Dimercaptopropanesulfonic
acid (
DMPS) has been approved for the treatment of
arsenic poisoning through promoting
arsenic excretion and modulating
arsenic species. To clarify how
DMPS regulates the excretion of
arsenic species, we investigated the effects of
DMPS on the biomethylation of
arsenite (As(3+)) in HepG2 cells. In the experiments, we found that
DMPS at low concentrations dramatically decreased the content of
arsenic in HepG2 cells and inhibited the cellular methylation of As(3+). Three aspects, the expression of human
arsenic (III)
methyltransferase (hAS3MT), the accumulation of cellular
reactive oxygen species (ROS) and the in vitro enzymatic methylation of
arsenic, were considered to explain the reasons for the inhibition of
DMPS in
arsenic metabolism. The results suggested that
DMPS competitively coordinated with As(3+) and
monomethylarsonous acid (MMA(3+)) to inhibit the up-regulation of
arsenic on the expression of hAS3MT and block
arsenic involving in the enzymatic methylation. Moreover,
DMPS eliminated
arsenic-induced accumulation of ROS, which might contribute to the antidotal effects of
DMPS on
arsenic posing.