XXXX plus near-u.v. light initiates DNA damage and repair in Chinese hamster cells.

@entity3653 @entity2555 @entity26 @entity5834 @entity106 @entity2142
Earlier results on the photodynamic action of several carcinogenic @entity2555 , and particularly @entity3653 ( @entity106 ), have been extended to determine if @entity106 + near-u.v. light produces damage to DNA. @entity106 by itself (30 min, approximately 24 degrees C) introduces relatively few breaks into genomic DNA. The addition of near-u.v. light, however, inserts large numbers of single-strand breaks in a dose-dependent way. Incubation following exposure initially results in the rapid repair of these breaks. A primary role for DNA damage in photodynamic cell killing is not supported by other observations, however. First, @entity5834 , an inhibitor of radiation-associated DNA repair processes, has only a minor effect on the @entity26 -dependent killing of cells exposed to @entity106 + u.v. light. Second, along with the repair of DNA breaks, the insertion of additional breaks becomes evident leading to a massive breakdown of genomic DNA due to an @entity2142 . And third, lethally affected cells rapidly lose their surface attachment. Because light induces damage in DNA when @entity106 is present, it is likely that @entity106 becomes closely associated with DNA. Thus, a starting point for mutagenic and carcinogenic action in the absence of light is suggested although activation of @entity106 by a P-450 system does not appear to be a prerequisite of @entity106 -DNA association. Still, DNA as such may not be the initial or the primary target for light-induced cell killing. In addition to interacting with DNA, @entity106 is sequestered by membranes, suggesting that killing results from an @entity26 -dependent release of catabolic enzymes. These enzymes, which may come from lysosomes, degrade DNA but concomitantly release surface-attached cells into the medium.
