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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Equal mole doses of the anions of disodium carbamyl phosphate (carbamyl P) or sodium cyanate, antisickling agents, have been compared in C57B1 mice. Using 15 mice per group, two groups were given the equivalent ip dose of carbamyl P or cyanate anion (7 mmoles/kg/day) in a divided dose, in the morning and six hours later, for 17--18 days. The control group received sodium chloride (13.8 mmoles of Na+ or Cl-/kg/day). Surviving mice per group were sodium chloride, 15/15; disodium carbamyl P, 14/15; and sodium cyanate, 0/15, all mice died by day 2. Surviving mice appeared normal throughout the study, and no abnormalities were seen at necropsy. The hematologic measurements were the same for sodium chloride or disodium carbamyl P, including hemoglobin, packed cell volume, erythrocyte counts, leucocyte counts, and differential counts. The mean hemoglobin carbamylation was 1.24 (+/- 0.06 SE) moles of valine hydantoin/mole of hemoglobin tetramer in mice receiving disodium carbamyl P for 18 days, sufficient for antisickling activity. The enzymatic degradation of carbamyl P to NH3, CO2, and Pi was measured in serial blood samples in additional C57B1 and DBA/2J mice following ip injections of carbamyl P or cyanate. Both NH3 and Pi increased immediately after giving carbamyl P, but no increase occurred after cyanate administration. Thus enzymatic degradation of carbamyl P occurs in vivo and appears to be an important detoxification mechanism. When equivalent mole doses of anion are administered, disodium carbamyl P is less toxic than sodium cyanate in mice.
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PMID:Antisickling agents: effects of carbamyl phosphate or cyanate on survival, erythrocytes, and leucocytes in the mouse. 53 3

The objective of this study was to examine the binding of carcinogenic polycyclic aromatic hydrocarbons in well-characterized nuclear subfractions from transformable cells in culture. A cloned line of AKR mouse embryo cells was exposed to culture medium containing [3H]-3-methyl-cholanthrene (MC) (0.4 mug/ml) 670 Ci/mole). Cellular uptake and nuclear binding were determined after 4 hr of exposure. The addition of unlabeled MC up to 10 mug/ml did not cause reduction of [3H]MC cellular uptake or nuclear binding. From 2 to 5% of the total cellular MC was localized in the nuclei. All nuclear subfractions obtained from mechanically sheared nuclei and separated on sucrose gradients showed some MC binding; however, a high-affinity, high-specific-activity binding of MC was associated only with the slower-sedimenting component shown to represent that fraction of nuclear chromatin that is transcriptionally active. Conditions that caused the precipitation of this chromatin also resulted in the precipitation of the radioactive compound, thus suggesting that the MC was physically bound to the chromatin. Unlabeled MC (10 mug/ml) saturated this high-affinity MC binding to the transcripitionally active chromatin but did not saturate the binding to the other nuclear fractions. The binding of another potent carcinogen, [3H]-1,2,5,6-dibenzanthracene, and the "weak" carcinogen, [3H]-1,2,3,4-dibenzanthracene (3,4-DBA), to whole nuclei and nuclear subfractions was also determined. The concentration, specific activity, and time of treatment were identical with those used for MC. The level of binding of [3H]-1,2,5,6-dibenzanthracene was approximately 3-fold greater in whole nuclei on a per mass DNA basis than in those of either the MC or the 3,4-DBA. The binding of MC and 3,4-DBA to whole nuclei was approximately equal. As with MC, the [3H]-1,2,5,6-dibenzanthracene demonstrated a peak of high specific activity binding to the slower-sedimenting fraction of chromatin while the 3,4-DBA displayed considerably less binding to this fraction.
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PMID:Binding of polycyclic aromatic hydrocarbons to transcriptionally active nuclear subfractions of AKR mouse embryo cells. 127 1

Expired ethanol and acetaldehyde were measured after an oral injection of ethanol in C57BL/6J and DBA/2J mouse strains by a combination of several techniques in a sequence involving a method for trapping expired radioactive compounds, separation of compounds by gas chromatography, isolation of radioactive ethanol and acetaldehyde, and their quantitative analysis by liquid scintillation spectrophotometry. With the specific activities used in evaluation of the technique (0.1 Ci/mole, acetaldehyde; 1.1 Ci/mol, ethanol) the lower limit of sensitivity using 500 microliters from a 10 ml trap is 955 pmoles for acetaldehyde and 101 pmoles for ethanol. However, in the animal experiments, injected ethanol has a specific activity of 1.1 Ci/mol which would make the specific activity of expired metabolically formed acetaldehyde the same. This results in a lower limit of sensitivity for acetaldehyde of 80 pmoles. The two strains were monitored for 80 min following an oral injection of 3.8 g/Kg of (2-14C) ethanol. Comparing the two strains on the expiration of each compound the curves were identical.
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PMID:A quantitative analysis of ethanol and acetaldehyde expired by inbred mouse strains. 739 48