Nunes E, Candreva E C, Keszenman D, Salvo V A
Department of Biophysics, Faculty of Medicine, Montevideo, Uruguay.
Mutat Res. 1993 Oct;289(2):165-70. doi: 10.1016/0027-5107(93)90066-o.
We have analyzed the mutagenic effect of elevated temperatures (hyperthermia: HT) either upon direct exposure or after a previous heat shock (HS) in the haploid auxotrophic Saccharomyces cerevisiae strain SC7K lys2-3 in the logarithmic phase of growth. We demonstrated a significant antimutagenic effect of HS (38 degrees C for 1 h) followed by hyperthermia (48 degrees C, up to 60 min). Using cycloheximide (CHM) during the HS exposure we reversed the antimutagenic effect. We suggest that, upon HS, the enzymes involved in repair of premutational damage are more resistant to denaturation, i.e., by the induced HSP genes, and could work efficiently to prevent damage fixation in critical targets. CHM blocks the antimutagenic effect of the HS treatment by inhibiting the inducible synthesis of HSP.
我们分析了高温（热疗：HT）对处于对数生长期的单倍体营养缺陷型酿酒酵母菌株SC7K lys2-3直接暴露时或先前热休克（HS）后的诱变作用。我们证明了热休克（38摄氏度，1小时）后再进行热疗（48摄氏度，长达60分钟）具有显著的抗诱变作用。在热休克暴露期间使用放线菌酮（CHM），我们逆转了抗诱变作用。我们认为，热休克时，参与预突变损伤修复的酶对变性更具抗性，即通过诱导的热休克蛋白（HSP）基因，并且可以有效地防止关键靶点的损伤固定。放线菌酮通过抑制热休克蛋白的诱导合成来阻断热休克处理的抗诱变作用。
