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

1. Chloride concentration and osmolalities were compared in consecutively collected samples of proximal tubular fluid, peritubular capillary plasma and systemic plasma. 2. Mean chloride concentrations (m-mole/l) were 141.3+/-2.6 in tubular fluid, 114.8+/-1.7 in peritubular capillary plasma and 119.4+/-1.8 in systemic plasma. 3. Mean osmolalities (m-osmole/kg H2O) were 297+/-2.2 in tubular fluid, 293+/-2.4 in peritubular capillary plasma and 299+/-1.8 in systemic plasma. 4. These differences are discussed in relation to the anatomical and functional organization of the peritubular capillaries and renal tubules.
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PMID:Comparison of chloride concentration and osmolality in proximal tubular fluid, peritubular capillary plasma and systemic plasma in the rat. 60 57

1. The exchange of chloride and bicarbonate across the human erythrocyte membrane has been followed by measuring the changes in extracellular pH which occur when chloride-rich erythrocytes are added to chloride-free media containing varying concentrations of bicarbonate and carbonic anhydrase. 2. The dependence of the rate of chloride/bicarbonate exchange on the extracellular concentration of bicarbonate was consistent with the existence of a saturable membrane anion transporter exhibiting Michaelis--Menten kinetics. In a medium containing sodium gluconate buffered to pH 7.0 with imidazole--malate the Km for bicarbonate activation of transport was 0.39 (+/- 0.03) mM and the Vmax was 2033 (+/- 80 m-mole anions exchanged/3 X 10(13) cells. min, at 10 degrees C. 3. Chloride/bicarbonate exchange was temperature-dependent with an Arrhenius activation energy of 19.4 kcal/mole in the temperature range 2--10 degrees C. 4. Exchange of intracellular chloride for extracellular bicarbonate was inhibited by the presence of extracellular halides. Inhibition by chloride, bromide and fluoride was competitive and the affinity of the transport system decreased in the order HCO-3 greater than Cl- greater than Br- greater than F-. The kinetics of inhibition by iodide were complex, but inhibitory effects of low concentrations of iodide were less than those of chloride and bromide.
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PMID:Chloride/bicarbonate exchange in human erythrocytes. 63 49

Aqueous chlorine reacts with tyrosine to form ring-chlorinated products. Ring substitution occurs at Cl:tyrosine mole ratios greater than 1. Because the nitrogen function of amides is much less reactive than that of amines, the aromatic ring of N-acetyltyrosine is chlorinated at chlorine:substrate mole ratios less than 1. When an aqueous solution of the gastric protein pepsin was chlorinated (37 degrees C, 45 min), tyrosine residues were chlorinated at pH 2 but not at pH 8. The carbohydrate, protein, and chloride concentrations in stomach fluid from fasted rats were determined. When varying concentrations of aqueous chlorine (20-180 mg/L Cl2) were added to the stomach fluid at pH 2, tyrosine residues were mono- and dichlorinated on the aromatic ring. The amount of mono- to dichlorination products varied with the concentration of aqueous chlorine. A mechanism is proposed. The implications for toxicological studies involving chlorinated drinking water are discussed.
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PMID:Reactions of aqueous chlorine in vitro in stomach fluid from the rat: chlorination of tyrosine. 191 6

Fluka humic acid used as a model substrate in these studies was analysed for elemental and the oxygen-containing functional groups. It was chlorinated at C:Cl molar ratios of 1:1 and 1:0.3 and subsequently separated into molecular weight fractions by ultrafiltration. The freeze-dried, chlorinated humic acid and the respective molecular weight fractions were analyzed for TOC, TOX, alkylating activity using 4-(p-nitrobenzyl)pyridine and mutagenicity by the Ames/Salmonella/microsome assay with strains TA-98 and TA-100. Results indicated that predominantly non-volatile, direct-acting mutagenic and/or alkylating agents were formed during humic acid chlorination and that these agents were unevenly distributed among the various molecular weight fractions. Formation of mutagenic and alkylating agents were highly dependent upon level of chlorination and total organic carbon. Higher levels of mutagenic and alkylating activities were produced with increasing concentration of chlorine in the range of 0.4-1.2 chlorine equivalents per mole of carbon. However, both these activities in the freeze-dried, chlorinated humic acid solutions containing the non-volatiles or the fresh solutions decreased gradually with increasing pH and storage time, apparently due to degradation and hydrolysis of some of the components.
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PMID:Mutagenicity and alkylating activity of the aqueous chlorination products of humic acid and their molecular weight fractions. 252 78

The genotoxicity of 5 compounds: 2 fulvic acids, a trade humic acid, a synthetic humic material (SHM), and 2,5-dihydroxybenzoic acid, was assessed after chlorination, by means of the SOS Chromotest for tester strain E. coli PQ 37 without metabolic activation. Chlorination was carried out for humic material concentration of 0.5 mg total organic carbon per liter, and chlorine concentrations in the range of 0.1-2.0 chlorine equivalents per mole of carbon. Among all the considered criteria that can account for potent toxicity: chemical degradation determined by the UV absorption decrease, chlorine consumption, average molecular weight, only the polymerization index (O.D. 665 nm/O.D. 465 nm) can be related to the genotoxicity of humic samples. This latter criterion appears a possible predictor of genotoxic potency, revealed subsequent to the aqueous chlorination of humic materials. Looking at the various genotoxic activities of the tested compounds, SHM can be considered a better model of natural humic materials than the trade humic acid.
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PMID:SOS Chromotest study concerning some appreciation criteria of humic substances' genotoxic potency. 252 69

The mutagenicity of products formed by chlorination after ozonation of naphthoresorcinol in aqueous solution was assayed with Salmonella typhimurium strains TA98 and TA100 in the presence and absence of S9 mix from phenobarbital- and 5,6-benzoflavone-induced rat liver. Ozonated and subsequently chlorinated naphthoresorcinol was directly mutagenic, as was ozonated naphthoresorcinol, in both strains tested. The mutagenic activity at chlorination with 8 equivalents of chlorine per mole of naphthoresorcinol after ozonation was markedly higher than that at only ozonation. Of the identified ozonation products of naphthoresorcinol, muconic acid, after chlorination with 2 or 4 equivalents of chlorine per mole of the compound, induced direct mutagenicity against TA98 and TA100. The chlorination of glyoxal with 0.5 and 1 chlorine equivalents per mole of the compound was shown to produce direct mutagenicity toward TA98. The identification of the chlorination products of these compounds is also discussed.
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PMID:Mutagenicity on chlorination of products formed by ozonation of naphthoresorcinol in water. 266 98

Survival data are presented for a fecal strain of Escherichia coli exposed to three concentrations of chlorine dioxide at four temperatures. Chick's first-order reaction equation is generalized to a pseudo nth-order model. Nonlinear least squares curve-fitting of the survival data to the nth order model was performed on an analogue computer. The data were observed to follow fractional order kinetics with respect to survival concentration, with an apparent activation energy of 12,000 cal/mole. Initial experiments support the thesis that the mechanism of chlorine dioxide kill occurs via disruption of protein synthesis.
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PMID:Kinetics and mechanism of bacterial disinfection by chlorine dioxide. 533 39

The anti-tumour drug cisplatin is a potent nephrotoxic agent. Renal Na+/K+-activated and Mg2+-activated ATPases are shown to be equally sensitive to cisplatin inhibition in vitro. An aged solution of cisplatin, containing hydrolysis products, is a thousand times more inhibitory to ATPase (ID50 8.0 X 10(-7) M) than freshly made cisplatin solutions (ID50 6.5 X 10(-4) M). Chloride ion concentrations of 0-150 mM in the assay mixtures do not affect either the extent of inhibition of ATPase by cisplatin or the time required for inhibition to develop. We conclude that cisplatin reacts directly with ATPase rather than that a hydrolysis product is responsible for the inhibition. Various amino acid complexes with cisplatin were tested for their ability to inhibit ATPase. Cysteine/cisplatin in a mole ratio of 1 : 1 is completely ineffective. Mono-substituted methionine/cisplatin is more inhibitory than cisplatin alone but di-substituted methionine/cisplatin is less effective. The reason for these observations and their significance to nephrotoxicity are discussed.
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PMID:The inhibition of renal ATPase by cisplatin and some biotransformation products. 612 88

A major concern of the chlorination of aquatic humic materials is the ubiquitous production of trihalomethanes. A large number of other chlorinated organic compounds, however, have been shown to be formed by chlorine's reaction with humic substances. In this study, humic material was concentrated from a coastal North Carolina lake and chlorinated at a chlorine to carbon mole ratio of 1.5 at pH 12. A high pH was necessary for complete dissolution of the humic material and for production of adequate quantities of oxidation and chlorination products for extraction, separation and mass spectrometric identification. After concentration in ether, samples were methylated, separated with a 50-m OV-17 glass capillary column or a 25 m SP-2100 fused-silica column and identified. A Hewlett-Packard 5710A gas chromatograph interfaced to a VG Micromass 7070F double-focusing mass spectrometer was used. Low resolution, accurate mass measurements were made with a combined EI-Cl source. The ability to do low resolution, accurate mass measurements made possible a rapid scan function necessary for capillary column gas chromatography. Accurate mass measurements allowed increased confidence in the identification of compounds, most of which are not available as standards. The products identified in these studies were chlorinated aliphatic straight-chain acids dominated by di- and trichloroacetic acid and the chlorinated dicarboxylic acids: succinic, fumaric and maleic acids. Chlorinated and unchlorinated aliphatic mono- and dicarboxylic acids and unchlorinated polycarboxylic aromatic acids comprise the remaining bulk of the compounds identified.
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PMID:Reaction products of aquatic humic substances with chlorine. 621 70

Aqueous chlorination of humic acids results in the formation of compounds with direct-acting mutagenic activity in the Ames/Salmonella plate assay for tester strains TA98, TA100, TA1535, TA1537 and TA1538. The addition of a rat-liver microsomal fraction (S9) plus cofactors causes a substantial decrease of activity, the extent of which is tester strain dependent. The non-chlorinated humic acids are not mutagenic either in the presence or absence of S9. Formation of mutagenic activity and of total organic halogen (TOX) is linearly related to humic concentration in the range of 0.2-1.6 mg/ml total organic carbon (TOC), and to chlorine concentration in the range of 0.1-1.0 chlorine equivalents per mole of carbon. The mutagenic activity is due predominantly to non-volatile compounds. Mutagenic activity is also detectable, after sample concentration by lyophilization, upon chlorination at a humic acid level of 0.02 mg/ml TOC. The specific mutagenic activities (per mg TOX), and also the degree of chlorine incorporation into humic acid, at 0.02 mg/ml TOC are similar to those present after chlorination at 1 mg/ml TOC. Production of mutagens is greatly dependent on the chlorination pH, with a pattern of decreasing mutagenic activity with increasing pH. This order of activity can be at least partially explained by the alkali liability of the compounds. Chlorination of commercial humic acids is proposed as a model for examination of mutagen formation during water chlorination.
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PMID:Formation of mutagens following chlorination of humic acid. A model for mutagen formation during drinking water treatment. 622 25


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