LaVelle J M
Environ Mutagen. 1986;8(5):717-25. doi: 10.1002/em.2860080507.
In a previous report chromate potentiated the mutagenicity of sodium azide, apparently by affecting repair and/or replication of DNA. Further evidence in support of such a mechanism for chromate potentiation is reported here. Chromate does not react directly with azide or its major mutagenic metabolite, azidoalanine, eliminating such reactions as possible mechanisms for potentiation. Further, azide was unable to potentiate the mutagenicity of chromate in Salmonella typhimurium strain TA104, which is sensitive to chromate mutagenicity but not to azide. Thus, it appears that the potentiation is not due to an action of azide in modulating chromate mutagenicity. Finally, the interaction was not altered by deficiency in recA gene product in S typhimurium GW19, nor by enhancement of SOS repair in the pKM101 containing strain TA100. Thus, induction of recA-dependent functions seems to play no role in the comutagenic actions of chromate. The simplest explanation for potentiation seems to be that chromate is able either to limit error-free recovery from azide-induced DNA damage or to promote error-prone repair or error-prone processing at sites of lesions.
在之前的一份报告中，铬酸盐增强了叠氮化钠的致突变性，显然是通过影响DNA的修复和/或复制来实现的。本文报道了支持铬酸盐增强作用这种机制的进一步证据。铬酸盐不与叠氮化物或其主要诱变代谢物叠氮丙氨酸直接反应，排除了此类反应作为增强作用的可能机制。此外，叠氮化物无法增强鼠伤寒沙门氏菌TA104菌株中铬酸盐的致突变性，该菌株对铬酸盐的致突变性敏感，但对叠氮化物不敏感。因此，增强作用似乎并非由于叠氮化物在调节铬酸盐致突变性方面的作用。最后，鼠伤寒沙门氏菌GW19中recA基因产物的缺陷，以及含有pKM101的菌株TA100中SOS修复的增强，均未改变这种相互作用。因此，recA依赖性功能的诱导似乎在铬酸盐的协同致突变作用中不起作用。增强作用最简单的解释似乎是，铬酸盐要么能够限制从叠氮化物诱导的DNA损伤中进行无差错恢复，要么能够促进损伤部位的易错修复或易错加工。
