Open AccessTriazine Derivatives Inhibit Rat Hepatocarcinogenesis but Do Not Enhance Gap Junctional Intercellular Communication
Author(s) -
Hori Takaaki,
Asamoto Makoto,
Krutovskikh Vladimir,
Iwahori Yoshio,
Maeda Mitsuaki,
ToriyamaBaba Hiroyasu,
Takasuka Nobuo,
Tsuda Hiroyuki
Publication year - 1997
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1997.tb00295.x
Subject(s) - intracellular , gap junction , triazine , cell junction , chemistry , microbiology and biotechnology , cancer research , biology , biochemistry , cell , polymer chemistry
We report here novel candidate chemopreventive agents active against experimental hepatocarcino‐genesis. The triazine derivatives 6‐(2‐chlorophenyl)‐2,4‐diamino‐l,3,5‐triazine (2CPDAT), 6‐(3‐chlorophenyl)‐2,4‐diamino‐l,3,5‐triazine (3CPDAT), 6‐(4‐chlorophenyl)‐2,4‐diamino‐l,3,5‐triazine (4CPDAT), 6‐(4‐pyridyl)‐2,4‐diamino‐l,3,5‐triazine (PyDAT), and 6‐(pyridine JV‐oxid‐4‐yl)‐2,4‐diamino‐l,3,5‐triazine (PyNODAT), synthesized in our laboratory, in addition to 6‐(2,5‐dichloro‐phenyl)‐2,4‐diamino‐l,3,5‐triazme (DCPDAT), or irsogladine, which is a widely used anti‐ulcer drug, were investigated for potential chemopreventive effects in a rat liver medium‐term bioassay system. A significant inhibitory influence on enzyme‐altered liver foci was found for 2CPDAT, 3CPDAT, 4CPDAT, and PyNODAT, but not for DCPDAT or PyDAT, The involvement of gap jnnctional intercellular communication in the inhibition was studied, but no change in gap Junctional intercellular communication capacity in rat liver cells in vitro or in gap junction protein (connexin 32) expression in rat liver in vivo was noted. These results indicate that, although these irsogladine analogues exert inhibitory effects on rat liver carcinogenesis, their action is independent of modification of gap Junctional intercellular communication.