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Vol. 291, Issue 2, 492-502, November 1999
Department of Pharmacology, Wayne State University School of
Medicine, Detroit, Michigan (L.H.L., D.A.P.); and Division of Basic
Medical Sciences, Mercer University School of Medicine, Macon, Georgia
(R.K.Z.)
Inorganic mercury (Hg2+) induced time- and
concentration-dependent cellular injury in freshly isolated proximal
tubular (PT) and distal tubular (DT) cells from normal (control) rats
or uninephrectomized (NPX) rats. PT cells from NPX rats were more
susceptible than PT cells from control rats, and DT cells were slightly
more susceptible than PT cells to cellular injury induced by
Hg2+ (not bound to a thiol). Preloading cells with
glutathione increased Hg2+-induced cellular injury in PT
cells from control rats. However, coincubation of PT or DT cells from
control or NPX rats with Hg2+ and glutathione (1:4)
provided significant protection relative to incubations with
Hg2+ alone. No support was obtained for a role for
-glutamyltransferase in glutathione-dependent protection. However,
the organic anion carrier does appear to play a role in accumulation
and toxicity of mercuric conjugates of cysteine in PT cells from
control, but not NPX, rats. Coincubation with Hg2+ and
cysteine (1:4) had little effect on, or slightly enhanced, Hg2+-induced cellular injury at low concentrations of
Hg2+ in all cells studied. Coincubation with
Hg2+ and albumin (1:4) markedly protected PT and DT cells
from control and NPX rats at all concentrations except the highest
concentration of Hg2+ in DT cells from NPX rats.
2,3-Dimercapto-1-propanesulfonic acid protected cells both when
preloaded or added simultaneously with Hg2+. Thus, renal
cells from NPX rats are more susceptible to Hg2+-induced
injury, PT and DT cells respond differently to exposure to
Hg2+, and thiols can significantly modulate the toxic
response to Hg2+.
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