Microbial Arsenic Metabolism and Reaction Energetics

Reviews on the geochemistry, biochemistry, or microbial ecology of arsenic—and there are many—commonly start with statements about the toxicity of this metalloid (Newman et al. 1998; Rosen 2002; Smedley and Kinniburgh 2002; Oremland and Stolz 2003; Oremland et al. 2004, 2009; Silver and Phung 2005; Lloyd and Oremland 2006; Stolz et al. 2006, 2010; Bhattacharjee and Rosen 2007; Paez-Espino et al. 2009; Tsai et al. 2009; Slyemi and Bonnefoy 2012; Cavalca et al. 2013b; Kruger et al. 2013; van Lis et al. 2013; Watanabe and Hirano 2013; Zhu et al. 2014). These introductions are sometimes followed by famous anecdotes of foul play (e.g., was Napoleon I poisoned by his British captors?) and reminders that arsenic was used as a popular medicine, tonic, and aphrodisiac since the 18th century. Recall that the 1908 Nobel Prize in medicine was awarded to Paul Ehrlich, in part, for the discovery of an organoarsenical (Salvarsan) as a treatment for syphilis—this was arguably also the first documented application of what would later become known as “chemotherapy.” Readers are then often reminded that arsenic is still used today in pesticides and herbicides, in animal feed, as a wood preservative, in electronic devices, and in specialized medical treatments. Arsenic is toxic in both of its common oxidation states, the oxidized arsenate, As(V), and the reduced arsenite, As(III). As a molecular analog of phosphate, arsenate uses a phosphate transport system to enter the cell and there inhibits the phosphorylation of ADP and thereby the synthesis of ATP. Arsenate can also substitute for phosphate in various biomolecules, thus disrupting key pathways, including glycolysis. Arsenite is even more toxic than arsenate and enters the cell much like glycerol molecules via aqua-glyceroporins (Cullen …