FIG 4.

Overview of mechanisms of bacterial antimonite resistance and oxidation. (A) A hypothetical model of IscR's regulation of bacterial Sb(III) oxidation. (i) Sb(III) induced the production of H₂O₂ via the bacterial oxidative stress response and subsequently H₂O₂ oxidized Sb(III) to Sb(V). (ii) H₂O₂ was partially consumed by catalase KatA. (iii) Sb(III) induced the expression of [Fe-S] assembly transcription factor IscR, which could positively contribute to GSH formation. Then, H₂O₂ was partially consumed by GSH. (B) Cellular events are represented on this model according to the published literature. Sb(III) is taken up through glycerol channel and extruded from the cell by Acr3 and ArsAB, and transportation of Sb(V) remains unknown. Bacteria obtained Sb(III) resistance by the ars operon. In addition, Sb(III) oxidation, Sb(V) reduction, and Sb(III) methylation were also involved in bacterial Sb detoxification. For energy generation, Sb(III) could induce activation of the TCA cycle and produce energy to protect against the toxicity of Sb.