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Additional resources for Cisplatin. Current Status and New Developments
This delayed crosslinking was especially striking in cisplatin-treated cells in which interstrand crosslinking appeared to increase as much as 20-fold over a 12 hr period. The delay in crosslink formation may reflect the time required for monofunctionally bound drug to react with the second DNA site. Further incubation beyond 12 hr resulted in loss of crosslinks, possibly due to a repair process. Assays of total crosslinking in the same experiment showed somewhat differ ent patterns (upper panels in Fig.
In order to improve quantitation, control cells labeled 3 with H-thymidine and exposed to 150 rads at 0° were mixed with the experi 14 3 mental C-labeled cells prior to deposition on the filters. The elution of H 14 DNA serves as an internal reference for normalization of the elution of C-DNA. DNA strand breaks are measured by the increased elution rate of shortened single strands. Crosslinks have the opposite effect, and are measured by inserting a known frequency of strand breaks by means of χ ray.
Whereas ara-C modified both the extent of the shoulder and the magnitude of the slope. The shoulder region of a survival curve reflects the capacity of cells to absorb damage without expressing a lethal effect, a phen omenon possibly, although not necessarily, related to the presence of a repair mechanism (Drewinko et al, 1979). The slope of the linear part of the curve quantifies the sensitivity of the interaction between the toxic agent and the vital cellular structure, in this case, DNA. Thus, these findings suggest, first, that the primary damage of cis-ΌΌ?