Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Acidity, urinary

Schoeninger, M.J. and DeNiro, M.J. 1984 Nitrogen and carbon isotopic composition of bone collagen from marine and terrestrial animals. Geochimica et Cosmochimica Acta 48 625-639. Schuette, S. A., Hegsted, M., Zemel, B. and Linkswiler, H.M. 1981 Renal acid, urinary cyclic AMP, and hydroxyproline excretion as affected by level of protein, sulfur amino acids and phosphorus intake. Journal of Nutrition 111 2106-2116. [Pg.258]

Following delivery of 1,200 mg of HFC-134a by inhalation from metered-dose inhalers to four healthy adult male volunteers (16 actuations of 75 mg per inhalation each inhalation within 30 s of the previous inhalation), the only fluorinated urinary component was trifluoroacetic acid. Urinary trifluoroacetic acid accounted for less than 0.0005% of the administered dose, indicating minimal metabolism (Monte et al. 1994). [Pg.159]

B. Proteus species produce urease (A) that produces ammonia and urea, alkalizing urine. Urine requires acidification for effective therapy. Hippuric (B), mandelic, or ascorbic acids or methionine are urinary acidifying agents. The normal acidic urinary environment is disturbed by recurrent Proteus in-... [Pg.523]

On the other hand, acidic drugs tend to ionize under conditions of alkaline pH and so are unable to permeate the renal tubular epithelium and are preferentially excreted. Tire converse applies to conditions of acidic urinary pH. This has been demonstrated experimentally for many drugs weak bases are excreted more rapidly in acidic urine, whereas weak acids are excreted more rapidly in alkaline urine. In the horse, phenylbutazone, which is a weak organic acid with a pKa of 4.6, has a more delayed clearance time under conditions of aciduria than under conditions of alkaline urine. [Pg.21]

Since D-amino acids are poorly utilized, diets containing sufficient quantities of D-enanticmers will result in elevated levels of plasma and urinary amino acids. Urinary excretion of D-methionine by infants fed a formula supplemented with DD-methionine has led to misdiagnosis of inborn errors of metabolism (77). D-Amino acids derived from processed food proteins may confuse medical diagnoses. Determining D-amino acid contents of caimon foods would estimate the significance of this problem. Some preliminary results are shown in Table VI. [Pg.183]

Studies on the effect of oxalic acid in spinach on calcium balance in humans have shown a small decrease or no effect on calcium balance (12). However, when subjects were given test meals of either Swiss chard (13) or amaranth (, 1, which are rich in oxalic acid, urinary excretion of calcium indicated that the absorption of calcium from these sources was less than that of an equal amount of calcium from milk. Absorption of calcium from milk was also reduced when given along with amaranth (14). [Pg.128]

Half-life. Plasma half-life, about 10 hours under alkaline urinary pH conditions or 3 hours if an acidic urinary pH is maintained. [Pg.538]

Shih and colleagues (1994) injected rats subcutaneously with a single dose of sarin (75 ftg/kg) and measured excretion of the hydrolyzed metabolites, the alkylmethylphos-phonic acids, including IMPA and other methylphosphonic acids. Urinary elimination was found to be quite rapid and the terminal elimination half-life of sarin metabolites in urine was 3.7 h. Most of the administered dose of sarin was retrieved from the urine in metabolite form after 2 days. [Pg.800]

Since allopurinol blocks xanthine conversion to uric acid, urinary xanthine excretion is increased, creating a risk of xanthine crystal formation in the urinary system or even in muscles this can result in nephrolithiasis (12). It is still an open question whether a predisposition to renal disease or renal disease itself is required to precipitate these adverse effects. It is also not known whether increased excretion of orotic acid, due to an interaction of allopurinol with pyrimidine formation, has any consequences for these adverse effects or for its role in reducing glucose tolerance. [Pg.81]

In multiple comparisons using four indices of renal dysfunction (i.e. urinary p2-microglobulin, protein, glucose and amino acid), urinary protein and p2-mi-croglobulin in women and urinary protein in men were the most contributory factors to the mortality rates [110]. [Pg.796]

Penicillins and cephalosporins have short half-lives (0.5-1.5 h) in domestic animals because these antibiotics are secreted by the proximal renal tubules and, due to their high degree of ionization, are not reabsorbed from the distal nephron. The half-lives of lipid-soluble weak organic acids (e.g. sulphadi-methoxine, sulphadiazine, phenobarbitone) and organic bases (e.g. trimethoprim, procainamide, amphetamine) of which a significant fraction (> 20%) of the dose is eliminated by renal excretion may be influenced by the urinary pH reaction. Under acidic urinary conditions, which are normally present in carnivorous species, weak acids are reabsorbed from the distal renal tubules, whereas the excretion of weak bases is enhanced. [Pg.34]

Freedman, D. S., Brown, J. P., Weir, D. G., and Scott, J. M., The reproducibiUty and use of the tritiated folic acid urinary excretion test as a measure of folate absorption in clinical practice Effect of methotrexate on absorption of folic acid. /. Clin. Pathol. 26, 261-267 (1973). [Pg.284]

Uric acid stones account for approximately 10% of all renal calculi. Formation of uric acid stones is favored by acid urinary pH. Measures to prevent uric acid stone formation include a low-purine diet or treatment with allopurinol, which lowers levels of uric acid by inhibiting the enzyme xanthine oxidase. A high rate of urine flow, on the order of 3 liters per 24 hours, especially at night, or administration of bicarbonate to maintain urine pH alkaline facilitates dissolution of uric acid stones and prevents their recurrence after surgery. [Pg.143]

Answer E. Back to basic principles. Zero-order elimination means that plasma levels of a drug decrease linearly with time. This occurs with ASA at toxic doses, with phenytoin at high therapeutic doses, and with ethanol at all doses. Enzymes that metabolize ASA are saturated at high plasma levels —> constant rate of metabolism = zero-order kinetics. Remember that application of the Henderson-Hasselbalch principle can be important in drug overdose situations. In the case of aspirin, a weak acid, urinary alkalinization favors ionization of the drug —>4 tubular reabsorption —>T renal elimination. [Pg.261]

In the severely ill infant, measurements of serum ammonia and lactate, urinary organic acids, urinary and serum amino acids and erythrocyle galacto.se I-phosphale uridyl transferase will be required. If the baby has a problem which is apparent intermittently, then blood and urine should be collected for analysis during the acute phase. [Pg.63]

There was carried out a screening of flavonoids, phenylacrylic acids and various hydroxylated phenyl acetic acids, urinary metabolites of flavonoids, against three metallopeptidases, containing Zn as cofactor, to study their mechanism of activity in vitro [77]. [Pg.891]

New su I phonic acid urinary metabolites, thiotaurine and quinaldylglycyltaurine... [Pg.648]

A new, strongly acidic product, quinaldyl(carboxyl-14C)glycyltaurine (198), a sulphonic acid urinary metabolite, has been discovered163 and its chemical structure established by subcutaneous injections and oral administrations of quinaldic acid-carboxyl-14C to hungry cats. Hydrolysis of 198 demonstrated the presence of glycine, taurine, quinaldic acid and quinaldylglycine in the hydrolysate. [Pg.649]

Fig. 3.13. Organic acid urinary profiles of a patient with hereditary progressive deafness and a control patient both individuals were administered orally 20 g of leucine. 3-HIVA, 3-hydroxyisovaleric acid 3-MCG, 3-methyl-crotonylglycine. Reproduced from [164]. Fig. 3.13. Organic acid urinary profiles of a patient with hereditary progressive deafness and a control patient both individuals were administered orally 20 g of leucine. 3-HIVA, 3-hydroxyisovaleric acid 3-MCG, 3-methyl-crotonylglycine. Reproduced from [164].
Renal excretion of basic drugs such as amphetamine theoretically can be enhanced by acidification of the urine. Acidification can be accomplished by the administration of ammonium chloride or ascorbic acid. Urinary excretion of an acidic compound is particularly sensitive to changes in urinary pH if its is within the range of 3.0-7.5 for bases, the corresponding pH range is 7.5-10.5. [Pg.1124]

They breakdown usually to ionic mercury at the acidic urinary pH. [Pg.444]

The increased plasma kynuremne pool and the induced xanthurenic acid urinary excretion have several implications in the assessment of diazinon noncholinergic toxicity. An increase in xanthurenic acid formation may alter glucose metabolism. Xanthurenic acid has been reported to form a complex with insulin and damage pancreatic P cells. Elevated plasma kynurenin may alter kynurenin transport into the brain. Since more than 40% of brain kynurenin originates from the systemic circulation, cerebral biosynthesis of neuroactive kynurenin metabolites such as quinolinic acid and kynurenic acid may change. Finally, the availability of L-iryptophan for other L-lryptophan-dependent processes may be reduced. Tryptophan is the metabolic precursor for. serotonin and nicotinic adenine dinucleotidc. Diabetes, bladder cancer, and neurological disorders may be the toxic consequences of diazinon-altered L-tryptophan metaboli.sm (Seifert and Pewnim, 1992 Pewnim and Seifert, 1993). [Pg.707]

Steroids Biie acids Fatty acids Urinary acids Ketones Prostagiandins Oximes, TMS, t-BDMS ethers Methyl esters, TMS ethers Methyl esters, TMS, t-BDMS esters Methyl esters, TMS, t-BDMS esters Oximes Methyl esters, oximes, TMS, ethers Steroid profiles Liver disease, peroxisomal deficiencies Phospholipids, triglycerides Acidurias, diabetes Diabetes Healing processes, pain... [Pg.2911]

L-glyceric aciduria urinary excretion of oxalic acid, urinary L-glyceric acid oxalate stones D-glyceric dehydrogenase deficiency Autosomal recessive Williams, H.E., and Smith, L.H., Jr. L-glyceric aciduria a new genetic variant of primary hyperoxaluria. N. Engl. J. Med. 278, 233-239 (1968)... [Pg.232]

Flynn, T.M. and I.A. Southwell, 1979. l,3-Dimethyl-2-oxabicyclo [2,2,2]-octane-3-methanol and 1,3-dimethyl-2-oxabicyclo[2,2,2]-octane-3-carboxylic acid, urinary metabolites of 1,8-cineole. 32 ... [Pg.897]

In summary these children had features in common which made it difficult to identify the underlying enzyme abnormality and its relationship to their presentation in renal failure. Both had raised plasma uric acids not unusual in severe renal failure but in these children the magnitude was the important factor The crystals or stones causing the nephropathy could both have been identified as uric acid Urinary uric acid on a creatinine basis was not raised in either The severe renal damage at such an early age in both underlines the importance of early and correct identification of these defects, especially APRT deficiency, which can be treated successfully with allopurinol and such severe renal damage need never occur. ... [Pg.8]


See other pages where Acidity, urinary is mentioned: [Pg.20]    [Pg.68]    [Pg.234]    [Pg.545]    [Pg.3962]    [Pg.19]    [Pg.220]    [Pg.43]    [Pg.618]    [Pg.343]    [Pg.119]    [Pg.463]    [Pg.586]    [Pg.18]    [Pg.188]    [Pg.276]   
See also in sourсe #XX -- [ Pg.247 , Pg.275 ]




SEARCH



© 2024 chempedia.info