Zhang Q M, Yonei S
Laboratory of Radiation Biology, Faculty of Science, Kyoto University, Japan.
J Bacteriol. 1991 Jun;173(11):3488-91. doi: 10.1128/jb.173.11.3488-3491.1991.
Treatment of exponentially growing cells of Escherichia coli with membrane-binding drugs such as chlorpromazine (CPZ) and procaine resulted in an induction of manganese-superoxide dismutase (Mn-SOD). A slight decrease was observed in the amount of Fe-SOD. The induction of Mn-SOD required de novo synthesis of this enzyme, since it was suppressed by rifampin. The treatment did not cause the induction of Mn-SOD when performed under anaerobic conditions. In E. coli cells with a sodA-lacZ operon fusion, CPZ and procaine induced beta-galactosidase in the presence of oxygen, whereas it was not expressed and was not induced by CPZ and procaine under anaerobic conditions. Although CPZ reduced the ability of cell suspensions to take up oxygen, it increased the cyanide-resistant fraction of the total respiration. Therefore, it appeared likely that the induction of the sodA gene was a response to an increase in superoxide radical production mediated by these membrane-binding drugs in E. coli cells, possibly by disruption of the electron transport systems in the cell membranes.
用膜结合药物如氯丙嗪（CPZ）和普鲁卡因处理指数生长的大肠杆菌细胞，会诱导锰超氧化物歧化酶（Mn-SOD）的产生。观察到铁超氧化物歧化酶（Fe-SOD）的量略有下降。Mn-SOD的诱导需要该酶的从头合成，因为它会被利福平抑制。在厌氧条件下进行处理时，不会导致Mn-SOD的诱导。在具有sodA-lacZ操纵子融合的大肠杆菌细胞中，CPZ和普鲁卡因在有氧条件下诱导β-半乳糖苷酶，而在厌氧条件下它不表达且不会被CPZ和普鲁卡因诱导。尽管CPZ降低了细胞悬液摄取氧气的能力，但它增加了总呼吸中抗氰化物的部分。因此，sodA基因的诱导似乎是对这些膜结合药物在大肠杆菌细胞中介导的超氧自由基产生增加的一种反应，可能是通过破坏细胞膜中的电子传递系统。
