Mercury (Hg) is a global pollutant of environmental and health concern; its methylated form, methylmercury (MeHg) is a potent neurotoxin. Sulfur-containing molecules play a role in MeHg production by microorganisms. While sul des are considered to limit Hg methylation, sulfate and cysteine were shown to favor this process. However, these two forms can be endogenously converted by microorganisms into sul de. Here, we explore the effect of sul de (produced by the cell or supplied exogenously) on Hg methylation. For this purpose, Pseudodesulfovibrio hydrargyri BerOc1 was cultivated in non-sul dogenic conditions with addition of cysteine and sul de as well as in sul dogenic conditions. We report that Hg methylation depends on sul de concentration in the culture rather than on the initial form of sulfur (cysteine, sul de or sulfate) added, and was independent of hgcA expression. Interestingly, MeHg production was maximal at 0.1-0.5 mM of sul des. Besides, a strong positive correlation between MeHg in the extracellular medium and the increase of sul de concentrations was observed, suggesting a facilitated MeHg export with sul de and/or higher desorption from the cell. We demonstrate that sul des (exogenous or endogenous) play a key role in controlling mercury methylation, and should be considered when investigating the impact of Hg on natural environments.

Mercury (Hg) is a global pollutant of environmental and health concern; its methylated form, methylmercury (MeHg) is a potent neurotoxin. Sulfur-containing molecules play a role in MeHg production by microorganisms. While sulfides are considered to limit Hg methylation, sulfate and cysteine were shown to favor this process. However, these two forms can be endogenously converted by microorganisms into sulfide. Here, we explore the effect of sulfide (produced by the cell or supplied exogenously) on Hg methylation. For this purpose, Pseudodesulfovibrio hydrargyri BerOc1 was cultivated in non-sulfidogenic conditions with addition of cysteine and sulfide as well as in sulfidogenic conditions. We report that Hg methylation depends on sulfide concentration in the culture rather than on the initial form of sulfur (cysteine, sulfide or sulfate) added, and was independent of hgcA expression. Interestingly, MeHg production was maximal at 0.1-0.5 mM of sulfides. Besides, a strong positive correlation between MeHg in the extracellular medium and the increase of sulfide concentrations was observed, suggesting a facilitated MeHg export with sulfide and/or higher desorption from the cell. We demonstrate that sulfides (exogenous or endogenous) play a key role in controlling mercury methylation, and should be considered when investigating the impact of Hg on natural environments.

No abstract

No abstract