Histamine extraction

Other chemicals of possible concern for health and safety found ia yeast proteias iaclude tyramiae (0—2.25 mg/g) and histamine (0.2—2.8 mg/g), formed by decarboxylation of the corresponding amino acids (38). These compounds are also found ia other fermeated (including pickled) foods. Their preseace ia yeast extracts used as condiments coatributes very Htde to human iatake. Likewise, the nephrotoxic compouad lysiaoalaniae has beea ideatified ia alkah-treated yeast extracts, at a level of 0.12 mg/g. However, the chemical occurs at similar low coaceatratioas ia almost all heat- and alkaU-treated foods. 

Sea urchin toxins extracted from spines or pedicellariae have a variety of pharmacological actions, including electrophysiological ones (75). Dialyzable toxins from Diadema caused a dose-dependent increase in the miniature end-plate potential frequency of frog sartorius muscle without influencing membrane potential (76). A toxin from the sea urchin Toxopneustes pUeolus causes a dose-dependent release of histamine (67). Toxic proteins from the same species also cause smooth muscle contracture in guinea pig ileum and uterus, and are cardiotoxic (77). 

Studies of the histamine Hj-receptor antagonists substances were extracted from 97... 

Acid acetone extracts of human and rodent leukocytes (RBL-cells) have been found to contain immunoreactive SOM (iSOM) and immunoreactive SP (iSP) as determined by radioimmunoassay [144], Quantities of the peptides varied from 325 pg iSOM/107 cells for human monocytes and 272 pg iSOM/107 cells for RBL-cells to 4.4 pg iSOM/107 cells for human T cells. iSP was highest in murine bone marrow-derived mast cells (64 pg iSP/107 cells) and RBL-cells (23 pg iSP/107 cells) and lowest in human T and B lymphocytes (2.5 and 1.2 pg iSP/107 cells, respectively). Interestingly, the murine bone marrow-derived mast cells had the highest ratio of iSP to iSOM. Preliminary chromatographic results show a large and a small SOM (SOM-28 and SOM-14, respectively). SOM-14 (3 x 10 9 M) has been shown to inhibit histamine release and LTC4 generation from murine bone marrow-derived mast cells stimulated by anti-IgE serum [144]. 

IEC was applied to determine biogenic polyamines such as putrescine (4a), cadaverine (4b), tyramine (5), histamine (6), spermidine (38), agmatine (39) and tryptamine (40), contained in aqueous trichloroacetic extracts of leafy vegetables, such as cabbage and lettuce. A cation exchange column loaded with potassium ions and a special buffer were used. Spermidine (38) was the major amine detected in this group (7-15 Xg/g fresh weight)144. 

Other mechanisms A few other effects of hypericin, and a crude hypericum extract have been found, including affinity for NMDA, inositol triphosphate, and adenosine receptors. However, these are not likely to be significant to its therapeutic effects because concentrations required for these interactions are not likely to be achieved by oral administration (Cott 1997). Vasoactive effects are possible because hypericum extracts blocked the vasoconstricting effects of histamine and prostaglandin F2o in porcine coronary arteries, and some vasorelaxation occurs in one particular fraction. These effects are hypothesized to be mediated by inhibition of phosphodiesterase (Melzer et al. 1991). 

Finally, a thorough receptor binding study by Raffa and colleagues (1998) showed that hypericin extracts had no effect at adrenergic (alpha or beta), adenosine, angiotensin, benzodiazepine, dopamine, bradykinin, neuropeptide Y, PCP, NMDA, opioid, cholecystokinin A, histamine HI, or nicotinic ACh receptors. Although comprehensive, this study did not look at the binding of any other hypericum constituents. 

In mast cells, histamine release induced by IgE or A23187 was also inhibited by feverfew extract [48] which also reduced spasmolytic activity of smooth muscle induced by acetylcholine, 5HT, histamine, prostaglandin E2 and bradykinin [20]. 

Histamine is released from whole rabbit blood by both cotton extracts and endotoxins, however, the ability of AECD to release histamine is greater than would be expected from endotoxin content alone. Antweiler (63), however, was unable to show in vivo histamine release by endotoxins obtained from cotton extracts in rabbits nor could he show an acute fall in blood pressure of cats after I.V. endotoxin injection, as occurred with subsequent injections of compound 48/80 or other dust extracts. He concludes that endotoxins are not responsible for any histamine releasing activity of cotton dust. 

Boiling an acidified cotton extract does not lower its anaphylatoxin activity whereas endotoxins lose their activity by this procedure. Furthermore, it is argued that the endotoxin hypothesis is not compatible with the fact that different parts of the cotton plant contain different amoxmts of histamine liberating factor, particularly as plant parts which are more contaminated by handling, i.e. cotton hairs, have no histamine liberating activity. 

Both histamine and 5-HT have been demonstrated in extracts 5-HT is responsible for some of the bronchoconstrictor activity of cotton dust extracts. Brom-lysergic acid, a specific 5-HT inhibitor, partially reduces activity, suggesting the presence of an "unknown contractor." This does not appear to be acetylcholine or bradykinin. Thus, although histamine, 5-HT, and the "unknown contractor" can cause immediate contractor responses, delayed onset contractions may still be due to secondary release of histamine (105). 

Histamine release from pig lung occurs in response to extracts from cotton pericarp, seed, leaf, root and bract (112). Extracts of sisal release histamine from both pig and human lung, but the reactivity is less than cotton dust extracts. The use of chopped lung for histamine assay is not always reliable, however, nor is it sufficiently sensitive. 

Pig platelets have recently been shown to release histamine when exposed to cotton dust or plant extracts (115) and this assay compares closely with chopped lung assays. Mill dust and gin trash extracts give some release and extracts of leaves from other plant sources, including pecan and grape, give similar reactions. Byssinosan (116). an aminopolysaccharide isolated from cotton dust, and THF antigen (83) are relatively inactive. 

Cotton dust extracts have been shown to affect cyclic nucleotide levels (122). Guinea pig lungs, in response to AECD, show a decrease in cAMP levels with a concomitant increase in cGMP. Further, there is a high correlation (r = 0.95) between lung histamine levels and cAMP/cGMP ratios. Other workers (123) have shown stimulation of cAMP in human peripheral blood lymphocytes in response to AECD. 

Within 30 minutes of their administration, 6 -adrenergic drugs often reverse most of the functional deficit in Monday morning byssinotics. As there is no mucous secretion, airway smooth muscle contraction is considered the primary response. Exposure of man to histamine aerosols produces pulmonary function changes similar to those seen after exposure to dust extract. However, exposure to histamine aerosol invariably initiates constriction of smooth muscle more rapidly than exposure to cotton dust ( <15 minutes), and dissipates within minutes, while the acute effects of inhalation of cotton dust and dust extracts lasts for hours. The slowly developing and prolonged effects of dust and extracts suggest that mediators other than histamine are involved. 

Small airway constriction and recruitment of leukocytes on pulmonary surfaces are prominent, documented responses to the inhalation of cotton dust. Currently, one or both of these effects are generally ascribed to endotoxin (8-10), to antigen-antibody reactions (11), to lacinilene C-7 methyl ether (1, 13), to a low molecular weight ( 1000 daltons), neutral, highly water soluble substance that is stable in boiling water and found in cotton bracts (14), to chemotaxins present in cotton mill dust extracts (15, 16) or to histamine releasing substances (17). 

Histamine Releasing Agents in Extracts of Cotton Mill Dust and Cotton Bract... 

The platelet hist UIline release assay demonstrated that cotton mill dust extract, cotton bract extract, cotton leaf extract, dialyzed CMD extract, polyphenols, compound 48/80, rutin, trimethylamine HCl, quercetin, catechin, tannic acid, ellagic acid and sodium metasilicate all release histamine directly (48). Thus not only do tannin compounds induce histamine release, but they may also form higher molecular weight polymers and contain components that survive acid hydrolytic conditions (48). Tannins are widely distributed in the plant kingdom. 

Cotton dust and cotton bract extract contracted smooth muscle with forces equivalent to a 0.32jj0.05 jug/ml concentration of 5HT and 0.7+0.1 ug/ml concentration of 5-HT, respectively ( ). However, cotton bract extracts were blocked by methysergide, a 5-HT antagonist, while cotton dust extracts were not. Diphenhydramine, a histamine antagonist, failed to significantly affect either of the extracts ( ). 

Antweller ( ) in 1961 injected Salmonella abortus equl and E. coll endotoxins Intraperltoneally into rats and looked for mast cells in the mesentery and the histamine content of the abdominal fluid. Negative results were obtained with amounts of the endotoxins (up to 10 yg) thought to be similar to that in cotton dust although large doses of endotoxin were known to cause rapid histamine release in cats and dogs. He concluded that endotoxins did not produce histamine release or the biological effect of cotton dust extracts. 

In 1961 Pernls et al. (34) showed that histamine or histamine-like substances are liberated by endotoxins and by saline extracts of cardroom waste cotton by the guinea pig ileum method (a much more sensitive method than that used by Antweller). 

Histamine Liberation. Histamine liberation is not caused by fungal extracts, fungal cultures. Bacillus cultures, or their extracts, but is caused by cotton dust extracts and by known endotoxins when a sensitive method is used. 

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