29th Annual Meeting of the American Society of Photobiology

Downtown Marriot

Chicago, Il.

July 7th-12th, 2001


The Bystander Effect: Ionizing Radiation and UVA

Hill, Helene1, Howell, Roger1, Azzam, Edouard1, de Toledo, Sonia 1, Bishayee, Anupam1 and Lenarczyk, Marek1
NJ Medical School1

Abstract-
In studies involving ionizing radiation, damages of various types have been recognized in unirradiated neighboring cells termed bystanders. Damages that have been observed in bystander cells include increased sister chromatid exchanges, chromosomal instability, micro-nucleus formation, enhanced mitogenic responses, increased mutation frequencies, cell death, induction of the G1 checkpoint and induction of damage-response proteins. Bystander phenomena have been induced by both low LET (X-rays, -rays, -rays) and high LET ( particles) radiations. Most bystander phenomena have required cell-cell contact and are presumed to be mediated by gap junction intercellular communication. Connexin cell surface proteins have been implicated as conduits for the as-yet unidentified translocated agents. Bystander effects are diminished by scavengers of reactive oxygen species. Of interest to photobiologists is the report of Bagdonis, et al. (Radiation Research, 152, 174-179 (1999) that a phenomenon akin to the bystander effect may be produced by UVA photons. Some aspects of UVA are similar to ionizing radiation in that both interact with cellular macromolecules through reactive oxygen species. This present report will review bystander effects studied by the authors with the aim of stimulating photobiological research in this area. Photobiologists should consider that bystander phenomena may be important to the understanding of the mechanism of action of PDT and of PUVA; that sun damage to skin may be passed on to unirradiated bystanders; that immunological responses could be modulated through bystander effects. Relatively simple tissue culture methods are now available to study these effects in situ as well as in progeny of bystander cells.

Keywords: DNA damage, damage response proteins, gap junction intercellular communication, genetic instability