Big Chemical Encyclopedia

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

Articles Figures Tables About

Urinary excretion products

In recent experiments on the metabolism of NDPA, NHPPA and NOPPA in vivo in rats (20) we have shown that the major urinary excretion product in each case is the 3-glucuronide of NHPPA (Table II). [Pg.45]

The principal metabolite of phenytoin is 5-(p-hydroxyphenyl)-5-phenylhydantoin (parahydroxy phenytoin) which, as the glucuronate, forms over 70% (65-81%) of the urinary excretion products. Free phenytoin accounts for less than 5% of the total (G9). Little phenytoin is excreted in the feces although free and hydroxylated phenytoin are excreted into the saliva and bile (N5). [Pg.72]

The nucleoside formed from hypoxanthine and ribose is known as inosine (Ino or I) and the corresponding nucleotide as inosinic acid. Further substitution at C-2 of -H by -OH and tautomerization yields xanthine (Xan). Its nucleoside is xanthosine (Xao, X). A similar hydroxylation at C-7 converts xanthine to uric acid, an important human urinary excretion product derived from nucleic acid bases. [Pg.203]

A female-specific 15(3 hydroxylase acts on steroid sulfates such as corticosterone sulfate and forms the major urinary excretion product of that hormone in female rats.292 These sex-specific differences in enzymes are thought to be related to secretions of growth hormone that are in turn controlled by the "programming" of the hypothalamus by androgen during the neonatal period in rats272 or during human fetal development. [Pg.1260]

Glycine can be reduced to acetate and ammonia by the selenium-dependent clostridial glycine reductase system (Eq. 15-61). A variety of additional products can be formed from glycine as is indicated in Fig. 24-20. Hippuiic acid (Box 10-A), the usual urinary excretion product in the "detoxication" of benzoic acid, is formed via benzoyl-CoA (Eq. 24-43) ... [Pg.1399]

Returning to the major tryptophan catabolic pathway, marked by green arrows in Fig. 25-11, formate is removed hydrolytically (step c) from the product of tryptophan dioxygenase action to form kynurenine, a compound that is acted upon by a number of enzymes. Kynureninase (Eq. 14-35) cleaves the compound to anthranilate and alanine (step d), while transamination leads to the cyclic kynurenic acid (step e). Hie latter is dehydroxylated in an unusual reaction to quinaldic acid, a prominent urinary excretion product. [Pg.1444]

Fig. 10. Pentazocine metabolic pathways and urinary excretion products in man and monkey. Fig. 10. Pentazocine metabolic pathways and urinary excretion products in man and monkey.
The N7-guanine adduct (22) is a urinary excretion product derived from the reaction of sulfur mustard with DNA. It can be isolated from urine by SPE on C18. GC/MS analysis of the derivatized adduct was problematic. A sensitive method was developed for the underivatized compound using LC/ESI/MS/MS, monitoring the fragmentation MH+, m/z 256 —> [CH2CH2SCH2CH2OH]+, m/z 105 on a triple-sector quadrupole instrument (60). LC separation was on a C18 column eluted with water-acetonitrile-formic acid. The detection limit was 8pg injected (S/N 5 1), 0.2 ng/ml in urine. Rao et al. (61) also reported characterization by LC/ESI/MS but using 25 mM NH4HC03 in 20 % MeOH as eluent. [Pg.308]

Analytical methods have been reported for unchanged agent and six of the urinary excretion products described above. These are TDG, TDGO, the bis A-acetylcysteine conjugate (1), two 3-lyase metabolites (2) and (3), and the guanine adduct (6). These methods have been applied to animal and/or human exposures to sulfur mustard. [Pg.409]

Disposition in the Body. Parathion is activated in the liver by metabolism to paraoxon. Parathion and paraoxon are further metabolised to diethylthiophosphoric acid (DETP), diethyl-phosphoric acid (DEP), and 4-nitrophenol which are the major urinary excretion products although DETP and DEP are unstable in stored urine. Urinary 4-nitrophenol concentrations may be indicative of the extent of exposure to parathion. 4-Nitrophenol is rapidly excreted in the urine and is not detectable 48 hours after exposure by inhalation or ingestion, but excretion is more prolonged after exposure of intact skin due to the much slower absorption of parathion by this route. Aminoparathion has been detected in postmortem blood and tissues. [Pg.854]

Mammals, including humans, detoxify inorganic arsenic by methylation, yielding cacodylic acid (dimethylarsinic acid) as the chief urinary excretion product. Disposition by urinary excretion is usually prompt. Elimination of the arsonic acid (monomethyl) compounds has not been extensively studied, but urinary excretion of the unaltered compound and/or a further methylated form would seem likely. [Pg.164]

The principal nitrogenous urinary excretion product in humans resulting from the catabolism of AMP is... [Pg.266]

Vanillylmandehc Acid (VMAj is a major catecholamine metabolite formed by the actions of catechol-0-methyl-transferase and MAO. It is excreted by the kidney and represents an average of 40% to 50% of the urinary excretion production of norepinephrine and epinephrine. Norepinephrine is the major source of VMA, with metabolism through MHPG as the major pathway. VA4A is not significantly conjugated and therefore is measured without a hydrolysis step. VMA was first isolated and identified in the urine of a patient with a pheochromocytoma, and its analysis is commonly performed to detect the presence of pheochromocytomas and neuroblastomas. [Pg.1061]

The conversion of tyrosine to 3,4-dihydroxyphenylalanine occurs both in vivo in man (590) and in vitro by the action of tissue tyrosinase (205, 688). Mammals can decarboxylate both tyrosine (402,407) and dihydroxyphenyl-alanine (406), tyrosine decarboxylase and dihydroxyphenylalanine (dopa) decarboxylases being quite distinct and separable (405), though both are dependent on pyridoxal phosphate (73, 758, and review 72). In mammals dihydroxyphenylalanine is the most readily decarboxylated of all amino acids, and it is therefore not unreasonable to assume that this is the substrate normally decarboxylated in adrenaline biosynthesis cf. 74, 75). Support for this concept derives from the fact that both the substrate and the product of the reaction (3,4-dihydroxyphenylethylamine diagram 11) can or do occur in the adrenal (298, 299, 802), and the amine is moreover, like adrenaline and noradrenaline, a normal urinary excretion product (245, 404). [Pg.66]

HemminkiK. 1984. Urinary excretion products of formaldehyde in the rat. Chem Biol Interact 48 243-248. [Pg.397]

Hippuric acid (Box 10-A), fhe usual urinary excretion product in the "detoxication" of benzoic acid, is formed via benzoyl-CoA (Eq. 24-43) ... [Pg.486]

Urinary excretion products, either free or conjugated... [Pg.877]

X Uric acid contains two rings and is similar to the purines adenine and V y guanine (adenine is shown in Fig. 5.25). In fact, it is the urinary excretion product formed from the oxidation of these two purine bases. It is not very soluble in water, particularly if the pH is near the pK of its acidic OH group. If present in excess amounts, Na+ urate tends to precipitate in joints, causing the severe pain of gout experienced by Ms. Topaigne. [Pg.68]

A rate-limiting enzyme catalyzes the first step in the conversion of a toxic metabolite to a urinary excretion product. Which of the following mechanisms for regulating this enzyme would provide the most protection to the body ... [Pg.156]

Fatty acids are a major fuel in the body. After eating, we store excess fatty acids and carbohydrates that are not oxidized as fat (triacylglycerols) in adipose tissue. Between meals, these fatty acids are released and circulate in blood bound to albumin. In muscle, liver, and other tissues, fatty acids are oxidized to acetyl CoA in the pathway of 3-oxidation. NADH and FAD(2H) generated from 3-oxidation are reoxidized by O2 in the electron transport chain, thereby generating ATP (see Fig. 2). Small amounts of certain fatty acids are oxidized through other pathways that convert them to either oxidizable fuels or urinary excretion products (e.g., peroxisomal P-oxidation). [Pg.338]

Fig. 39.19. Degradation of tryptophan. One of the ring carbons produces formate. The nonring portion forms alanine. Kynurenine is an intermediate, which can be converted to a number of urinary excretion products (e.g., xanthurenate), degraded to CO2 and acetyl CoA, or converted to the nicotinamide moiety of NAD and NADP, which also can be formed from the vitamin niacin. Fig. 39.19. Degradation of tryptophan. One of the ring carbons produces formate. The nonring portion forms alanine. Kynurenine is an intermediate, which can be converted to a number of urinary excretion products (e.g., xanthurenate), degraded to CO2 and acetyl CoA, or converted to the nicotinamide moiety of NAD and NADP, which also can be formed from the vitamin niacin.
A second catabolic reaction of L-threonine (Eq. 24-37, step b) is cleavage to glycine and acetaldehyde. The reaction is catalyzed by serine hydroxymethyl-transferase (Eq. 14-30). Some bacteria have a very active D-threonine aldolase. A quantitatively more important route of catabolism in most organisms is dehydrogenation (Eq. 24-37, step to form 2-amino-3-oxobutyrate. This intermediate can be cleaved by another PLP-dependent enzyme to acetyl-CoA plus glycine (Eq. 24-38, step d). It can also be decarboxylat-ed (Eq. 24-38, step e) to aminoacetone, a urinary excretion product, or oxidized by amine oxidases to methylglyoxal (Eq. 24-37, The latter can... [Pg.457]

Albumin binding of TXA2 has been noticed earlier (25), but in that study the opposite effect of albumin was studied, viz. a non-covalent binding which exerted a protective effect on the labile TXA (Fig. 2). In neither case are the further fates of the thromboxane derivatives known, such as the major, final urinary excretion products. Such knowledge would probably solve the assay problems in the thromboxane field. [Pg.5]

One of the major urinary excretion products of cortisol. It is one of the compounds of the 17-oxogenic steroid and 17-hydroxy-corticosteroid group. [Pg.339]

The course of progesterone metabolism formulated in Fig. 17 is quite well substantiated by the observations made following administration of 21-carbon steroids. When nonisotopic progesterone was fed or given intramuscularly to man, pregnane-3o ,20a-diol (LXXXIV) was the major urinary excretion product, although only 10% to 20% of the hormone given was obtained in the form of this metabolite very small amounts of... [Pg.403]


See other pages where Urinary excretion products is mentioned: [Pg.1391]    [Pg.408]    [Pg.414]    [Pg.94]    [Pg.534]    [Pg.643]    [Pg.1039]    [Pg.1345]    [Pg.107]    [Pg.16]    [Pg.353]    [Pg.478]    [Pg.418]    [Pg.426]    [Pg.453]    [Pg.774]    [Pg.381]    [Pg.389]   
See also in sourсe #XX -- [ Pg.292 ]




SEARCH



Testosterone urinary excretion products

Urinary excretion

© 2024 chempedia.info