Excretion urinary

Relatively Httie is known about the bioavailabiUty of pantothenic acid in human beings, and only approximately 50% of pantothenic acid present in the diet is actually absorbed (10). Liver, adrenal glands, kidneys, brain, and testes contain high concentrations of pantothenic acid. In healthy adults, the total amount of pantothenic acid present in whole blood is estimated to be 1 mg/L. A significant (2—7 mg/d) difference is observed among different age-group individuals with respect to pantothenic acid intake and urinary excretion, indicating differences in the rate of metaboHsm of pantothenic acid. 

Thiamine requirements vary and, with a lack of significant storage capabiHty, a constant intake is needed or deficiency can occur relatively quickly. Human recommended daily allowances (RDAs) in the United States ate based on calorie intake at the level of 0.50 mg/4184 kj (1000 kcal) for healthy individuals (Table 2). As Httle as 0.15—0.20 mg/4184 kJ will prevent deficiency signs but 0.35—0.40 mg/4184 kJ are requited to maintain near normal urinary excretion levels and associated enzyme activities. Pregnant and lactating women requite higher levels of supplementation. Other countries have set different recommended levels (1,37,38). 

Human exposure to environmental contaminants has been investigated through the analysis of adipose tissue, breast milk, blood and the monitoring of faecal and urinary excretion levels. However, while levels of persistent contaminants in human milk, for example, are extensively monitored, very little is known about foetal exposure to xenobiotics because the concentrations of persistent compounds in blood and trans-placental transmission are less well studied. Also, more information is needed in general about the behaviour of endocrine disruptive compounds (and their metabolites) in vivo, for example the way they bind to blood plasma proteins. 

The pharmacokinetics of azacitidine shows that it is rapidly absorbed after s.c. administration with the peak plasma concentration occurring after 0.5 h. The bioavailability of s.c. azacitidine relative to i.v. azacitidine is approximately 89%. Urinary excretion is the primary route of elimination of azacitidine and its metabolites. The mean elimination half-lives are about 4 h, regardless of i.v. or s.c. administration. 

Diuretics promote the urinary excretion of sodium and water by inhibiting the absorption of filtered fluid across the renal tubular epithelium. The ensuing reduction in Na reabsorption reduces the Na content of the body, the critical determinant of extracellular and plasma fluid volumes. Thus, the use of diuretics is primarily indicated in the treatment of edematous diseases and of arterial hypertension. 

As a general rule, increases of renal blood flow and/ or glomerular filtration rate (GFR) correlate rather well with increased urinary excretion of solutes and water. The underlying causes for this correlation are not fully understood, but they reflect incomplete adjustments of tubular reabsorption to an increase of tubular electrolyte load. 

The co-administration of drugs which inhibit the transporters involved in biliary excretion can reduce the biliary excretion of drugs which are substrates of the transporter, leading to elevated plasma concentrations of the drugs. For example, biliary and urinary excretion of digoxin, both mediated by P-gp, are inhibited by quinidine which is an inhibitor of P-gp. 

Bames, D.W.H., Bishop, M., Harrison, G.E. and Sutton, A. 1961 Comparison of the plasma concentration and urinary excretion of strontium and calcium in man. InternationalJournal of Radiation Biology 3 637-646. 

Nitrophenol and 4-nitrophenol glucuronide are excreted in urine. The studies of urinary excretion of methyl parathion metabolites, including those reported in this section, generally hydrolyze the glucuronide prior to analysis and report the resulting total 4-nitrophenol values. 

Urinary excretion of metabolites of methyl parathion is rapid and efiicient in animals (Braeckman et al. 1983 Hollingworth et al. 1967). In mice, 70-80% of the activity was excreted in the urine within... 

Morgan DP, Hetzler HL, Slach EF, et al. 1977. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Arch Environ Contam Toxicol 6 159-173. 

The earliest reports of controlled release steroids were those of Jackanicz (63), Yolles (64), Anderson (65), and Wise (66). Most of those early studies were based on poly[ (L+)-lactic acid). Implants and granular particles were fabricated with progesterone, norgestrel, and norethisterone. In vivo urinary excretion studies were conducted on [I Cjprogesterone beads (64). The reported results were somewhat questionable as only 20% of the original implanted drug could be accounted for. 

Creatinine is formed in muscle from creatine phosphate by irreversible, nonenzymatic dehydration and loss of phosphate (Figure 31-6). The 24-hour urinary excretion of creatinine is proportionate to muscle mass. Glycine, arginine, and methionine all participate in creatine biosynthesis. Synthesis of creatine is completed by methylation of guanidoacetate by S-adenosylmethio-nine (Figure 31-6). 

The study of the mechanism of urinary excretion of amylase and the amylase clearance has been the subject of many studies in recent years. Levitt et. al (79) studied the renal clearance of amylase in renal insufficiency, acute pancreatitis and macro-amylasemia. In acute pancreatitis, the kidney cleared amylase at a markedly increased rate. The ratio of the amylase clearance rate to the creatinine clearance rate (Cgm/Ccr) averaged 3 times normal early in the course of acute pancreatitis, and this elevation could persist after the serum amylase returned to normal. Comparison of an lase clearance to creatinine clearance was to minimize irrelevant changes due to variation in renal function. The increased clearance of amylase makes the urinary amylase a more sensitive indicator of pancreatitis. 

Table VI lists several drugs Inducing hepatic microsomal enzymes (5). These enzymes can metabolize the drug as well as other substrates. Barbiturates, grlseofulvln, and glutethlmlde Induce enzymes which metabolize coumarln and phenlndlone derivatives and thus reduce their anticoagulant activity. Dlphenylhydantoln and phenylbutazone stimulate cortisol hydroxylase activity and Increase the urinary excretion of B-hydroxy cortisol and decrease the concentration of cortisol In the plasma.

Various minor hematological effects have been noted in animals. Rats exposed to 50-800 ppm of trichloroethylene continuously for 48 or 240 hours showed time- and dose-related depression of delta-aminolevulinate dehydratase activity in liver, bone marrow, and erythrocytes (Fujita et al. 1984 Koizumi et al. 1984). Related effects included increased delta-aminolevulinic acid (ALA) synthetase activity, reduced heme saturation of tryptophan pyrrolase and reduced cytochrome P-450 levels in the liver and increased urinary excretion of... 

The primary urinary metabolites of trichloroethylene in humans are trichloroethanol, trichloroethanol glucuronide, and TCA (Monster et al. 1979 Nomiyama and Nomiyama 1971 Sato et al. 1977). The halftime for renal elimination of trichloroethanol and trichloroethanol glucuronide has been determined in several studies to be approximately 10 hours following trichloroethylene exposure (Monster et al. 1979 Sato et al. 1977). The urinary excretion of TCA is much slower, and data from several studies indicate that the halftime of urinary TCA is approximately 52 hours because the metabolite is very tightly and extensively bound to plasma proteins (Monster et al. 1976 Sato et al. 1977). 

Sex differences in the urinary excretion of metabolites of trichloroethylene have been reported (Inoue et al. 1989 Nomiyama and Nomiyama 1971). In trichloroethylene-exposed workers, urinary levels of trichloro compounds and trichloroethanol were significantly higher in men than in women, while urinary levels of TCA did not differ between the two sexes (Inoue et al. 1989). However, it was reported that excretion of TCA in urine was greater in women than in men within 24 hours of exposure (Nomiyama and Nomiyama 1971). 

This model accurately predicted the time curves for blood concentration and urinary excretion of metabolites by male volunteers exposed to 100 ppm trichloroethylene (Sato et al. 1991). It was found that, while the amount of metabolite excretion increases with body weight, the concentration does not, because of a corresponding increase in urinary volume. Also, women and obese people, compared with slim men, have lower concentrations but longer residence times of blood trichloroethylene because of their higher fat content (Sato et al. 1991). As a consequence, the model predicted that 16 hours after exposure to trichloroethylene, one could expect a woman s blood level to be 30% higher and an obese man s level to be twofold higher than that of a slim man (Sato 1993). 

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