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Vol. 54, Issue 2, 353-363, August 1998
Division of Basic Medical Sciences, Mercer University School of
Medicine, Macon, Georgia 31207 (R.K.Z.), and
Department of Biology,
Georgia State University, Atlanta, Georgia 30303 (L.P., V.T.C., D.W.B.)
Mechanisms by which the dithiol chelating agent
2,3-dimercaptopropane-1-sulfonate (DMPS) significantly alters the renal
tubular transport, accumulation, and toxicity of inorganic mercury were studied in isolated perfused pars recta (S2) segments of proximal tubules of rabbits. Addition of 200 µM DMPS to the bath
provided complete protection from the toxic effects of 20 µM inorganic mercury in the lumen. The protection was
linked to decreased uptake and accumulation of mercury. Additional data
indicated that, when DMPS and inorganic mercury were coperfused through
the lumen, very little inorganic mercury was taken up from the lumen.
We also obtained data indicating that DMPS is transported by the organic anion transport system and that this transport is linked to the
therapeutic effects of DMPS. Interestingly, very little inorganic
mercury was taken up and no cellular pathological changes were detected
when inorganic mercury and DMPS were added to the bath. We also tested
the hypothesis that DMPS can extract cellular mercury while being
transported from the bath into the luminal compartment. Our findings
showed that, when DMPS was applied to the basolateral membranes of S2
segments after they had been exposed to mercuric conjugates of
glutathione of the laminal membrane, the tubular content of mercury was
greatly reduced and the rates of disappearance of mercury from the
lumen changed from positive values to markedly negative values. We
conclude that inorganic mercury is extracted from proximal tubular
cells by a transport process involving the movement of DMPS from the
bathing compartment to the luminal compartment.
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