Toxicological Sciences, Vol 50, 98-105, Copyright © 1999 by Society of Toxicology
AR Parrish, XH Zheng, KD Turney, HS Younis and AJ Gandolfi
Although the kidney represents a target for the accumulation and toxicity
of arsenic, little is known about the molecular targets of arsenic in this
organ. Therefore, these studies were designed to examine the molecular
impact of arsenite [As(III)] and arsenate [As(V)] at low (nanomolar)
concentrations. Precision-cut rabbit renal cortical slices were challenged
with As(III) or As(V) for up to 8 h. Neither form of the metal induced
overt cytotoxicity as assessed by intracellular K+ levels over this time
period at concentrations from 0.01-10 microM. In addition, no alterations
in the expression of Hsp 60, 70, or 90 were observed. However, induction of
heme oxygenase-1 (Hsp 32) was seen following a 4-h challenge with As(III),
but not with As(V). As(III) and As(V) induced DNA binding of AP-1 at 2- and
4-h exposure; following a 6-h exposure there was no difference. Although no
alteration in the DNA binding activity of ATF-2 was induced by As(III) or
As(V), both forms enhanced the DNA binding activity of Elk-1. Enhanced DNA
binding activity of AP-1 and Elk-1 correlated with increased gene
expression of c-fos, but not c-jun, at 2 h. c-myc gene expression was also
induced by As(III) and As(V), albeit at a later time point (6 h). These
results suggest that acute arsenic challenge, by either As(III) or As(V),
is associated with discrete alterations in the activity of signaling
pathways and gene expression in renal tissue.
ARTICLES
Enhanced transcription factor DNA binding and gene expression induced by arsenite or arsenate in renal slices
Department of Anesthesiology, College of Medicine, University of Arizona, Tucson 85721, USA.
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