Open AccessOxidative stress, signal transduction, and intercellular communication in radiation carcinogenesis
Author(s) -
Trosko James E.,
Inoue Tohru
Publication year - 1997
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1002/stem.5530150710
Subject(s) - biology , oxidative stress , carcinogenesis , signal transduction , intracellular , microbiology and biotechnology , transduction (biophysics) , oxidative phosphorylation , cancer research , genetics , biophysics , biochemistry , cancer
During the evolution of multicellular organisms, survival in an aerobic environment came about by adaptive responses, both to the endogenous oxidative metabolism within the cells of the organism as well as the chemicals and low‐level radiation to which they are exposed. In addition to defense mechanisms shared with single‐cell organisms, multicellular organisms are equipped with gap junctions which allow electrotonic and/or metabolic synchronization of processes between coupled cells. The connexin genes, which code for the proteins comprising the gap junctions, provide homeostatic regulation of cell proliferation, differentiation, and adaptive responses of individual cells through a mechanism of “gap junctional intercellular communication”. The biological consequences of the response of a multicellular organism to low‐level radiation exceeding the background level of oxidative damage to a cell in a tissue could be apoptosis, cell proliferation, or cell differentiation. Stem Cells 1997; 15(suppl 2): 59‐67