OXIDATIVE STRESS, SIGNAL-TRANSDUCTION, AND INTERCELLULAR COMMUNICATION IN RADIATION CARCINOGENESIS

During the evolution of multicellular organisms, survival in an aerobi c 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 additi on to defense mechanisms shared with single-cell organisms, multicellu lar 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 jun ctions, provide homeostatic regulation of cell proliferation, differen tiation, and adaptive responses of individual cells through a mechanis m of ''gap junctional intercellular communication.'' The biological co nsequences of the response of a multicellular organism to low-level ra diation exceeding the background level of oxidative damage to a cell i n a tissue could be apoptosis, cell proliferation, or cell differentia tion.