The chemical and biological factors controlling microbial
formation
of methylmercury (MeHg) are widely studied separately, but the combined
effects of these factors are largely unknown. We examined how the
chemical speciation of divalent, inorganic mercury (Hg(II)), as controlled
by low-molecular-mass thiols, and cell physiology govern MeHg formation
byGeobacter sulfurreducens. We compared MeHg formation
with and without addition of exogenous cysteine (Cys) to experimental
assays with varying nutrient and bacterial metabolite concentrations.
Cysteine additions initially (0–2 h) enhanced MeHg formation
by two mechanisms: (i) altering the Hg(II) partitioning from the cellular
to the dissolved phase and/or (ii) shifting the chemical speciation
of dissolved Hg(II) in favor of the Hg(Cys)2complex. Nutrient
additions increased MeHg formation by enhancing cell metabolism. These
two effects were, however, not additive since cysteine was largely
metabolized to penicillamine (PEN) over time at a rate that increased
with nutrient addition. These processes shifted the speciation of
dissolved Hg(II) from complexes with relatively high availability,
Hg(Cys)2, to complexes with lower availability, Hg(PEN)2, for methylation. This thiol conversion by the cells thereby
contributed to stalled MeHg formation after 2–6 h Hg(II) exposure.
Overall, our results showed a complex influence of thiol metabolism
on microbial MeHg formation and suggest that the conversion of cysteine
to penicillamine may partly suppress MeHg formation in cysteine-rich
environments like natural biofilms.