Histamine phosphate

Histamine acid phosphate, 659 Histamine dihydrochloride, 659 Histamine diphosphate, 659 Histamine hydrochloride, 659 Histamine phosphate, 659 Histantil, 932 Histapyrrodine, 660 Histapyrrodine hydrochloride, 660 Histaspan, 457 Histergan, 557 Histex, 433 Histryl, 560 Histylamine, 1022 HMMA, 322 HoggarN, 576... 

Dog A, female, 13 kg, gastric fistula and esophagotomy, operated March 1945. Sections A and B represent an experiment of November 22, 1948, and section C an experiment of January 4, 1949. In the latter 2 mg atropine sulfate were injected 42 minutes before the injection of histamine phosphate. Rate of secretion and concentration of total acid and pepsin are shown by line graphs in order to more completely characterize the samples. The spontaneous mucus specimens represent 30-minute samples. UA = uronic acid HN = total hexosamine HN = excess hexosamine mmoles/liter. From Grossberg et al. (G70). 

NB Cited by AI-Badr AA and El-Subba HI, Histamine Phosphate, APDS, 27,168 (2000). 

Note The pre- and post-treatment of the chromatograms with the basic tri-ethylamine solution, which can be replaced by an alcoholic solution of sodium hydroxide [1,4] or a phosphate buffer solution pH = 8.0 (c = 0.2 mol/1) [5], serves to stabilize the fluorescence of the amino derivatives [2]. A final spraying with methanolic hydrochloric acid (chci = 5 mol/1) or 70% perchloric acid renders the detection reaction highly specific for histamine [4] and for catecholamines and indolamines [5]. 

Most GPCRs interact with and activate more than one G-protein subfamily, e.g., with Gs plus Gq/n (histamine H2, parathyroid hormone and calcitonin recqrtors), Gs plus G (luteinising hormone receptor, 32-adrenoceptor) or Gq/11 plus G12/13 (thromboxane A2, angiotensin ATb endothelin ETA receptors). Some receptors show even broader G-protein coupling, e.g., to Gi, Gq/n plus Gi n ( protease-activated receptors, lysophosphatidate and sphingosine-1-phosphate receptors) or even to all four G-protein subfamilies (thyrotropin receptor). This multiple coupling results in multiple signaling via different pathways and in a concerted reaction of the cell to the stimulus. 

Opioids. Reactions to morphine, codeine phosphate, meperidine, fentanyl and its derivatives are uncommon. Because of their direct histamine-releasing properties, especially regarding morphine and codeine, distinction between anaphylaxis and non-immune-mediated histamine release is not always easy. Only 12 cases were recorded in the last 2 years epidemiologic survey in France, 9 of them being related to morphine administration [9]. 

Histamine is synthesised by decarboxylation of histidine, its amino-acid precursor, by the specific enzyme histidine decarboxylase, which like glutaminic acid decarboxylase requires pyridoxal phosphate as co-factor. Histidine is a poor substrate for the L-amino-acid decarboxylase responsible for DA and NA synthesis. The synthesis of histamine in the brain can be increased by the administration of histidine, so its decarboxylase is presumably not saturated normally, but it can be inhibited by a fluoromethylhistidine. No high-affinity neuronal uptake has been demonstrated for histamine although after initial metabolism by histamine A-methyl transferase to 3-methylhistamine, it is deaminated by intraneuronal MAOb to 3-methylimidazole acetic acid (Fig. 13.4). A Ca +-dependent KCl-induced release of histamine has been demonstrated by microdialysis in the rat hypothalamus (Russell et al. 1990) but its overflow in some areas, such as the striatum, is neither increased by KCl nor reduced by tetradotoxin and probably comes from mast cells. 

Theory The gravimetric assay of histamine acid phosphate is based upon the formation of insoluble histamine-nitranilic acid complex as depicted in the following equation ... 

Histamine is synthesized by decarboxylation of histidine by L-histidine decarboxylase (HDC), which is dependent on the cofactor pyridoxal-5 -phosphate [21]. Mast cells and basophils are the major source of granule-stored histamine, where it is closely associated with the anionic proteoglycans and chondroitin-4-sulfate. Histamine is released when these cells degranulate in response to various immunologic and non-immunologic stimuli. In addition, several myeloid and lymphoid cell types (DCs and T cells), which do not... 

Lo WW, Fan TP Histamine stimulates inositol phosphate accumulation via the H] receptor in cultured human endothelial cells. Biochem Biophys Res Commun 1987 148 47-53. 

Most people have heard of antihistamines, even if they have little concept of the nature of histamine. Histamine is the decarboxylation product from histidine, and is formed from the amino acid by the action of the enzyme histidine decarboxylase. The mechanism of this pyridoxal phosphate-dependent reaction will be studied in more detail later (see Section 15.7). 

This enzyme [EC 4.1.1.22] catalyzes the conversion of histidine to histamine and carbon dioxide. The enzyme requires either pyridoxal phosphate or pyruvate as a cofactor. 

While the evidence implicating histamine as the causative agent of scombroid poisoning is compelling, Japanese investigators at one time isolated a histamine like substance called saurine that was possibly involved in scombroid poisoning (15). Saurine has since been identified as the phosphate salt of histamine (16). 

The principal pathways for the biogenesis and metabolism of histamine are well known. Histamine is formed by decarboxylation of the amino acid, L-histidine, a reaction catalyzed by the enzyme, histidine decarboxylase. This decarboxylase is found in both mammalian and non-mammalian species. The mammalian enzyme requires pyridoxal phosphate as a cofactor. The bacterial enzyme has a different pH optimum and utilizes pyruvate as a cofactor (26.27). 

Non-pyridoxal Phosphate Dependent. Figure 2 depicts the postulated mechanism for a non-pyridoxal phosphate catal) zed decarboxylation of histidine to histamine involving a pyruvoyl residue instead of pyridoxal -5 - phosphate (20). Histidine decarboxylases from Lactobacillus 30a and a Micrococcus sp. have been shown to contain a covalently bound pyruvoyl residue on the active site. The pyruvoyl group is covalently bound to the amino group of a phenylalanine residue on the enzyme, and is derived from a serine residue (21) of an inactive proenzyme (22). The pyruvoyl residue acts in a manner similar to pyridoxal phosphate in the decarboxylation reaction. 

Histamine formation at 4°C was studied with resting cell suspensions of several histidine decarboxylating bacteria (Table III). Cells were harvested from cultures grown at 38°C in Trypticase soy broth (BBL, Cockeysville, MD.), suspended in 0.2 M phosphate buffer (pH 6.0) containing 0.1% histidine, and incubated anaerobically at 4°C for 21 days. After incubation, the cells were removed by filtration, and histamine was measured in the supernatant liquid. 

Among the compounds commonly determined in research laboratories are diacetyl, 2,3-butandiol, glycerol, citramalic acid, amino acids (especially proline), histamine, ammonia, succinic acid, phosphate, ash, alkalinity of the ash, ethyl, acetate, methyl anthranilate, total volatile esters, higher alcohols (both total and individually) phenolic compounds, etc. An elegant method for determining ethyl esters, capronate, caprylate, caprinate, and laurate using carbon disulfide extraction and GLC has been published (123). 

Sanderson G, Scholfield CN (1986) Effects of adenosine uptake blockers and adenosine on evoked potentials of guinea-pig olfactory cortex. Pflugers Arch 406(l) 25-30 Sattin A, Rail TW (1970) The effect of adenosine and adenine nucleotides on the cyclic adenosine 3, 5 -phosphate content of guinea pig cerebral cortex slices. Mol Pharmacol 6(1) 13-23 Sawynok J, Zarrindast MR, Reid AR, Doak GJ (1997) Adenosine A3 receptor activation produces nociceptive behaviour and edema by release of histamine and 5-hydroxytryptamine. Eur J Pharmacol 333(1) 1-7... 

---