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PubMed1983

Mutagenicity of potassium alkanediazotates and their use as model compounds for activated nitrosamines.

The mutagenicity of a series of potassium alkanediazotates in the Ames assay was studied. These compounds were isolated as solids and are soluble in dimethyl sulfoxide. Upon addition to water, they form diazohydroxides (which are postulated intermediates in the decomposition of alpha-hydroxylated nitrosamines). The diazohydroxides decompose to electrophilic intermediates which may react with macromolecules or water. In the Ames assay, potassium diazotates produced his+ revertants in Salmonella typhimurium strains TA 100 and TA 1535 but not in strains TA 98, TA 1537, or TA 1538. Methane, methane-d3, ethane, propane, and phenylmethanediazotates were mutagenic in strain TA 100, and all diazotates with the exception of phenylmethanediazotate, produced revertants in TA 1535. The order of mutagenic potency of these compounds was: methane approximately equal to methane-d3 greater than ethane, greater than phenylmethane (TA 100) greater than propane greater than phenylmethane (TA 1535) = 0. All diazotates were direct-acting mutagens and produced revertants even when no liver 9000 X g supernatant (S9) fractions were present. S9 fractions inhibited the mutagenicity of potassium diazotates, and equivalent concentrations of S9 fractions (3 mg protein per plate) from either rat or hamster liver, whether induced or not, were equally effective. Bovine serum albumin was not as effective as S9 fractions in inhibiting diazotate mutagenesis, but heat-inactivated (70 degrees for 20 min) S9 fractions were as inhibitory of methanediazotate mutagenicity as native S9 fractions were at low protein concentrations. The half-lives of mutagenicity of methane- and ethanediazotates in aqueous solutions were identical (less than or equal to 15 sec); after less than 2 min in solution, these diazotates were rendered completely inactive. The implications of these studies for mechanisms of nitrosamine action and the use of potassium alkanediazotates as model compounds for activated nitrosamines are discussed.

Animals↗
PubMed1984

Arecoline tumorigenicity in Swiss strain mice on normal and vitamin B deficient diet.

Arecoline, a major alkaloid present in betel nut, was administered daily by gavage feeding to Swiss male and female mice at a dose of 1 mg/day/mouse five times a week, either alone or in combination with KNO3 or KNO3 + lime. Swiss mice of both sexes kept on a vitamin B complex-deficient diet were tested in a similar manner and compared with those receiving a normal diet. In the mice receiving a normal diet it was observed that arecoline induced tumors in 40% of males but failed to produce tumors in any of the females. Arecoline tumorigenicity in females was evident only when they received a vitamin B-deficient diet. Arecoline tumorigenicity was not evident in males when they were treated simultaneously with KNO3 + lime and kept on a normal diet. However, the same treatment administered to male mice kept on a vitamin B complex-deficient diet induced tumors in 39%.

Animals↗
PubMed2003

In vitro cytotoxicity of traditional versus contemporary dental ceramics.

STATEMENT OF PROBLEM: The biocompatibility of new dental ceramics has not been assessed with the same scrutiny as has been applied to alloys and composites. Yet, the biocompatibility of ceramics is critical to the long-term success of dental prostheses because ceramics are in close contact with oral tissues for extended periods. MATERIAL AND METHODS: Five dental ceramics (2 traditional feldspathic veneer porcelains [Vita Omega and Duceragold], 2 lithium disilicate pressable materials [Stylepress and Empress-2], and a pressable leucite-based material [Empress-1]) were tested for their ability to alter cellular mitochondrial dehydrogenase activity after fabrication using a tetrazolium assay, after aging for 2 weeks in a biologic solution and after post-aging polishing with either a fine diamond or diamond polishing paste. Cellular responses were compared with polytetrafluoroethylene controls (analysis of variance, Tukey pairwise post-hoc comparison, alpha=.05). RESULTS: The feldspathic porcelains caused only mild (<25% of controls) mitochondrial suppression regardless of aging or polishing. The pressable leucite-based material initially caused a 5% stimulation (not significant) of mitochondrial activity, which decreased significantly (P<.05) by 30% with aging to levels comparable to the feldspathic porcelains, and did not change with polishing. Both lithium disilicate materials caused an initial suppression of mitochondrial activity that decreased significantly with aging, but Empress-2 was severely cytotoxic initially (<20% of controls, P<.01), and became more cytotoxic again after polishing. Stylepress was less cytotoxic initially (85% of controls, not significant) and did not become cytotoxic again after polishing. CONCLUSIONS: Dental ceramics are not equivalent in their in vitro biologic effects, even within the same class of material, and biologic safety should not be assumed. Most ceramics caused only mild in vitro suppression of cell function to levels that would be acceptable on the basis of standards used to evaluate alloys and composites. However, 1 Li-disilicate material (Empress-2) exhibited cytotoxicity that would not be deemed biologically acceptable on the basis of prevailing empirical standards for dental alloys and composites.

Aluminum Silicates↗
PubMed1985

Inhibition of DNA synthesis by chromium compounds.

Cr(VI) irreversibly inhibited DNA synthesis in cultured mouse L cells to 50% of controls at 10 microM; 3.3 mM Cr(III) did not. At 0.3 mM, Cr(III) and Cr(VI) inhibited DNA synthesis in permeabilized L cells to 50% of control values. Cr(III) was a stronger inhibitor of DNA synthesis in the DNA-Escherichia coli DNA polymerase I system than was Cr(VI). The inhibitory effect of Cr(VI) depended on the ratio of Cr/DNA and Cr/enzyme; on the other hand, the increase in the concentration of DNA polymerase did not affect the inhibition of Cr(III), Cr(III), below the inhibitory concentration, produced an increase in the incorporation of [3H]dTMP into DNA; this was not observed with Cr(VI).

Animals↗
PubMed1997

Baralyme dehydration increases and soda lime dehydration decreases the concentration of compound A resulting from sevoflurane degradation in a standard anesthetic circuit.

UNLABELLED: Soda lime and Baralyme brand carbon dioxide absorbents degrade sevoflurane to CF2 = C(CF3)OCH2F, a potentially nephrotoxic vinyl ether called Compound A. Dehydration of these absorbents increases both the degradation of sevoflurane to Compound A and the degradation of Compound A. The balance between sevoflurane degradation and Compound A degradation determines the concentration of Compound A issuing from the absorbent (the net production of Compound A). We studied the effect of dehydration on the net production of Compound A in a simulated anesthetic circuit. Mimicking continuing oxygen delivery for 1, 2, or 3 days after completion of an anesthetic, we directed a "conditioning" fresh gas flow of 5 L/min or 10 L/min retrograde through fresh absorbent in situ in a standard absorbent system for 16, 40, and/or 64 h. The conditioned absorbent was subsequently used (without mixing of the granules) in a standard anesthetic circuit in which a 3-L rebreathing bag substituted for the lung. Metabolism was mimicked by introducing 250 mL/min carbon dioxide into the "lung," and the lung was ventilated with a minute ventilation of 10 L/ min. At the same time, we introduced sevoflurane in a fresh gas inflow of 2 L/min at a concentration sufficient to produce an inspired concentration of 3.2%. Because of increased sevoflurane destruction by the absorbent, progressively longer periods of conditioning (dehydration) and/or higher inflow rates increased the delivered (vaporizer) concentration of sevoflurane required to sustain a 3.2% concentration. Dehydration of Baralyme increased the inspired concentration of Compound A by up to sevenfold, whereas dehydration of soda lime markedly decreased the inspired concentration of Compound A. IMPLICATIONS: Economical delivery of modern inhaled anesthetics requires rebreathing of exhaled gases after removal of carbon dioxide. However, carbon dioxide absorbents (Baralyme/soda lime) may degrade anesthetics to toxic substances. Baralyme dehydration increases, and soda lime dehydration decreases, degradation of the inhaled anesthetic sevoflurane to the toxic substance, Compound A.

Anesthetics, Inhalation↗
PubMed1982

Effect of furosemide on the electrical parameters of frog skin.

When added to the mucosal solution bathing isolated frog skin at concentrations ranging from 5 X 10(-4) to 3 X 10(-3) M, the diuretic furosemide increased both the active transport of sodium and the electrical potential difference across the tissue in a dose-dependent way. The same effect was observed in chloride-free solutions. Mucosal furosemide also decreased the passive unidirectional fluxes of chloride. We believe that as far as electrical parameters are concerned mucosal furosemide has a double effect in frog skin: it increases the active conductance to sodium across the mucosal membrane, thus increasing active transport, and decreases the passive permeability to chloride, thus altering the passive conductance of the skin. The relative increase in short-circuit current was, however, invariably greater than the increase of the active conductance, suggesting the influence of yet a third effect. The effect of mucosal furosemide on active sodium transport was blocked by amiloride (5 X 1-(-5) M) and was independent of vasopressin. Qualitatively the effect was similar to the effect produced by triphenylmethylphosphonium ion.

Amiloride↗
PubMed2003

The color change in CO2 absorbents on drying: an in vitro study using moisture analysis.

UNLABELLED: Alkali hydroxide-free absorbents change color markedly when they dry, whereas absorbents containing alkali hydroxides do not. We investigated whether this observation can be explained by the weaker hygroscopic properties of pure calcium hydroxide compared with alkali hydroxides. Samples of the alkali hydroxide-free absorbents Amsorb or Superia and samples of these two absorbents with 1% or 3% NaOH or 3% KOH added were dried in a moisture analyzer at 105 degrees C to determine their moisture content and to assess the color of the samples during drying (each group, n = 5). Additionally, we repeated the experiments with pulverized samples of Baralyme and Spherasorb, which contain approximately 4% KOH and 1% NaOH, respectively. Amsorb and Superia changed color long before they were dry. After the addition of 1% NaOH, and as with the Spherasorb samples, the drying time required for a color change was longer, and the intensity of the resulting violet was less. This effect was even stronger when 3% NaOH was added. The samples with added KOH and the Baralyme did not change color at all on drying. We conclude that the differences in color change on drying in absorbents with varying NaOH or KOH content cannot be explained by larger water retention because of the hygroscopic properties of the alkali hydroxides. IMPLICATIONS: In an in vitro study, the moisture content and color change on drying were determined in samples of Amsorb or Superia and in the same absorbents with added NaOH or KOH. With increasing concentrations of alkali hydroxide, a delay in the color change upon drying was observed. However, the moisture content did not change.

Absorption↗
PubMed1978

Platelet 5-hydroxytryptamine transport, an electroneutral mechanism coupled to potassium.

Transport of 5-hydroxytryptamine into plasma membrane vesicles isolated from porcine blood platelets is stimulated when a potassium gradient (in greater than out) is imposed across the vesicle membrane. This stimulation occurs in the absence of measurable electrical potential across the membrane. Addition of valinomycin induces a membrane potential of approximately 50 mV (interior negative) as estimated by uptake of the lipophilic cation triphenylmethylphosphonium, but has surprisingly little effect on 5-hydroxytryptamine transport. Addition of 2,4-dinitrophenol dissipates the valinomycin-induced membrane potential. In the absence of valinomycin, 2,4-dinitrophenol has no effect on 5-hydroxytryptamine transport but valinomycin and 2,4-dinitrophenol together inhibit transport, probably by dissipation of the K+ gradient. These results are consistent with an electroneutral mechanism in which 5-hydroxytryptamine influx is directly coupled to potassium ion efflux and argue against an electrogenic mechanism in which there is a net influx of positive charge with 5-hydroxytryptamine.

Animals↗
PubMed2005

Potassium oxonate, an enzyme inhibitor compounded in S-1, reduces the suppression of antitumor immunity induced by 5-fluorouracil.

S-1 is an oral formulation combining tegafur (FT), 5-chloro-2,4-dihydroxypyridine (CDHP), and potassium oxonate (Oxo) in a molar ratio of 1:0.4:1. We examined whether Oxo reduces the immunosuppression induced by 5-fluorouracil (5-FU) in the rat. The body weight of rats treated with S-1 (FT + CDHP + Oxo) for seven consecutive days was significantly higher than that of rats treated with a combination of FT plus CDHP (FT + CDHP) for a similar period. The number of peripheral leukocytes was significantly higher in the S-1-treated rats (S-1 group) than that in the FT + CDHP-treated rats (FT + CDHP group). There was no apparent difference between the two treated groups in phenotypic changes of CD3-, CD45-, CD4-, or CD8-positive cells from the spleen or mesenteric lymph nodes. However, the natural killer activities of both spleen cells and mesenteric lymph node cells were significantly higher in the S-1 group than in the FT + CDHP group. Interleukin (IL)-2 production by spleen cells stimulated with concanavalin A was significantly lower in the FT + CDHP group than in the S-1 group. Although IL-2 production by mesenteric lymph node cells in the S-1 group was lower than that in untreated rats, it was higher than that in the FT + CDHP group. These findings suggest that Oxo in S-1 may reduce the suppression of antitumor immunity induced by 5-FU.

Animals↗