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Cobalt and nickel impair DNA metabolism by the oxidative stress independent pathway

Abstract

The oxidative stress evolved under cobalt and nickel exposures is thought to exert toxicity, though the exact routes of such metal poisoning remain ambiguous. We revisited the metal toxicity in Escherichia coli to show that the cobalt and nickel exposures as low as 0.5 and 1mM levels, respectively, visibly inhibit growth. We also observed that acidic conditions aggravated, while alkaline conditions alleviated the metal toxicity. Besides, 1mM manganese, which is non-cytotoxic, as judged by the growth of E. coli, synergistically elevated cobalt and nickel stress. However, the metal toxicity did not lead to oxidative stress in E. coli. On the other hand, we show that cobalt and nickel, but not manganese, reduced the rate of DNA replication to 50% within 2 hours. Interestingly, the metal ions promoted DNA double-strand breaks but did not induce SOS repair pathways, indicating that the metal ions could block SOS induction. To test this, we show that cobalt and nickel, but not manganese, suppressed nalidixic acid-induced SOS response. Finally, using an in vitro assay system, we demonstrated that cobalt and nickel inhibit RecBCD function, which is essential for SOS induction. Therefore, our data indicate that cobalt and nickel affect DNA replication, damage DNA, and inhibit SOS repair pathway to exert toxicity.

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Publication details

The article was received on 09 Aug 2017, accepted on 12 Oct 2017 and first published on 12 Oct 2017


Article type: Paper
DOI: 10.1039/C7MT00231A
Citation: Metallomics, 2017, Accepted Manuscript
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    Cobalt and nickel impair DNA metabolism by the oxidative stress independent pathway

    V. Kumar, R. K. Mishra, G. Kaur and D. dutta, Metallomics, 2017, Accepted Manuscript , DOI: 10.1039/C7MT00231A

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