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PubMed1979

Chlorine dioxide metabolism in rat.

Chlorine dioxide (ClO2) is under consideration as an alternative to chlorination as a disinfectant for public water supplies. A new assay was developed to qualitatively and quantitatively measure the metabolites of 36ClO2 in water and biological fluids. Studies in the rat indicated that the metabolites of ClO2 were Cl-, ClO-2, and ClO-b. At maximum absorption the percentage of ClO; formed in plasma from an initial oral dose of 10 mg/l 36ClO, was higher than from a 100 mg/l dose. The 36Cl concentration in washed packed cells indicated that 36Cl readily exchanges with chloride of saline.

Animals↗
PubMed1979

Kinetics of Cl02 and effects of Cl02, Cl02-, and Cl03- in drinking water on blood glutathione and hemolysis in rat and chicken.

Since chlorination of drinking water produces organochlorinated substances (some possibly carcinogenic), the use of chlorine dioxide disinfectant would avoid halogenation. There is scarcely any data published on the effects of ClO2 in drinking water on human or animal health. The kinetics of 36ClO2 was studied in rats. Radioactivity was rapidly absorbed from the gastrointestinal tract following the administration of (0.07 microCi) 36ClO2 orally. 36Cl in plasma reached at peak at 1 hr. The half life for the elimination of 36Cl from the rat was 44 hr, corresponding to a rate constant of 0.016 hr-1. After 72 hr radioactivity was highest in plasma, followed by kidney, lung, stomach, duodenum, ileum, liver, spleen, thymus, and bone marrow. 36Cl excretion was greatest at 24 and 48 hrs after the administration of 36 ClO2. Forty-three percent of the total initial dose was excreted at 72 hr in the urine and feces. No 36 Cl was detected in expired air throughout the 72 hr studied. ClO2, ClO2-, and ClO3- (1, 10, 100, 1000 ppm) given daily in drinking water decreased blood glutathione, decreased osmotic fragility, and changed the morphology of erythrocytes in both chicken and rat after two months. Methemoglobin was not detected throughout these studies.

Animals↗
PubMed1977

[Absorption and retention of ampicillin in calves and sheep].

Ampicillin-sodium and ampicillin-trihydrate were used in the experiments as an active substance at the rate of 800 IU/mg. Ampicillin-sodium was applied in the form of 5 per cent solution, and ampicillin-trihydrate--in the form of a 5 per cent water suspension prepared extempore prior to their administration. Both forms of ampicillin were used once, muscularly, at rates of 0.01 and 0.025 g/kg body weight with calves and sheep. The results of these comparative studies showed that the levels of the serum concentrations of ampicillin and the time of their deposition in both species of animals correlated with the dose, the chemical composition, and the species of animal. The period of retaining the antibiotic in the blood varied in calves and in sheep. Parallel to these studies the excretion of ampicillin from the body was also followed up--in the ewes' milk at muscular administration, rated 0.025 g/kg body weight. It was found that ampicillin-sodium and ampicillin-trihydrate quickly penetrate in the udder, and are observed in the milk at the 30th minute (0.25 microgram--0.38 microgram/cm3).

Ampicillin↗
PubMed1995

IGFBP-3 and IGFBP-5 association with endothelial cells: role of C-terminal heparin binding domain.

IGFBP-3 and IGFBP-5, but not the other 4 IGF binding proteins, specifically bound to endothelial cell (EC) monolayers. Charged compounds, such as heparin and heparan sulfate, competed for this binding. Of the 6 IGFBPs, IGFBP-3 and IGFBP-5 had the greatest heparin affinity. Peptides of 18 amino acids were synthesized, corresponding to a common basic region of IGFBP-3 (P3), IGFBP-5 and IGFBP-6 (P6) which contained a heparin binding sequence. P3 and P6 inhibited IGFBP-3 and -5 binding to endothelial cell monolayers and the peptides bound directly to EC extracellular matrix. This suggested that the C-terminal basic segment of IGFBP-3/-5 is important for the association of the binding protein with the EC monolayer.

Amino Acid Sequence↗
PubMedDate not supplied

Acute toxic nephropathies: clinical pathologic correlations.

Man's ever increasing exposure to numerous drugs and chemicals, which are the results of medical and industrial progress, produces a by-product of acute toxic nephropathies. These include acute toxic renal failure, drug-induced acute oliguric renal failure, acute hemorrhagic glomerulonephritis, nephrotic syndrome, tubular disturbances and potassium deficiency. In depth information is provided for the previously mentioned disorders.

Acute Kidney Injury↗
PubMed1994

Specific heparan sulfate saccharides mediate the activity of basic fibroblast growth factor.

In a previous study, we showed that heparitinase releases a 14-saccharide sequence (Oligo-H) from heparan sulfate (HS) with the structure delta GlcUA beta 1,4GlcNSO3-alpha 1,4[IdceA(2S)alpha 1,4GlcNSO3]5 alpha 1,4IdceA alpha 1,4GlcNAc (where IdceA(2S) represents iduronic acid 2-sulfate), which binds to basic fibroblast growth factor (bFGF) with high affinity (Turnbull, J. E., Fernig, D., Ke, Y., Wilkinson, M. C. & Gallagher, J. T. (1992) J. Biol. Chem. 267, 10337-10341). This paper describes further work on the binding properties of HS saccharides and their capacity to mediate bFGF activity in a mitogenesis assay in which responsiveness is dependent on the addition of HS or heparin. Saccharides prepared by heparinase or nitrous acid digestion and heparitinase-resistant fragments five disaccharide units (degree of polymerization (dp) = 10) or less in size were unable to activate bFGF. However, heparitinase-resistant saccharides of dp12-16 were active in the assay; the dp14 and dp16 fractions were equivalent in activity to heparin and more active than the parent HS. Saccharides of the same size and basic structure as the active fractions (> or = dp12) bound to bFGF with high relative affinity. Active saccharides were composed mainly of N-sulfated disaccharides, the predominant unit being IdceA(2S)-GlcNSO3. This was enriched at least 5-fold in the active saccharides by comparison with the original HS. In addition, the dp12 and dp14 active fractions had a notably low content of trisulfated disaccharides (IdceA(2S)-GlcNSO3(6S)) (where GlcNSO3(6S) represents N-sulfated glucosamine 6-sulfate), which are the major repeat units of heparin. The data show that sequences similar in size and basic structure to Oligo-H can mediate the mitogenic activity of bFGF. Overall, the results provide further evidence that specific HS sequences are generated biosynthetically in order to fulfill particular biological functions such as activation of bFGF.

3T3 Cells↗
PubMed1996

Ammonium persulfate: a safe alternative oxidizing reagent for measuring urinary iodine.

The chloric acid method is most commonly used to obtain accurate and reproducible measurements of iodine and remove interfering substances. Unfortunately chloric acid is a potential hazard, requiring an explosion-proof hood, among other precautions. We have developed a simple, convenient, and economic method for measuring urinary iodine by using 1 mol/L ammonium persulfate, a nonexplosive, nonhazardous chemical, as the oxidizing reagent. The oxidation procedure can be completed in 30 min at a temperature of 91-95 degrees C. The iodine in the urine is then measured by a modification of the traditional colorimetric method of Sandell and Kolthoff. Urine samples (110) collected from a mixed population of healthy males and females, ranging in age from 6 to 79 years and living in the US, were analyzed for urine iodine content by two methods: the proposed ammonium persulfate method and the chloric acid method. The ammonium persulfate method has an intraassay CV of 9.1% at 0.42 +/- 0.04 micromol/L (mean +/- SD), 7.8% at 1.46 +/- 0.11 micromol/L, and 4.0% at 3.54 +/- 0.14 micromol/L. The interassay CV is 10.2% at 0.46 +/- 0.05 micromol/L, and 7.9% at 3.27 +/- 0.26 micromol/L. Recovery of iodine added to urine in vitro was 107%, 94%, and 97% for 0.42 micromol/L, 0.77 micromol/L and 3.64 micromol/L, respectively. The lower limit of detectability was 0.0034 microgram of iodine. Values for iodine in 110 urines measured by the reference chloric acid method ranged from 0.06 to 8.03 micromol/L and by the ammonium persulfate method from 0.05 to 7.4 micromol/L. The persulfate method (y) correlated extremely closely with the reference chloric acid method (x) by the Pearson correlation (y = 0.923x + 0.810 micromol/L, and r = 0.994, Sy/x = 1.841).

Ammonium Sulfate↗
PubMedDate not supplied

[Experience in the determination of iodine in the urine by the kinetic cerium arsenite method].

The authors describe the kinetic cerium arsenite method for measuring iodine in the urine using reagents made in Russia. The urine is prepared for analysis by wet calcination with a mixture of chlorous and perchloric acids. The method of synthesizing chlorous acid, preparing reagents, collecting urine, and procedure of analysis are described. The method was used for assessing iodine excretion with the urine in schoolchildren of Novosibirsk and Kemerovo.

Adolescent↗