Nanomaterials such as silver nanoparticles and graphene-based composites are known to exhibit biocidal activities. However, interactions with surrounding medium or supporting substrates can significantly influence this activity. Here, it is shown that superior antimicrobial properties of natural shellac-derived graphene oxide (GO) coatings is obtained on metallic films, such as Zn, Ni, Sn, and steel. It is also found that such activities are directly correlated to the electrical conductivity of the GO-metal systems; the higher the conductivity the better is the antibacterial activity. GO-metal substrate interactions serve as an efficient electron sink for the bacterial respiratory pathway, where electrons modify oxygen containing functional groups on GO surfaces to generate reactive oxygen species (ROS). A concerted effect of nonoxidative electron transfer mechanism and consequent ROS mediated oxidative stress to the bacteria result in an enhanced antimicrobial action of naturally derived GO-metal films. The lack of germicidal effect in exposed cells for GO supported on electrically nonconductive substrates such as glass corroborates the above hypothesis. The results can lead to new GO coated antibacterial metal surfaces important for environmental and biomedical applications.

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Inteins are mobile genetic elements that self-splice at the protein level. Mycobacteria have inteins inserted into several important genes, including those corresponding to the iron-sulfur cluster assembly protein SufB. Curiously, the SufB inteins are found primarily in mycobacterial species that are potential human pathogens. Here we discovered an exceptional sensitivity of Mycobacterium tuberculosis SufB intein splicing to oxidative and nitrosative stresses when expressed in Escherichia coli. This effect results from predisposition of the intein's catalytic cysteine residues to oxidative and nitrosative modifications. Experiments with a fluorescent reporter system revealed that reactive oxygen species and reactive nitrogen species inhibit SufB extein ligation by forcing either precursor accumulation or N-terminal cleavage. We propose that splicing inhibition is an immediate, posttranslational regulatory response that can be either reversible, by inducing precursor accumulation, or irreversible, by inducing N-terminal cleavage, which may potentially channel mycobacteria into dormancy under extreme oxidative and nitrosative stresses.