| Toxicological effects of mercury (Hg) on mammalian cells has been studied intensively, however little is known about the mechanisms of toxicity to bacterial cells lacking an Hg resistance (mer) operon. I researched physiological effect of Hg to Shewanella oneidensis MR-1. MR-1 is eight-fold more sensitive to ionic mercury [Hg(II)] under aerobic conditions than in fumarate reducing conditions, with both chronic and acute Hg exposure. Since more Hg is associated with cellular material in fumarate reducing conditions than in aerobic conditions, this increased sensitivity in aerobic conditions is not due to increased import of Hg into the cell. In fumarate reducing conditions, glutathione may provide protection against Hg, as glutathione levels decrease in a dose-dependent manner, but this does not occur in aerobic conditions. Hg(II) does not change the redox state of thioredoxin in MR-1 in either fumarate reducing conditions or aerobic conditions. However, treatment with 0.5 muM Hg(II) increases lipid peroxidation in aerobic conditions but not in fumarate reducing conditions in MR-1. It is concluded that the enhanced sensitivity of MR-1 to Hg(II) in aerobic conditions is not due to differences in intracellular responses, but due to damage at the cell envelope.;Xanthobacter autotrophicus Py2, an aerobic Alphaproteobacteria, was chosen as a model system to study interaction between Hg and soil bacteria. This study demonstrates that the proposed mer operons in Py2, mer1 and mer2, are mer operons based on the observation that 1) their gene transcription is activated by Hg(II); 2) they confer Hg(II) and MeHg resistance when expressed in Escherichia coli; 3) they confer Hg(II) reduction and MeHg demethylation when expressed in Escherichia coli. There is a new mer gene, referred to as merS, in both mer operons. The merSs' transcripts reside on the same polycistronic RNA with merAs and their protein products have glutathione reductase activity. |
