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Excretion pattern, urinary

Urinary excretion patterns of thiocyanate suggest that there are quantitative species differences in acrylonitrile metabolism (Ahmed and Patel 1981). Thiocyanate was identified as a metabolite in rats, mice, rabbits and Chinese hamsters. About 20 to 23% of the administered dose was excreted as thiocyanate in rats, rabbits and Chinese hamsters, while 35% was excreted as thiocyanate in mice (Gut et al. 1975). It has also been observed that mice metabolize acrylonitrile more rapidly than rats (Ahmed and Patel 1981 Gut et al. 1975). Maximum blood cyanide concentrations were observed 1 hour after dosing in mice, but 3 hours after dosing in rats (Ahmed and Patel 1981). In mice, thiocyanate was present in the urine within 4 hours of dosing, while in rats, thiocyanate was present in urine only at time intervals longer than 4 hours (Gut et al. 1975). [Pg.54]

The table below shows the urinary excretion patterns of electrolytes of diuretic drugs. For each of the diuretic agents listed below, choose the urinary excretion pattern that the drug would produce. [Pg.212]

The answers are 373-d, 374-c, 375-a. (Kut ung, pp 253— 254, 256-257.) The urinary excretion pattern of electrolytes for the thiazide diuretic agents (e.g., hydrochlorothiazide) shown in the table that accompanies the question is represented by choice a. These drugs block the reabsorption of Na and Cl at the early distal convoluted tubule of the nephron. In addition, they promote the excretion of K and Mg. At high doses, the thiazide diuretics (especially hydrochlorothiazide) may cause a... [Pg.220]

Most conclusive evidence of the biochemical individuality of every human specimennot restricted to those who exhibit marked idiosyncrasieshas been obtained by the recent studies of urinary excretion patterns using paper chromatography and other methods.2,3,4 Typical results from one study2 illustrating how various items in the patterns vary from individual to individual are shown in Figure 13. [Pg.134]

Urinary excretion patterns of six individuals. Gu = glucose C = creatine ... [Pg.136]

The twin variance studies cited above5,6 indicate that dietary differences are not primarily responsible for the differences in the urinary excretion patterns. Additional evidence is of several sorts. Two experiments,8,9 each involving placing individuals on uniform diets, have... [Pg.136]

These findings show clearly that even when the animal diets are uniform, highly distinctive urinary excretion patterns are exhibited. The results with different inbred strains show that inheritance is the basic reason for the differences in pattern. It would require extremely extensive genetic studies to demonstrate the inheritance process for each item, but this does not seem crucially important from the standpoint of elucidating the phenomenon of individuality. [Pg.137]

Molecular genetic characterization and urinary excretion pattern of metabolites in two families with MCAD deficiency due to compound heterozygosity with a 13 base pair insertion in one allele. [Pg.15]

Time of Administration The presence or absence of food in the gastrointestinal tract, corticosteroid secretion rhythm, circadian cycle, urinary excretion pattern, fluid intake, and drug-metabolizing enzyme rhythms all can influence the effect of the medication. [Pg.29]

About half of the absorbed biotin is excreted as the metabolites bisnorbiotin, occurring from fl-oxidation of the valeric acid side chain, and biotin sulfoxide, occurring from the oxidation of the sulfur in the heterocyclic ring. The circulating plasma and urinary excretion patterns show a ratio of 3 2 1 for biotin, bisnorbiotin, and biotin sulfoxide. Minor metabolites are bisnorbiotin methyl ketone and biotin sulfone. Careful balance studies in humans, where perhaps only 1 mg is the total body content, showed that urinary excretion of biotin often exceeded dietary intake, and that in aU cases, fecal excretion was as much as three to six times greater than dietary intake because of microfloral biosynthesis. [Pg.1108]

Chiandetti L, ZaccheHo F. Acute metabolic decompensation in methylmalonic acidosis time sequence in the urinary excretion pattern of precursor organic acids and their major metabolites. Perspect Inherit Metab Dis 1987 7 57-70. [Pg.2246]

BlO. Berry, H. K., Variations in urinary excretion patterns in a Texas population. Amer. J. Phys. Anihropol. 11, 559-575 (1953). [Pg.200]

The urinary excretion pattern of the 11-oxy-17-OS during the first few days bears more resemblance to that found in adults (Table 10), but again paper chromatography shows other compounds with similar polarity to be present (C6). The rate of excretion of a major unknown substance is given in Table 10, and it will be seen that the urinary content of this and of the known compounds rapidly decline over the first few days. The results shown were determined by scanning paper chromatograms stained with Zimmermann reagent. Identification of the named steroids was not complete and consisted of a comparison of 1 / values in various solvent systems before and after acetylation of the compounds. [Pg.175]

The urinary excretion of glycosaminoglycans by juvenile cases of vitamin A deficiency and of protein-calorie malnutrition (kwashiorkor) is less than normal (M41). The predominant differences are the absence of hyaluronic acid and the presence of chondroitin sulfate of low sulfate content (C12). Treatment of the cases with vitamin A deficiency restored the glycosaminoglycan spectrum to normal. Decreased urinary glycosaminoglycan levels have also been noted in primary hepatoma (K6). It has been suggested that the urinary excretion pattern of individual glycosaminoglycans is pathognomic of certain hereditary bone diseases (T3). [Pg.56]

T3. Teller, W. M., Urinary excretion patterns of individual acid mucopolysaccharides. Nature (London) 213, 1132-1133 (1967). [Pg.99]

Figure 1. Urinary excretion pattern for a one-time exposure to 2,4-D. Figure 1. Urinary excretion pattern for a one-time exposure to 2,4-D.
Based on the recent study and the suggestions that the pubertydelaying activity is lost after exposure of urine to air at room temperature (Coppola and Vandenbergh, 1985) and that the puberty-inhibition affect may be associated with the adrenal function (Drickamer and McIntosh, 1980), we decided to study quantitative chemical differences between the urinary excretion patterns of intact and adrenalectomized grouped females. The urinary volatile substances were subsequently identified and tested for biological activity. The samples were analyzed using the headspace technique described previously by our laboratory (Novotny et al., 1974). [Pg.79]

A few disorders have been identified causing secondary disturbances in LT elimination and degradation, e.g. defective hepatobiliary elimination of cysteinyl leukotrienes as seen in the Dubin-Johnson syndrome [3], impaired co-oxidation of LTB4 in the Sjogren-Larsson syndrome [4] or altered jff-oxidation in disorders of peroxisome biogenesis such as the Zellweger syndrome [5]. The metabolic changes seen in these disorders are characterised by altered urinary excretion patterns of leukotrienes. However, in these conditions LT synthesis itself is not affected. [Pg.659]

It should be kept in mind that toxemia data can be used for comparison with data on atherosclerosis only in those cases where kidney disturbances are not serious enough to alter the original pathological relations in the blood and the urinary excretion pattern. This means that data on severe cases of pre-eclampsia and eclampsia often cannot be used. But as termi-... [Pg.266]

Results from a biobank of samples from German university students show that the daily intake of both DEHP and DnBP, as estimated from urinary excretion patterns of metabolites, decreased substantially over 15 years, with the median DnBP intake falling to less than one-third of 1988 levels by 2003. Over the same period, there was some evidence of increasing exposure to the replacement phthalates DiNP (a DEHP replacement) and DiBP (a DnBP replacement) (Wittassek et al. 2007). It also was noted that the annual median intake of DEHP for German students, estimated from urine samples from this biobank, had an extremely close correlation (r = 0.97) with yearly German industrial DEHP production data over the same period (Helm 2007). [Pg.41]


See other pages where Excretion pattern, urinary is mentioned: [Pg.137]    [Pg.253]    [Pg.156]    [Pg.115]    [Pg.176]    [Pg.1108]    [Pg.238]    [Pg.268]    [Pg.43]    [Pg.42]    [Pg.206]    [Pg.182]   
See also in sourсe #XX -- [ Pg.170 , Pg.171 ]




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