mutagens. The mutagenic effects of the products formed after nitrosation of each indole at pH 3.6, were eliminated in the presence of S9 mix. This was not the case when the nitrosation assay was carried out at pH 2.6. At this pH the mutagenicity of the nitrosated products varied in the presence of S9 mix and depended upon the nature of the indole undergoing nitrosation, and the bacterial test strain utilised for the mutagenicity assay. This indicated that more than one mutagenic product was responsible for the observed effects. As well as pH, a number of other factors influenced the formation of mutagenic nitroso products. Most notably, the concentrations of precursor compounds (sodium nitrite, and indole) present in the NAP test were of critical importance. As the sodium nitrite concentration was reduced from that recommended by the W.H.O. (40 mM), so the mutagenicity decreased. For all three compounds significant mutagenic effects were lost at sodium nitrite concentrations below 15 mM. In conclusion the data presented in this paper clearly demonstrates that individuals are chronically exposed to naturally occurring substances which readily nitrosate in excess nitrous acid and yield bacterial mutagens.

Biotransformation↗
PubMed2002

Sodium accumulation during ischemia induces mitochondrial damage in perfused rat hearts.

OBJECTIVE: The present study aimed to elucidate the involvement of sodium overload and following damage to mitochondria during ischemia in the genesis of ischemia/reperfusion injury of perfused rat hearts. METHODS: Isolated, perfused hearts were exposed to different durations (15-35 min) of ischemia followed by 60-min reperfusion. At the end of ischemia or reperfusion, myocardial sodium and calcium contents and myocardial high-energy phosphates were determined. The cardiac mitochondrial ability to produce ATP was measured using saponin-skinned bundles. The effects of sodium on the mitochondrial membrane potential and the oxidative phosphorylation rate were examined using isolated mitochondria from normal hearts. RESULTS: Post-ischemic recovery of left ventricular developed pressure decreased in an ischemic duration-dependent manner. Ischemia induced an increase in myocardial sodium, but not calcium. This increase was dependent on the duration of ischemia. The oxygen consumption rate of skinned bundles from the ischemic heart decreased at the end of ischemia. Incubation of mitochondria with various concentrations of sodium chloride or sodium lactate in vitro resulted in a depolarization of mitochondrial membrane potential and a decrease in ATP-generating activity. This decrease was not restored after elimination of sodium compounds. CONCLUSIONS: The present findings suggest that ischemia induces an increase in sodium influx from the extracellular space and that accumulated sodium may induce irreversible damage to mitochondria during ischemia. This mitochondrial dysfunction may be one of the most important determinants for the genesis of ischemia/reperfusion injury in perfused rat hearts.

Analysis of Variance↗
PubMed1976

[Effect of insecticides on larvae of Musca domestica in swine manure],.

The effectiveness of four inorganic compounds and six preparations of insecticides was examined on larvae of Musca domestica in pig manure. The activity of sodiumfluoride and chlorinated hydrocarbons was low. Carbaryl indicated better effect. Good to very good results showed trichlofon and bromophos and the inorganic compounds sodium hexafluorsilicate, sodium tetraborate and calcium cyanamid. The influence of calcium cyanamid and sodium tetraborate led to considerable morphological deformations of pupae. With the latter compound and with fluorides a distinct prolongation of period of development was established in comparison with control. The effect of trichlorfon and bromophos decomposes rapily in pig manure. With trichlorfon an indirect ovicide effect was observed.

Animals↗
PubMed2006

HIV-1 replication is stimulated by sodium stibogluconate, the therapeutic mainstay in the treatment of leishmaniasis.

Leishmaniasis is an important opportunistic disease among patients infected with human immunodeficiency virus (HIV)-1. The pentavalent antimony compound sodium stibogluconate is a drug of choice for the treatment of leishmaniasis. Because sodium stibogluconate acts as an inhibitor of phosphotyrosyl phosphatases and such inhibitors can promote HIV-1 replication, we tested the effect of this compound on virus gene expression. Using pseudotyped reporter viruses and fully infectious laboratory-adapted and clinical strains of HIV-1, we report that sodium stibogluconate induces an increase in HIV-1 transcription and virus replication in primary CD4(+) T cells and in thymic histocultures. This activation is a slow process and appears to involve the transcription factors nuclear factor- kappa B and activator protein 1, as well as the Syk, Jun, and mitogen-activated protein kinase/extracellular signal-related kinase signal-transduction pathways. In addition, the effect seems to be partly mediated by a soluble factor. Altogether, these findings might reveal clinical implications for the treatment of leishmaniasis in HIV-1-infected patients.

Antimony Sodium Gluconate↗
PubMed1985

Independent regulation of myeloid cell growth and differentiation inducing proteins: in vivo regulation by compounds that induce inflammation.

Regulation of the in vivo production of myeloid cell growth-inducing (MGI-1) and differentiation-inducing (MGI-2) proteins has been studied in mice injected with the inflammation-inducing compounds sodium caseinate, thioglycollate and bacterial lipopolysaccharide. The results indicate that these inflammation-inducing compounds can induce in vivo production of MGI-1 and MGI-2; that different inducing agents can cause a different body-distribution of MGI-1 and MGI-2; that there is an independent regulation of in vivo production and distribution of MGI-1 and MGI-2; and that there is a granulocyte growth-inducing protein (MGI-IG = G-CSF) that is not identical to the differentiation-inducing protein (MGI-2). Resident peritoneal macrophages produce MGI-1 and MGI-2 in vitro, but inflammatory macrophages show a reduced ability to spontaneously produce these proteins after in vivo injection of caseinate or thioglycollate. The results thus also indicate that macrophage activation can affect the ability of macrophages to produce the myeloid cell regulatory proteins MGI-1 and MGI-2.

Animals↗
PubMed1983

Treatment of ifosfamide-induced urothelial toxicity by oral administration of sodium 2-mercaptoethane sulphonate (MESNA) to patients with inoperable lung cancer.

The protective effect of oral administration of the thiol compound sodium 2-mercaptoethane sulphonate (MESNA) against urothelial toxicity induced by ifosfamide (IF) was tested in a group of 45 patients with inoperable lung cancer under treatment with IF (2250 mg/m2 on days 2-5) as part of a polychemotherapy regimen repeated in a 4-week cycle. MESNA was given orally on the days of treatment with IF in 3 doses of 840 mg/m2, each administered at 0 hr (= injection of IF), 4 hr and 8 hr p.i. Out of a total of 88 courses of this treatment we observed 10 episodes of asymptomatic microscopic haematuria and no episodes of gross haematuria. In this group of 45 patients under protection with MESNA there were 5 complete remissions and 9 partial remissions (total 31%). A further group of 25 patients under polychemotherapy with IF were treated by conventional prophylactic measures (raised fluid intake and forced diuresis). In this group there were 1 complete and 5 partial remissions (total 24%), but nearly all patients developed either gross haematuria and/or symptoms of bladder irritation (cystitis and pollakisuria). There were no appreciable differences between the MESNA series and the conventional prophylaxis series with respect to either haematological or systemic toxicity of the cytostatic treatment. Our results support the view that MESNA, given orally in conjunction with combined cytostatic regimens which include IF, simplifies the treatment and provides optimum protection for the urinary epithelium. Protection with oral MESNA is particularly suitable for outpatients.

Administration, Oral↗
PubMed1985

Generation of free radical intermediates from foreign compounds by neutrophil-derived oxidants.

A large number of foreign compounds, including many drugs, industrial pollutants, and environmental chemicals, can be oxidized under appropriate conditions to potentially toxic free radical intermediates. We evaluated the ability of the oxidants produced by the neutrophil myeloperoxidase system to generate free radical intermediates from several such compounds. Sodium hypochlorite or hypochlorous acid produced by human peripheral blood neutrophils and trapped in the form of taurine chloramine were both found to be capable of producing free radicals from chlorpromazine, aminopyrine, and phenylhydrazine. These radical intermediates were demonstrated by visible light spectroscopy and by direct electron spin resonance (for the chlorpromazine and aminopyrine radicals) or by spin-trapping (for the phenyl radical generated from phenylhydrazine). Stable oxidants produced by the neutrophils (i.e., those present in the supernatants of stimulated neutrophils in the absence of added taurine) also were found to be capable of generating free radical intermediates. The production of the oxidants and the ability of neutrophil supernatants to generate these radicals were almost completely eliminated by sodium azide, a myeloperoxidase inhibitor. We suggest that the oxidation by neutrophils of certain chemical compounds to potentially damaging electrophilic free radical forms may represent a new metabolic pathway for these substances and could be important in the processes of drug toxicity and chemical carcinogenesis.

Aminopyrine↗
PubMed1995

Transport of a hydrophilic compound into the cerebrospinal fluid during experimental allergic encephalomyelitis and after lipopolysaccharide administration.

PURPOSE: The transport of the hydrophilic model compound sodium fluorescein into the cerebrospinal fluid (CSF) of rats was studied during experimental allergic encephalomyelitis (EAE), as a model for local central nervous system (CNS) inflammatory disease, and after a single injection of a pyrogenic dose of lipopolysaccharide (LPS), as a model for a general inflammation. METHODS: Transport of sodium fluorescein was measured by means of serial CSF and plasma sampling. Transport of this hydrophilic model compound was studied in Lewis rats suffering from EAA and three hours after LPS administration in male Wistar rats. RESULTS: During acute EAE, sodium fluorescein concentrations in the CSF increased twofold compared to control animals, whereas plasma kinetics were comparable within both groups. After i.v. LPS administration, however, plasma as well as CSF kinetic parameters of sodium fluorescein concentration were significantly changed from those seen in control animals. Transport of sodium fluorescein from plasma into the CSF was calculated as the ratio Area Under the Curve (AUC)CSF/AUCPLASMA. During acute EAE this ratio increased 2-fold compared to control animals, whereas after i.v. LPS administration it was not significantly different from the one obtained in control animals. CONCLUSIONS: These results suggest an opening of the blood-brain barrier (BBB) during a cerebral inflammatory response, like acute EAE, but not after LPS administration.

Animals↗
PubMed1995

Inhibition by sodium nitroprusside of the expression of inducible nitric oxide synthase in rat neutrophils.

A well-known nitric oxide (NO)-releasing compound, sodium nitroprusside (SNP), decreases in a dose-dependent manner NO synthase (NOS) activity induced in rat neutrophils by treatment with lipopolysaccharide (LPS). This inhibitory action of SNP seems not to be due to its direct effect on the enzyme activity. The strong nitrosonium ion (NO+) character of SNP could be responsible for its inhibition of NOS induction in neutrophils.

Amino Acid Oxidoreductases↗
PubMed1995

The iron component of sodium nitroprusside blocks NMDA-induced glutamate accumulation and intracellular Ca2+ elevation.

These studies were designed to compare the effects of nitric oxide (NO) generating compounds with those of several iron containing compounds which do not generate NO on glutamate receptor function. Stimulation of primary cultures of cerebellar granule cells with N-methyl-D-aspartate (NMDA) or kainate results in the elevation of intracellular calcium ([Ca2+]i) and cGMP and the release of glutamate. The iron containing compounds, sodium nitroprusside (SNP), potassium ferrocyanide (K4Fe(CN)6) and potassium ferricyanide (K3Fe(CN)6) decrease the NMDA-induced release of glutamate. SNP is the only compound of the above 3 agents which generates NO. A non-iron, NO generating compound, S-nitroso-N-acetylpenicillamin (SNAP), has no effect on the NMDA-induced glutamate release. Potassium ferrocyanide (Fe II), but not potassium ferricyanide (Fe III), blocks NMDA-induced cGMP elevations after 3 min exposure times. This contrasts with the NO generating compounds (both SNP and SNAP) which elevate cGMP levels. Furthermore, both potassium ferrocyanide (Fe II) and SNP (Fe II) suppress the elevation of [Ca2+]i induced by NMDA but neither potassium ferricyanide (Fe III) nor SNAP are effective in this regard. These effects are also independent of cyanide as another Fe II compound, ferrous sulfate (FeSO4) is also able to suppress NMDA-induced elevations of [Ca2+]i. SNP was unable to suppress kainate receptor functions. Collectively, these results indicate that Fe II, independently of NO, has effects on NMDA receptor function.

Animals↗
PubMed1999

Sodium ferric gluconate complex in sucrose is safe and effective in hemodialysis patients: North American Clinical Trial.

A new intravenous (i.v.) iron compound, sodium ferric gluconate complex in sucrose (Ferrlecit, R&D Laboratories, Inc, Marina Del Rey, CA), was administered over 8 consecutive dialysis days in equally divided doses to a total of either 0.5 or 1.0 g in a controlled, open, multicenter, randomized clinical study of anemic, iron-deficient hemodialysis patients receiving recombinant human erythropoietin (rHuEPO). Effectiveness was assessed by increase in hemoglobin and hematocrit and changes of iron parameters. Results were compared with historically matched controls on oral iron. High-dose i.v. treatment with 1.0 g sodium ferric gluconate complex in sucrose resulted in significantly greater improvement in hemoglobin, hematocrit, iron saturation, and serum ferritin at all time points, as compared with low-dose i.v. (0.5 g) or oral iron treatment. Despite an initial improvement in mean serum ferritin and transferrin saturation, 500 mg i.v. therapy did not result in a significant improvement in hemoglobin at any time. Eighty-three of 88 patients completed treatment with sodium ferric gluconate complex in sucrose: 44 in the high-dose and 39 in the low-dose group. Two patients discontinued for personal reasons. The other three discontinued because of a rash, nausea and rash, and chest pain with pruritus, respectively. In comparison with 25 matched control patients, adverse events could not be linked to drug therapy, nor was there a dose effect. In conclusion, sodium ferric gluconate complex in sucrose is safe and effective in the management of iron-deficiency anemia in severely iron-deficient and anemic hemodialysis patients receiving rHuEPO. This study confirms the concepts regarding iron therapy expressed in the National Kidney Foundation Dialysis Outcomes Quality Initiative (NKF-DOQI) that hemodialysis patients with serum ferritin below 100 ng/mL or transferrin saturations below 18% need supplementation with parenteral iron in excess of 1.0 g to achieve optimal response in hemoglobin and hematocrit levels.

Adult↗
PubMed1984

[Blood pharmacokinetics of fluorine in man after the oral administration of nicomethanol hydrofluoride].

The pharmacokinetic parameters of fluoride have been studied, after a single oral administration to human volunteers of two fluoridated compounds: sodium fluoride, and a new organic fluoride salt, nicomethanol hydrofluoride. The results obtained with these two compounds were very similar, suggesting that no abnormal accumulation of fluoride in the body occurs after using nicomethanol hydrofluoride.

Administration, Oral↗