title: Increase in histidine decarboxylase activity in tissues of mice bearing Colon-26 tumor cells.
abstract: The changes in histidine decarboxylase (HDC) activity, histamine and tele-methylhistamine contents were examined in tissues of mice after the inoculation of Colon-26 tumor cells subcutaneously into the lower back. The HDC activity in the spleen of mice increased significantly 14 days after the inoculation of Colon-26 and the increase in HDC activity continued for up to 28 days. However, the histamine content in the spleen of tumor-bearing mice was not changed significantly during the observation period. In the following experiments, two subclones of the Colon-26 cell line, cachexia-inducing clone-20 and non cachexia-inducing clone-5, were used and the induction of HDC activity in mice was examined in four tissues, spleen, lung, liver and kidney. Both clone-20 and clone-5 induced the increase in HDC activity to the same extent in the spleen and lung, but not in the liver and kidney. As observed using the Colon-26 original cell line, the histamine contents in the four tissues of tumor-bearing mice were not different from those in the control mice. In contrast, the levels of tele-methylhistamine, one of the major catabolites of histamine, in the tumor-bearing mice increased significantly compared with the control mice in all four tissues examined. There was a correlation between the increase in tele-methylhistamine level and the increase in HDC activity in the tissues. A histological study indicated that the tissue mast cells were not increased in spleen and lung of tumor-bearing mice. These findings indicated that the increase in HDC activity in the spleen and lung occurred in parallel with the growth of inoculated tumor cells in mice and suggested that the cells other than mast cells may be involved in the increase in HDC activity. The tumor-bearing state produced histamine with a high turnover rate in the mouse tissues, especially in the spleen and lung.
authors.affiliation: Department of Surgery, Okayama University Medical School, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Takeuchi
authors.forename: M
authors.initials: M
authors.lastname: Nishibori
authors.forename: M
authors.initials: M
authors.lastname: Uomoto
authors.forename: H
authors.initials: H
authors.lastname: Iwagaki
authors.forename: N
authors.initials: N
authors.lastname: Nakaya
authors.forename: N
authors.initials: N
authors.lastname: Tanaka
authors.forename: K
authors.initials: K
authors.lastname: Saeki
mesh_terms: D000230:Adenocarcinoma / Q000201:enzymology* / Q000276:immunology / Q000473:pathology; D000818:Animals; D002100:Cachexia / Q000473:pathology; D002999:Clone Cells; D006632:Histamine / Q000378:metabolism; D006640:Histidine Decarboxylase / Q000378:metabolism*; D007668:Kidney / Q000201:enzymology / Q000378:metabolism; D008099:Liver / Q000201:enzymology / Q000378:metabolism; D008168:Lung / Q000201:enzymology / Q000378:metabolism; D008297:Male; D008761:Methylhistamines / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D009368:Neoplasm Transplantation; D013154:Spleen / Q000201:enzymology / Q000378:metabolism; D013997:Time Factors
chemical_list: D008761:Methylhistamines; D006632:Histamine; D006640:Histidine Decarboxylase; C020404:tele-methylhistamine