Inhibition of protein synthesis antagonizes induction of sister-chromatid exchanges by exogenous agents.
Cycloheximide (CH) and puromycin (PM)strongly antagonize induction of sister-chromatid exchanges (SCEs) by exogenous agents regardless of the mechanism  for initiating damage. 5-Bromodeoxyuridine (BUdR) substitution was used to monitor SCEs, but the background level of BUdR-induced SCEs was unaffected by the presence of protein inhibitors. Antagonism between DNA-damaging agents and protein inhibitors was strongest in euchromatic regions. Possible relationships between SCE formation and the mechanism of antagonism by protein inhibitors are discussed.
D000818:Animals; D001973:Bromodeoxyuridine / Q000037:antagonists & inhibitors; D002460:Cell Line; D002869:Chromosome Aberrations; D006224:Cricetinae; D003412:Cricetulus; D003434:Crossing Over, Genetic / Q000187:drug effects*; D003513:Cycloheximide / Q000494:pharmacology*; D005020:Ethyl Methanesulfonate / Q000037:antagonists & inhibitors; D005467:Floxuridine / Q000037:antagonists & inhibitors; D006918:Hydroxyurea / Q000037:antagonists & inhibitors; D008741:Methyl Methanesulfonate / Q000037:antagonists & inhibitors; D011691:Puromycin / Q000494:pharmacology*; D012854:Sister Chromatid Exchange / Q000187:drug effects*
D005467:Floxuridine; D011691:Puromycin; D003513:Cycloheximide; D005020:Ethyl Methanesulfonate; D008741:Methyl Methanesulfonate; D001973:Bromodeoxyuridine; D006918:Hydroxyurea