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At least 19 recordsLinked to original sources
PubMed1986

Apoprotein A-I measured by radial immunodiffusion in heparin-MnCl2 supernates.

We compared measurements of apoprotein A-I (apoA-I) in plasma and in heparin-MnCl2 supernates analyzed by radial immunodiffusion. The apoA-I values were similar when the samples were fresh [n = 41, mean (SD), mg/L: plasma, 1393.4(349); heparin-MnCl2 supernates, 1364.9(332), p less than 0.01], but were greater than 8% lower in heparin-MnCl2 supernates after storage for seven days at 4 degrees C [plasma, 1348.0(351); heparin-MnCl2 supernates, 1237.6(342), p less than 0.001]. Neither heparin nor MnCl2 interfered directly with the immunodiffusion assay, and treating samples with tetramethylurea and urea to maximize the exposure of apoA-I did not prevent the decrease. MnCl2 (46 mmol/L) added to isolated HDL (d 1.063-1.21) decreased apoA-I values by 5.6% when measured immediately and by 16.7% after storage at 4 degrees C for seven days. High-density lipoprotein cholesterol values were unchanged by MnCl2. The results indicated that apoA-I was more stable in plasma than in heparin-MnCl2 supernates, probably because of an interaction between apoA-I and MnCl2.

Apolipoprotein A-I↗
PubMed1975

Induction of mouse lung adenomas by amines or ureas plus nitrite and by N-nitroso compounds: effect of ascorbate, gallic acid, thiocyanate, and caffeine.

Lung adenomas were induced in strain A mice by chronic treatment with N-nitroso compounds (given in drinking water) and with amines or ureas in food plus NaNO2 in drinking water. We studied the effects of varying the concentrations of three N-nitroso compounds and NaNO2 concentration in the morpholine plus NaNO2 and methylurea plus NaNO2 systems. Sodium ascorbate (NaASC) at the highest level tested (11.5 or 23 g/kg food) gave 89-98% inhibition of adenoma induction by the NaNO2 plus piperazine, morpholine, and methylurea systems. In 7 groups, NaASC produced increases of 15-59% in adenoma induction by nitrosomorpholine (NM) and mononitrosopiperazine (MNP), possibly because the mice consumed more of the nitrosamine solution. Adenoma induction by morpholine plus NaNO2 was strongly inhibited by gallic acid, moderately inhibited by caffeine, and unaffected by thiocyanate (all added to the food). Gallic acid inhibited or had no effect on the action of NM and MNP. We discussed the proposal that NaASC (or perhaps gallic acid) be administered with readily nitrosatable drugs.

Adenoma↗
PubMed1988

Inhibitory effects of para-aminobenzoic acid on the formation and mutagenicity of N-nitroso compounds.

Naturally occurring para-aminobenzoic acid (PABA) inhibited the formation of N-methyl-N-nitrosourea (MNU) from a nitrosation mixture of N-methylurea and nitrite at pH 3. The suppressive effect of PABA on the formation of MNU is higher than that of ascorbic acid. The presence of the MNU was assayed by its mutagenicity in a higher plant, Arabidopsis thaliana. In addition, PABA markedly reduced the mutagenicity of N-methyl-N'-nitro-N-nitrosoguanidine in A.thaliana, but had no or only a low inhibitory effect on the mutagenicity of preformed MNU and on the promutagen N-nitrosodimethylamine.

4-Aminobenzoic Acid↗
PubMed1992

Characterization of BIBS 39 and BIBS 222: two new nonpeptide angiotensin II receptor antagonists.

Two new nonpeptide angiotensin II (AII) receptor antagonists, 4'-[(2-n-butyl-6-cyclohexylaminocarbonylamino-benzimidazole-1-yl)- methyl ] biphenyl-2-carboxylic acid (BIBS 39) and 2-n-butyl-1-[4-(6-carboxy-2,5-dichlorobenzoylamino)-benzyl]-6-N- (methylaminocarbonyl)-n-pentylamino-benzimidazole (BIBS 222) were characterized in radioligand binding assays, and in vitro and in vivo experiments. BIBS 39 displaced [125I] AII from its specific binding sites with a K(i) value of 29 +/- 7 nM for the AII subtype I (AT1) receptor and a K(i) value of 480 +/- 110 nM for the AII subtype 2 (AT2) receptor. BIBS 222 showed a K(i) value of 20 +/- 7 nM for the AT1 subtype and a K(i) value of 730 +/- 170 nM for the AT2 subtype. Thus BIBS 39 was 17 times more selective for the AT1 subtype and BIBS 222 37 times. Both compounds were specific for AII receptors as they did not show high affinity for other receptors. BIBS 39 shifted the AII concentration-contractile response curves in isolated rabbit aorta to the right in a parallel fashion. A pA2 value of 8.14 +/- 0.08 and a slope of 1.06 +/- 0.07 were calculated. BIBS 222 caused nonparallel shifts to the right and reduced the maximal response induced by AII by about 25%. A KB value of 9.01 (+/- 3.22) x 10(-8) M was determined. At 10(-5) M, neither compounds altered the contractile responses to noradrenaline and KCl. In pithed rats, BIBS 39 dose dependently shifted the dose-response curve of AII to the right without affecting the maximal response.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin Receptor Antagonists↗
PubMed1987

Aged and bound herbicide residues in soil and their bioavailability. Part 2: Uptake of aged and non-extractable (bound) [carbonyl-14C]methabenzthiazuron residues by maize.

[Carbonyl-14C]methabenzthiazuron (MBT) was applied to growing winter wheat in an outdoor lysimeter. The amount applied corresponded to 4 kg Tribunil/ha. 140 days after application the 0-2.5 cm soil layer was removed from the lysimeter. This soil contained about 40% of the applied radioactivity. Using 0,01 M CaCl2 solution or organic solvents, the extractable residues were removed from the soil. The bioavailability of the non-extractable as well as aged residues remaining in the soil was investigated in standardized microecosystems containing 1.5 kg of dry soil. During a 4 weeks period the total uptake (4 maize plants/pot) amounted up to 3.6; 2.2; and 0.9% of the radioactivity from soils containing aged MBT residues, MBT residues non-extractable with 0.01 M CaCl2 or MBT residues non-extractable with organic solvents, respectively. About 20% of the radioactivity found in maize leaves represented chromatographically characterized parent compound. At the end of the plant experiment the soil was extracted again with 0.01 M CaCl2 and with organic solvents. The soil extracts and also the organic phases obtained from the aqueous fulvic acid solution contained unchanged parent compound.

Benzothiazoles↗
PubMed1991

Eugenol causes oxidant-mediated edema in isolated perfused rabbit lungs.

Eugenol, an extract of cloves, has been associated with pulmonary edema when inhaled from commercially available clove cigarettes. We tested the hypothesis that eugenol directly causes lung edema through oxidant-mediated mechanisms by infusing eugenol (0.1 and 1.0 mM) into isolated rabbit lungs perfused with a cell-free albumin and physiologic salt solution. We observed lung edema (1.0 mM) as demonstrated by increased lung weight gain and wet-to-dry lung weight ratios without alterations in mean pulmonary artery pressure. The oxygen metabolite scavengers catalase (1,000 U/ml) and dimethylthiourea (30 mM) attenuated lung edema. Instillation of dimethylurea, superoxide dismutase, or heat-inactivated catalase did not prevent lung edema formation. We conclude that eugenol causes lung edema in isolated lungs through oxidant-mediated mechanisms in the absence of circulating formed blood elements. Eugenol may be a valuable compound in the laboratory investigation of edemogenic disorders.

Animals↗
PubMed1991

Environmental mutagens that induce the adaptive response to alkylating agents in Escherichia coli.

Many microorganisms exhibit an adaptive response to mutagenic alkylation damage. In Escherichia coli the response is regulated by the inducible Ada protein. A sensitive immunoassay employing two anti-Ada monoclonal antibodies has been developed here to monitor low levels of induction of the Ada protein. This protein was detected in non-induced E. coli which contained an average of two molecules of Ada per cell. The occurrence of the adaptive response in bacteria signals the existence of an ecological niche in which cells are exposed to direct-acting methylating compounds, but the structure and identity of these agents are unknown. Using the immunoassay to search for possible candidates, a number of methylating agents and precursors of such agents have been investigated. Carbamyl phosphate and methylamine yield N-methylurea, which reacts subsequently with nitrite to generate the strong inducer N-methyl-N-nitrosourea. The antibiotic streptozotocin also is a potent inducer of the adaptive response. Moreover, the abundant environmental mutagen methyl chloride acts as an inducer.

Adaptation, Physiological↗
PubMed1979

N-mineralization of formaldehyde-releasing N-compounds.

The mineralization of several N-compounds, such as MMU, DMU, and HMT, as well as their respective nitrificide action, have been investigated. It has been proved that the amount of available formaldehyde, as well as its rate of release, are responsible for the specific action of these compounds on the N-mineralization process. Factors affecting the rate of release, namely molecular structure, solubility, and temperature, are discussed as well. Importance of these N-compounds as slow-release N-fertilizers based on a new molecular-microbiological approach is described.

Bacteria↗
PubMed1989

Inhibition of chemical Epstein-Barr virus induction by dimethyl sulfoxide and related polar compounds.

Dimethyl sulfoxide and twelve related polar compounds, capable of inducing differentiation of murine erythroleukemia cells, markedly inhibited induction of Epstein-Barr virus antigens in virus producer and nonproducer lymphoblastoid cells exposed to 12-O-tetradecanoylphorbol-13-acetate, n-butyric acid, 5-iodo-2'-deoxyuridine, and a combination of 12-O-tetradecanoylphorbol-13-acetate and n-butyric acid. The concentration at which these compounds caused 90% inhibition of antigen induction corresponded to that optimal for induction of differentiation. At the same concentrations, polar compounds did not affect cell viability or virus induction by superinfection with Epstein-Barr virus recovered from P3HR-1 cells. The inhibitory activity was reversible. Three nonpolar differentiating compounds revealed no inhibitory activity.

Acetamides↗
PubMed1977

Individual susceptibility of mice to a mutagen in both germ and somatic cells.

Male Swiss mice received simultaneously, by gavage, 500 mg methylurea/kg body weight and 25 mg sodium nitrite/kg body weight, and in a further experiment 330 mg of methylurea/kg and 17 mg sodium nitrite/kg, for 5 consecutive days. This treatment resulted in a dose-dependent mutagenic effect in both the dominant-lethal and the micro-nucleus tests. Furthermore, in both mammalian tests, some animals were more susceptible to the mutagenic compounds than were others. However, the liver microsomal metabolizing system did not seem to be responsible for this variation of mutagenic induction.

Animals↗
PubMed1986

Mutagenicity of methylisocyanate and its reaction products to cultured mammalian cells.

Methylisocyanate (MIC) induced mutagenic responses in the absence of exogenous activation in the mouse lymphoma cell forward mutation assay at concentrations as low as 8-24 microM. MIC produced predominantly small mutant colonies, suggesting the possibility of clastogenic activity. The intermediate hydrolysis product, methylamine, was also mutagenic without exogenous activation but required several hundred-fold higher concentrations (ca. 3 mM). N,N'-Dimethylurea, the final product in the reaction of methylisocyanate and water, was totally refractory in either the presence or absence of S9 for concentrations up to 57 mM (5 mg/ml). The ethyl ester of N-methylcarbamic acid was also tested since it was the only available analogue to the highly reactive N-methylcarbamic acid intermediate. This compound was mutagenic only in the presence of S9 at doses exceeding 5-40 microM, which suggested the possibility that the free acid, produced by enzymatic hydrolysis, is also mutagenic. The mutagenic activity of the ester resulted solely in the production of small mutant colonies.

Animals↗
PubMed1990

[The pre- and postnatal carcinogenic effect of 3,3-diethyl-1-methyl-1-nitrosourea (DEMNU) in rats following intravenous application].

The pre- and postnatal administration of DEMNU induces a high frequency of tumors when applied via the intravenous route, and the latency periods show a dose dependence (table I). Tumors of the brain, spinal cord and cranial nerves clearly predominate. Furthermore, a large number of neoplasms of kidney, heart and soft tissue was observed (table II). As DEMNU is per se a very stable compound, it is suggested that this agent is metabolized by monooxygenases. 3-Ethyl-1-methyl-1-nitrosourea should be formed as an intermediate product via this pathway, which is relatively stable and might explain the mainly neurotropic carcinogenicity of DEMNU. Species differences in the carcinogenicity of trialkyl-nitrosoureas and the mode of metabolic activation are discussed.

Animals↗