The release of peroxidase by nontransformed or transformed fibroblasts or epithelial cells (effector cells) triggers apoptosis induction selectively in transformed fibroblasts or transformed epithelial cells (target cells) through intercellular apoptosis-inducing signaling. The release of peroxidase can be induced either by treatment with transforming growth factor beta 1 or by low doses of alpha particles, gamma rays or ultrasoft X rays. In addiation, data indicates that radiation quality does not determine the overall efficiency of peroxidase release and the effects among a wide range of radiation doses are indistinguishable. These findings suggested that peroxidase release might be being triggered through intercellular bystander signaling. We show here that maximal peroxidase release does indeed occur after coculture of a small number of irradiated cells with an excess of unirradiated cells and demonstrate an enhanced effector function of nontransformed cells after the addition of a small number of irradiated cells. These data strongly indicate that peroxidase release is indeed triggered through bystander signaling mechanisms in mammalian cells.
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Absorption, Radiation, Alpha Particles, Animals, Bystander Effect, Fibroblasts, Gamma Rays, Gene Expression Regulation, Enzymologic, Gene Expression Regulation, Neoplastic, Humans, Neoplasms, Experimental, Peroxidase, Radiation Dosage, Rats, Up-Regulation, X-Rays