TY - JOUR
T1 - Localization of histaminase (diamine oxidase) in rat small intestinal mucosa
T2 - Site of release by heparin
AU - Shakir, K. M.Mohamed
AU - Margolis, Simeon
AU - Baylin, Stephen B.
N1 - Funding Information:
Acknowlrdgemenrs-The authors thank Miss Kathleen Wieman for her excellent technical assistance. Dr. Shakir is supported by National Institutes of Health Fellowship No. AM 07109-02 and Dr. Baylin is recipient of Research Career Development Award No. l-K04-CA-000-27-01. The studies were supported by Grant No. 74-05 from the Maryland Chapter of the American Cancer Society, No. l-ROl-18404-01 from the National Cancer Institute, and Grant No. HL 1593@04 from the National Institutes of Health.
PY - 1977/12/15
Y1 - 1977/12/15
N2 - Previous studies have suggested that in the rat, small intestine is the source for rise in plasma histaminase levels seen after heparin administration. The cellular location of histaminase in intestine and the mechanism of heparin release have not been previously investigated. The present study identifies intestinal villus cells rather than crypt cells as the location of intestinal histaminase; at this site, the enzyme is not associated with brush border. Heparin added to incubations containing isolated intestinal cells did not release histaminase into the medium. Perfusion of intestinal vasculature with heparin caused a prompt release of this enzyme into venous effluent. The present investigation. therefore, suggests that heparin releases histaminase from vascular binding sites rather than directly from parenchymal cells. The use of isolated intestine with perfusion of the vasculature could serve as a useful tool for further defining the relationship between the sites of synthesis and the binding sites involved with heparin releasable enzymes such as histaminase.
AB - Previous studies have suggested that in the rat, small intestine is the source for rise in plasma histaminase levels seen after heparin administration. The cellular location of histaminase in intestine and the mechanism of heparin release have not been previously investigated. The present study identifies intestinal villus cells rather than crypt cells as the location of intestinal histaminase; at this site, the enzyme is not associated with brush border. Heparin added to incubations containing isolated intestinal cells did not release histaminase into the medium. Perfusion of intestinal vasculature with heparin caused a prompt release of this enzyme into venous effluent. The present investigation. therefore, suggests that heparin releases histaminase from vascular binding sites rather than directly from parenchymal cells. The use of isolated intestine with perfusion of the vasculature could serve as a useful tool for further defining the relationship between the sites of synthesis and the binding sites involved with heparin releasable enzymes such as histaminase.
UR - http://www.scopus.com/inward/record.url?scp=0017624709&partnerID=8YFLogxK
U2 - 10.1016/0006-2952(77)90438-5
DO - 10.1016/0006-2952(77)90438-5
M3 - Article
C2 - 413549
AN - SCOPUS:0017624709
SN - 0006-2952
VL - 26
SP - 2343
EP - 2347
JO - Biochemical Pharmacology
JF - Biochemical Pharmacology
IS - 24
ER -