Rossman T G, Molina M
Environ Mutagen. 1986;8(2):263-71. doi: 10.1002/em.2860080208.
Salts of metals which are carcinogenic, noncarcinogenic, or of unknown carcinogenicity were assayed for their abilities to modulate ultraviolet (UV)-induced mutagenesis in Escherichia coli WP2. In addition to the previously reported comutagenic effect of arsenite, salts of three other compounds were found to enhance UV mutagenesis. CuCl2, MnCl2 (and a small effect by KMnO4), and NaMoO4 acted as comutagens in E coli WP2, which has wild-type DNA repair capability, but were much less comutagenic in the repair deficient strain WP2s (uvrA). The survival of irradiated or unirradiated cells was not affected by these compounds. No effects on UV mutagenesis were seen for 16 other metal compounds. We suggest that the comutagenic effects might occur either via metal-induced decreases in the fidelity of repair replication or (in the case of CuCl2) via metal-induced depurination.
对具有致癌性、非致癌性或致癌性未知的金属盐进行了检测，以评估它们调节紫外线（UV）诱导的大肠杆菌WP2诱变的能力。除了先前报道的亚砷酸盐的共诱变作用外，还发现其他三种化合物的盐可增强UV诱变。CuCl2、MnCl2（以及KMnO4有轻微作用）和NaMoO4在具有野生型DNA修复能力的大肠杆菌WP2中作为共诱变剂，但在修复缺陷菌株WP2s（uvrA）中的共诱变作用要小得多。这些化合物对受辐照或未受辐照细胞的存活没有影响。其他16种金属化合物对UV诱变没有影响。我们认为，共诱变作用可能是通过金属诱导修复复制保真度降低，或者（对于CuCl2）通过金属诱导的脱嘌呤作用而发生的。
