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A Canary's Eye View — Metabolic Basis
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Histamine

Mechanisms and effects

  • Produced from the granules of mast cells (part of connective tissue) and basophils; also from platelets. Stored in mast cells [also the others?]. Produced by decarboxylation of histidine (see diagram).
  • Agents :
    • physical: trauma, cold
    • immuniologic (via IgE receptors)
    • C3a and C5a (anaphylatoxins)
    • interleukin-1
    • histamine-releasing factors from
      1. PMN's
      2. monocytes
      3. platelets: contact with collagen, thrombin, AFP and Ag-Ab.
      4. PAF
  • A result of allergic hypersensitivity or inflammation.
  • Histamine causes...
    • vasodilation
    • increased permeability of venules only
    • expansion of capillaries (probably by constricting the smaller veins that lead from them)
    • resulting local edema
    • increase in the volume of the vascular bed (net vasodilation)
    • lowered blood pressure.
    • chemotaxis for eosinophils

Inactivation:

  • Histaminase.
    • [Where? How produced?]
    • How induce histaminase? Can you supplement it?
  • Circulating histamine is inactivated in the liver via methylation and oxidation reactions.
    • Methylation: by enzyme histamine N-methyltransferase (HMT or HNMT) — catalyzes the N<tau>-methylation of histamine
    • Oxidation: by enzyme diamine oxidase (DAO)
    • Yamauchi et al: say inactivationis principally by (HMT) (DAO). Am J Physiol 1994 Sep;267(3 Pt 1):L342-9
  • Gordon (see below) says basically, methylation followed by oxidation. [?? Oxidation is a phase I process; how can that follow methylation, a phase II process?]
  • Michael A. Kaliner, M.D says
    • 4 to 8% of histamine by-products in urine: Histamine metabolized to N-methylhistamine by N-methyltransferase
    • 42 to 47% metabolized by monamine oxidase to N-methylimidazole acetic acid
    • 9 to 11% metabolized by diamine oxidase to imidazole acetic acid
    • 16 to 23% metabolized as a conjugate with ribose to form imidazole acetic acid riboside
    • < 3% is excreted unchanged into urine.
    • This information from Clinical Use of (H1) Antihistamines in Elderly Patients: Considerations in a Polypharmaceutic Patient Population, at Clinical Geriatrics Magazine Online, from the University of Pennsylvania School of Medicine, Office of Continuing Medical Education. Accessed 22 September 2002. References available there (not at the bottom of the page, but before the tables).
  • [I have problems with methylation, can I supplement these other pathways?]

Antagonists

  • Standard antagonists are pharmaceutical antihistamines. Kaliner (see above) provides some information. First-generation H1 antistamines hae extensive CNS "side effects." Second-generation H1 antihistamines are mainly metabolized by cytochrome P450 (CYP)3A4, in their first hepatic pass; he doesn't say how generations 1 and 2 are cleared.
  • Several suggestion are mentioned in Time of the Season: Warm Weather Allergies and Promising Natural Solutions, by Peter Chowka and Kathi Head, N.D.

See also my pages

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copyright © 2002 by Catherine Holmes Clark. Last updated datex 2002