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Urine hydrolyzed

Urine Hydrolyzed with H2SO4 extracted with isooctane injected into GC GC/ECD (for metabolite trichloro-ethanol) 75 ppb 98.2 Pekari and Aitio 1985b... [Pg.232]

The data of Stein and Muting differ substantially in the matter of methionine quantity, which, accordingly to the latter, is the quantitatively most important conjugated amino acid of normal urine. A similar opinion was also expressed by Albanese et al. (A2) in 1944, but Wallraff et al. (Wl) reported that methionine appears only occasionally in urine hydrolyzates and in amounts never exceeding 12 mg/24 hours. [Pg.135]

Urine Hydrolyze sample with NaOH extract with methanol and diethyl ether/hexane concentrate add TEA, HFBA, and MDA extract derivative with... [Pg.103]

SuperchlorinationShock Treatment. Superchlorination or shock treatment of pool water is necessary since accumulation of organic matter, nitrogen compounds, and algae consumes free available chlorine and impedes disinfection. Reaction of chlorine with constituents of urine or perspiration (primarily NH" 4, amino acids, creatinine, uric acid, etc) produces chloramines (N—Cl compounds) which are poor disinfectants because they do not hydrolyze significantly to HOCl (19). For example, monochloramine (NH2CI) is only 1/280 as effective as HOCl against E. coli (20). [Pg.298]

Opioids are easily absorbed subcutaneously and intramuscularly, as well as from the gastrointestinal tract, nasal mucosa (e.g., when heroin is used as snuff), and lung (e.g., when opium is smoked). About 90% of the excretion of morphine occurs during the first 24 hours, but traces are detectable in urine for more than 48 hours. Heroin (diacetyhnorphine) is hydrolyzed to monoacetylmorphine, which is then hydrolyzed to morphine. Morphine and monoacetylmorphine are responsible for the pharmacologic effects of heroin. Heroin produces effects more rapidly than morphine because it is more lipid soluble and therefore crosses the blood-brain barrier faster. In the urine, heroin is detected as free morphine and morphine glucuronide (Gutstein and Akil 2001 Jaffe et al. 2004). [Pg.63]

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. [Pg.95]

Urine Acidify and heat to hydrolyze add NaOH extract with anhydrous ethyl ether derivatize with diazoethane concentrate add hexane concentrate and cleanup on silica gel elute with benzene-hexane (PNP) GC/ECD 20 pg/L (20 ppb) 85-98 Shafiketal. 1973b... [Pg.176]

A recent method, still in development, for determining total 4-nitrophenol in the urine of persons exposed to methyl parathion is based on solid phase microextraction (SPME) and GC/MS previously, the method has been used in the analysis of food and environmental samples (Guidotti et al. 1999). The method uses a solid phase microextraction fiber, is inserted into the urine sample that has been hydrolyzed with HCl at 50° C prior to mixing with distilled water and NaCl and then stirred (1,000 rpm). The fiber is left in the liquid for 30 minutes until a partitioning equilibrium is achieved, and then placed into the GC injector port to desorb. The method shows promise for use in determining exposures at low doses, as it is very sensitive. There is a need for additional development of this method, as the measurement of acetylcholinesterase, the enzyme inhibited by exposure to organophosphates such as methyl parathion, is not an effective indicator of low-dose exposures. [Pg.177]

The metabolism of NMOR in the rat is outlined in Figure 4. o-Hydroxylation yields the unstable intermediates and the latter hydrolyzes to (2-hydroxyethoxy)acetaldehyde [7] which has been identified as a liver microsomal metabolite by isolation of the corresponding 2,4-dinitrophenylhydrazone (59). (2-Hydroxy-ethoxy)acetaldehyde, which exists predominantly as the cyclic hemiacetal was not detected in the urine of rats gavaged with 125 mg/kg NMOR. However, (2-hydroxyethoxy)acetic acid was a major urinary metabolite (16% of the dose). These transformations are analogous to those observed with NPYR and NNN. [Pg.68]

N-Hydroxy arylamines readily form glucuronide conjugates, but in contrast to the N-hydroxy arylamides, these are N-glucuronides which are unreactive and stable at neutral pH. The N-glucuronides are readily transported to the lumens of the urinary bladder and intestine where they can be hydrolyzed to the free N-hydroxy arylamines by mildly acidic urine or by intestinal bacterial 3-glucuronidases (13,14). Non-enzymatic activation of N-hydroxy arylamines can occur in an acidic environment by protonation (15,16) of the N-hydroxy group (VIII) as well as by air oxidation (reviewed in 17) to a nitrosoarene (IX). [Pg.346]

Carbofuran in animals may also be hydrolyzed to produce carbofuran-7-phenol. Hydrolysis of the 3-hydroxyderivative leads to formation of 3-hydrocarbofuran-7-phenol. Other degradation products include /V-hydroxymethyl carbofuran and, as in plants, 3-hydroxy- and 3-ketoderivatives. All of these compounds may become conjugated and excreted by animals in urine and, presumably, bile (Metcalf et al. 1968 Finlayson et al. 1979). At least 10 metabolites of carbofuran are known at present their interrelations are shown in detail by Menzie (1978). [Pg.807]

The CES family of proteins is characterized by the ability to hydrolyze a wide variety of aromatic and aliphatic substrates containing ester, thioester, and amide bonds (Heymann 1980, 1982). Cauxin is a member of the CES family, and is secreted from the proximal straight tubular cells into the urine in a species-, sex-, and age-dependent manner. Therefore, we postulated that cauxin was involved in an enzymatic reaction in cat urine and the products made by the reaction should vary with species, sex, and age. Based on this hypothesis, we searched for physiological substrates and products of cauxin in cat urine and identified 2-amino-7-hydroxy-5,5-dimethyl-4-thiaheptanoic acid, also known as felinine. [Pg.55]

MBCG is hydrolyzed to felinine and glycine by cauxin in the renal tubules and the bladder and/or ex vivo. The felinine produced in this manner is excreted into the urine. [Pg.57]

Almost at the same time Abderhalden (Al) showed the peptide character of the undialyzable part of urine. By means of the Fischer analysis method he isolated from the hydrolyzate of this mixture certain free amino acids, and for the first time introduced the name polypeptide for the analyzed constituent of urine. [Pg.127]

A similar ion-exchange resin method was used by Ling in 1955 (LI) for the examination of combined amino acids in urine. According to this procedure urine was desalted and simultaneously freed from amino acids by using Amberlite IR-112, H+-form resin. The effluent collected from the column was then fractionated on Amberlite IRA, OH--form resin, by successive elution with 0.16 N acetic acid, 0.08 N formic acid, 0.25 N formic acid, 0.08 N hydrochloric acid, and finally with 0.16 N formic acid. The solutions of all acids contained 10% of acetone. The collected fractions were hydrolyzed with hydrochloric acid and the liberated amino acids identified by means of paper chromatography. [Pg.130]

Amino Acid Content of Acid Hydrolyzates of Normal Urine ... [Pg.133]

As early as 1905 Abderhalden (Al) isolated from the hydrolyzate of the nondiffusible fraction of human urine four amino acids, i.e., leucine, alanine, glycine, and glutamic acid, and detected two others phenylalanine and aspartic acid. Some amino acids derived from this fraction have been quantitatively determined by Albanese et al. (A3) who found in the amount of the nondiffusible fraction corresponding to one liter of urine as much as 32.8 mg tryptophan, 18.0 mg phenylalanine, 16.2 mg methionine, 15.2 mg cystine, 13.1 mg arginine, 6.7 mg histidine, and 3.9 mg tyrosine. [Pg.135]

Further studies in humans indicate that a large proportion of the 2,5-hexanedione detected in urine after M-hexane exposure is the result of an artifact resulting from treatment with acid to hydrolyze urinary conjugates (Fedtke and Bolt 1987). When urine from a male volunteer exposed to 217 ppm -hexanc for 4 hours was hydrolyzed enzymatically with -glucuronidase, excretion of 4,5-dihydroxy-2-hexanone was approximately 4 times higher than that of 2,5-hexanedione. When the urine was hydrolyzed with acid,... [Pg.100]

Hexanedione is usually measured as total 2,5-hexanedione, a free form accounting for about 10% of the total and 4,5-dihydroxy-2-hexanone, which is converted to 2,5-hexanedione upon acid treatment (acidification of urine samples is routinely performed in order to hydrolyze conjugates that can interfere with analysis). 2,5-Hexanedione has also been detected after acid treatment of urine from individuals not occupationally exposed to w-hcxane (Fedtke and Bolt 1986a Perbellini et al. 1993). A reference value for 2,5-hexanedione in acid-treated urine in a non-occupationally exposed Italian population (n=123,... [Pg.151]

The diet treatments were level of phytate intake, either 0.2 or 2.0 g/day. Each level was consumed for 15 days, three consecutive repeats of the 5-day menu cycle. To provide 2.0 g/day of phytic acid, 36 g of wheat bran was baked into 6 muffins and two muffins were eaten each meal. Dephytinized bran was prepared by incubating the bran in water and allowing the endogenous phytase to hydrolyze the phytate, then the entire incubation mixture was freeze-dried (4) and 36 g baked into 6 muffins. Thus, the intake of all nutrients and neutral detergent fiber was the same for both phytate intakes. Five subjects consumed the whole bran muffins for 15 days followed by the dephytinized bran muffins for 15 days and the other 5 subjects in the reverse order. Brilliant blue dye was given at breakfast on the first day of each collection period to aid in demarcation of stools. Stool composites were made for days 1-5, 6-15, 16-20 and 21-30 and urine composites for days 6-15, and 21-30. Daily food composites were made, homogenized, freeze-dried and then analyzed to determine mineral nutrient intakes. [Pg.66]

The presence of hexamethylenediamine (4c) in hydrolyzed human urine is indicative of exposure to hexamethylene diisocyanate. The diamine was determined after derivatization with heptafluorobutyric anhydride followed by GC-CI-MS, using ammonia as the ionizing reagent and deuterated hexamethylenediamine as internal standard LOD 0.5 j.ig/L urine97. [Pg.1063]

Compound 87 in acid-hydrolyzed urine serves as a tracer for occupational exposure to the corresponding diisocyanate. It was derivatized with pentafluoropropionic anhydride and determined by LC using TSP-MS and plasmaspray (PSP) MS (discharge-assisted TSP-MS). The [M — 2](—) ion was measured instrumental LOD 0.1 pg/pL LOD about 0.2 -ig/L urine, RSD 10% for 0.5 pg/L230. Another determination of 87 in urine is with isobutyl chloroformate231. [Pg.1081]


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See also in sourсe #XX -- [ Pg.93 , Pg.94 ]




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