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Histidine metabolites

Despite our understanding of the biochemistry of niacin, we still cannot account for the characteristic photosensitive dermatitis in terms of the known metabolic lesions. There is no apparent relationship between reduced availability of tryptophan and niacin, and sensitivity of the skin to ultraviolet (UV) light. The only biochemical abnormalities that have been reported in the skin of pellagrins involve increased catabolism of the amino acid histidine leading to a reduction in the concentration of urocanic acid, a histidine metabolite that is the major UV-absorbing compound in normal dermis (see Figure 10.6). [Pg.222]

D17. Davis, R, E., and Leake, E., Histidine metabolite excretion and serum folate levels. [Pg.284]

Histidinemia is an autosomal recessive disorder that is benign in most affected individuals. The incidence from newborn screening is 1 10000, making histidinemia one of the most frequent of the inborn errors of metabolism. The enzyme defect is histidase, an enzyme normally expressed only in skin and liver. The block in conversion of histidine to urocanic acid results in an increased concentration of histidine in blood and urine and the abnormal presence of histidine metabolites in urine. [Pg.155]

Figlu, formiminoglutamic acid IpyA, imidazolepyruvic acid UroA, urocanic acid. L-histidine monohydrochloride is dissolved in water and given orally after an overnight fast. 350 mg of urocanic acid in a 1 mM solution of NaOH at pH 7.0 was injected slowly i.v. after an overnight fast. The plasma and urine samples should be frozen immediately after collection in order to prevent the decomposition of histidine metabolites. [Pg.160]

Imidazole natural products, especially those derived bio-synthetically from histidine, make up a small portion of the alkaloids found in nature. The majority of these alkaloids are thought to be produced from two histidine metabolites (1) histamine (11), which results from histidine decarboxylase-catalyzed decarboxylation [14], and (2) urocanic acid (12),... [Pg.474]

Histamine is a critical mediator in anaphylactic reactions. It is a diamine produced by decarboxylation of the amino acid histidine in the Golgi apparatus of mast cells and basophils. Once secreted, it is rapidly metabolized by histamine methyltransferase [2]. Plasma histamine levels are elevated in anaphylaxis, reaching a concentration peak at 5 min and declining to baseline by 30-60 min [3]. Therefore, histamine samples for assessing an anaphylactic reaction should be obtained within 15 min of the onset of the reaction. Urinary metabolites of histamine may be found for up to 24 h. [Pg.126]

In contrast to the lability of certain dN adducts formed by the BHT metabolite above, amino acid and protein adducts formed by this metabolite were relatively stable.28,29 The thiol of cysteine reacted most rapidly in accord with its nucleophilic strength and was followed in reactivity by the a-amine common to all amino acids. This type of amine even reacted preferentially over the e-amine of lysine.28 In proteins, however, the e-amine of lysine and thiol of cysteine dominate reaction since the vast majority of a-amino groups are involved in peptide bonds. Other nucleophilic side chains such as the carboxylate of aspartate and glutamate and the imidazole of histidine may react as well, but their adducts are likely to be too labile to detect as suggested by the relative stability of QMs and the leaving group ability of the carboxylate and imidazole groups (see Section 9.2.3). [Pg.303]

The Ames test involves the reversion from a his— to his+ phenotype in any one of multiple bacterial strains (usually five strains are tested simultaneously). If the addition of test compound to a his— strain of bacteria allows them to grow on histidine deficient media, the obvious conclusion is compound-induced mutagenesis and a high potential hazard for the compound being carcinogenic. This test can also be conducted in the presence or absence of metabolic activation, in order to provide more information on potential risks (i.e., the parent compound may not be mutagenic, but the primary metabolite may present a safety risk). In practice, a positive Ames test almost always leads to discontinuing work on a compound of interest, and so these data are always collected prior to nomination of a compound for development. [Pg.165]

The outstanding inclusion ability and the carboxylic functions of host I raised the idea of co-erystallizing it with imidazole (Im) which, due to its versatile nature 114), is one of the frequently used components in enzyme active sites, generally presented by histidine. Formally, a system made of imidazole and an acid component may mimic two essential components of the so-called catalytic triad of the serine protease family of enzymes the acid function of Aspl02 and the imidazole nucleus of His57 115) (trypsin sequence numbering). The third (albeit essential) component of the triad corresponding to the alcohol function of Seri 95 was not considered in this attempt. This family of enzymes is of prime importance in metabolitic processes. [Pg.128]

Figure 6.1 Histamine synthesis and metabolism in neurons. L-histidine is transported into neurons by the L-amino acid transporter. Once inside the neuron, L-histidine is converted into histamine by the specific enzyme histidine decarboxylase. Subsequently, histamine is taken up into vesicles by the vesicular monoamine transporter and stored there until released. In the absence of a high-affinity uptake mechanism in the brain, released histamine is rapidly degraded by histamine methyltransferase, which is located postsynaptically and in glia, to telemethylhistamine, a metabolite that does not show any histamine-like activity. Figure 6.1 Histamine synthesis and metabolism in neurons. L-histidine is transported into neurons by the L-amino acid transporter. Once inside the neuron, L-histidine is converted into histamine by the specific enzyme histidine decarboxylase. Subsequently, histamine is taken up into vesicles by the vesicular monoamine transporter and stored there until released. In the absence of a high-affinity uptake mechanism in the brain, released histamine is rapidly degraded by histamine methyltransferase, which is located postsynaptically and in glia, to telemethylhistamine, a metabolite that does not show any histamine-like activity.
We have been interested in analysis of mutagens in urine, (19-21) as have other groups. (22,23) The analysis of the mutagenicity of urine is complicated by several technical problems. Urinary metabolites are usually present in low concentrations and relatively little urine can be added directly to the Salmonella test system because urinary histidine interferes in the test. In addition, urine contains a variety of conju-... [Pg.8]

Histamine occurs in the brain, particularly in certain hypothalamic neurons, and evidence is strong that histamine is a neurotransmitter. Distribution of histamine, its synthetic enzyme (histidine decarboxylase), and methyl histamine (the major brain metabolite) is not uniform. Possible roles for histamine in the regulation of food and water intake, thermoregulation, hormone release, and sleep have been suggested. Additional information on histamine can be found in Chapter 38. [Pg.285]

Histamine is formed by decarboxylation of the amino acid l -histidine, a reaction catalyzed in mammalian tissues by the enzyme histidine decarboxylase. Once formed, histamine is either stored or rapidly inactivated. Very little histamine is excreted unchanged. The major metabolic pathways involve conversion to /V-methylhistamine, methylimidazoleacetic acid, and imidazoleacetic acid (IAA). Certain neoplasms (systemic mastocytosis, urticaria pigmentosa, gastric carcinoid, and occasionally myelogenous leukemia) are associated with increased numbers of mast cells or basophils and with increased excretion of histamine and its metabolites. [Pg.347]

Nevertheless, malonyl-CoA is a major metabolite. It is an intermediate in fatty acid synthesis (see Fig. 17-12) and is formed in the peroxisomal P oxidation of odd chain-length dicarboxylic acids.703 Excess malonyl-CoA is decarboxylated in peroxisomes, and lack of the decarboxylase enzyme in mammals causes the lethal malonic aciduria.703 Some propionyl-CoA may also be metabolized by this pathway. The modified P oxidation sequence indicated on the left side of Fig. 17-3 is used in green plants and in many microorganisms. 3-Hydroxypropionyl-CoA is hydrolyzed to free P-hydroxypropionate, which is then oxidized to malonic semialdehyde and converted to acetyl-CoA by reactions that have not been completely described. Another possible pathway of propionate metabolism is the direct conversion to pyruvate via a oxidation into lactate, a mechanism that may be employed by some bacteria. Another route to lactate is through addition of water to acrylyl-CoA, the product of step a of Fig. 17-3. Tire water molecule adds in the "wrong way," the OH ion going to the a carbon instead of the P (Eq. 17-8). An enzyme with an active site similar to that of histidine ammonia-lyase (Eq. 14-48) could... [Pg.947]

A large number of a, 3-didehydro-a-amino acids have been identified as constituents of relatively low molecular weight cyclic compounds from microbial sources. However, the presence of a,p-didehydroalanine in bacterial as well as in mammalian histidine ammonia lyase and in phenylalanine ammonia lyase shows that the occurrence of a,p-didehydro-a-amino acids is not limited to small molecules alone 8 These residues are incorporated in natural sequences by posttranslation modification. a,p-Didehydro-a-amino acids have also been postulated to be precursors in the biosynthesis of several heterocyclic metabolites including penicillin and cephalosporin 9 Other well-known compounds containing ,( -di-dehydro-a-amino acids are nisin 10,11 (a food preservative112 ), subtilin (a broad spectrum antibiotic) 13 and some of the metabolites isolated from Streptomyces strains such as gri-seoviridin 14 ... [Pg.636]

A Papua New Guinea sponge, Pseudoceratina sp., contains the unusual alkaloids ceratamines A (1142) and B (1143), and a biogenesis involving histidine and tyrosine is proposed (1173). The fermentation broth from Aspergillus fischeri var. thermomutatus has yielded CJ-12662 (1144) and UK-88051 (1145) (1174). The former metabolite was confirmed by X-ray spectroscopy and partial synthesis. A marine-derived Streptomyces sp. produces the novel pyrrolizidine 5-chlorobohem-amine C (1146), which was shown not to be an isolation artifact (1175). The Chinese medicinal plant Huperzia serrata has furnished 2-chlorohyperzine E (1147) (1176). [Pg.175]

Roquefortine.—Histidine (121) is a part precursor for roquefortine (119) (cf. Vol. 10, p. 25). Its incorporation involves desaturation with loss of the proton at C-2 and one of the protons at C-3. Experimental results with (2S,3S)- and (25,3jR)-[3-3H]histidine [as (121)] show that, in the biosynthesis of both roquefortine (119) and oxaline (120), the 3-pro-S proton is lost stereo-specifically.43 Dehydrogenation to generate these double-bonds of (E) configuration thus proceeds in a syn sense. Desaturation with the same syn stereochemistry has been observed in the biosynthesis of other diketopiperazine metabolites, e.g. mycelianamide and cryptoechinulin A, which both have (Z) double-bonds (cf. Vol. 7, p. 19 Vol. 8, p. 35). [Pg.22]

Metabolites of the ergoline type [as (128)], as well as those of type (119), have been isolated from Penicillium roqueforti. The incorporation has been observed of radioactive samples of tryptophan and mevalonate into both series of metabolites, and of histidine into those of type (119).44 Diversion from tryptophan into the two independent biosynthetic pathways is initiated on the one hand by the formation of (122) and on the other by reaction with histidine to give a diketopiperazine precursor for metabolites such as (119). Which route is followed is temperature-dependent. [Pg.22]


See other pages where Histidine metabolites is mentioned: [Pg.222]    [Pg.222]    [Pg.114]    [Pg.156]    [Pg.475]    [Pg.222]    [Pg.222]    [Pg.114]    [Pg.156]    [Pg.475]    [Pg.645]    [Pg.14]    [Pg.509]    [Pg.208]    [Pg.943]    [Pg.32]    [Pg.97]    [Pg.193]    [Pg.561]    [Pg.187]    [Pg.450]    [Pg.334]    [Pg.199]    [Pg.321]    [Pg.67]    [Pg.851]    [Pg.401]    [Pg.645]    [Pg.325]    [Pg.363]    [Pg.121]    [Pg.157]    [Pg.362]    [Pg.86]    [Pg.305]    [Pg.149]   
See also in sourсe #XX -- [ Pg.155 , Pg.156 ]

See also in sourсe #XX -- [ Pg.474 ]




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