An interrelatedness of the potentiation of radiation-induced bacterial cell killing by cisplatin and binuclear rhodium carboxylates.
Cisplatin and binuclear rhodium (Rh2) carboxylates appear to potentiate radiation-induced killing of Salmonella typhimurium cells largely as a consequence of one-electron reduction that leads to an active radiolytic product. This conclusion is supported by results from experiments wherein the hydrated electron and the hydroxyl radical are competed for in the presence of cisplatin and Rh2 carboxylates, and by the similarly shaped radiation survival curves for cisplatin and Rh2 carboxylates wherein potentiation is expressed beyond variable thresholds of radiation dose. Increasing concentrations of phosphate and chloride also inhibit radiation potentiation by both cisplatin and Rh2 carboxylates, further supporting the contention for similar mechanisms. Radiation potentiation by cisplatin is relatively much more sensitive to the inhibition by chloride.
Richmond
R C
RC
Department of Radiation Oncology, Norris Cotton Cancer Center, Dartmouth-Hitchcock Medical Center, Hanover, New Hampshire 03756.
Mahtani
H K
HK
D002264:Carboxylic Acids / Q000494:pharmacology*; D002470:Cell Survival / Q000187:drug effects / Q000528:radiation effects*; D002945:Cisplatin / Q000494:pharmacology*; D009942:Organometallic Compounds / Q000494:pharmacology*; D012238:Rhodium / Q000494:pharmacology*; D012486:Salmonella typhimurium / Q000187:drug effects / Q000528:radiation effects*; D013268:Stimulation, Chemical
D002264:Carboxylic Acids; D009942:Organometallic Compounds; D012238:Rhodium; D002945:Cisplatin