Leitão A C, Soares R A, Cardoso J S, Guillobel H C, Caldas L R
Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Brazil.
Mutat Res. 1993 Apr;286(2):173-80. doi: 10.1016/0027-5107(93)90181-e.
Mutagenesis induced by several genotoxic agents has been reported to be inhibited by cobaltous chloride. In order to study the effects of this metal in some SOS functions we evaluated mutagenesis, lysogenic induction and phage reactivation in Escherichia coli cells treated with CoCl2. We detected that cobaltous chloride, when present in the plating medium, was able to block mutagenesis and lysogenic induction promoted by UV irradiation. We also found that CoCl2 blocked protein synthesis, so we propose that this effect can be responsible for the antimutagenic and antilysogenic effects of this metal. On the other hand, if the cells were treated for a short period of time with CoCl2, in the absence of Mg, we observed that cobaltous chloride per se was able to promote lysogenic induction as well as to enhance the phage reactivation induced by UV irradiation. We conclude that depending on experimental conditions, cobaltous chloride may act either as an inhibitor or as an inducer of the SOS functions.
据报道,几种基因毒性剂诱导的诱变作用会受到氯化钴的抑制。为了研究这种金属在某些SOS功能中的作用,我们评估了用CoCl₂处理的大肠杆菌细胞中的诱变、溶原性诱导和噬菌体复活情况。我们检测到,当氯化钴存在于平板培养基中时,它能够阻断紫外线照射促进的诱变和溶原性诱导。我们还发现CoCl₂会阻断蛋白质合成,因此我们认为这种效应可能是这种金属产生抗诱变和抗溶原性效应的原因。另一方面,如果在没有镁的情况下,用CoCl₂对细胞进行短时间处理,我们观察到氯化钴本身能够促进溶原性诱导,并增强紫外线照射诱导的噬菌体复活。我们得出结论,根据实验条件,氯化钴可能作为SOS功能的抑制剂或诱导剂起作用。