Publication: Mercuric chloride-induced alterations
in stress protein distribution in rat kidney
Authors
Stacchiotti, A. ; Lavazza, A. ; Rezzani, R. ; Borsani, E. ; Rodella, L.F. ; Bianchi, R.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Mercuric chloride (HgCl2) induces acute
renal failure associated to tubular impairment in
experimental animals and humans. Stress proteins are a
superfamily of proteins, comprising heat- shock proteins
(HSP) and glucose-regulated proteins (GRP), enhanced
or induced in the kidney in response to stress. They act
as molecular chaperones that protect organelles and
repair essential proteins which have been denatured
during adverse conditions. The involvement of stress
proteins in mercury-nephrotoxicity has not yet been well
clarified. This study was undertaken to detect the tubular
distribution of four stress proteins (HSP25, HSP60,
GRP75, HSP72) in the rat kidney injected with HgCl2
and to quantify lysosomal and mitochondrial changes in
straight proximal tubules, the main mercury target.
Sprague-Dawley rats were administered i.p. with
progressive sublethal doses of HgCl2 (0.25 mg/kg, 0.5
mg/kg, 1 mg/kg and 3.5 mg/kg) or saline (as controls)
and sacrificed after 24 h. In dosages over 0.50 mg/kg,
stress proteins increased and changed localization in a
dose-dependent manner. HSP25 was focally expressed in
altered proximal tubules at 1 mg/kg but in the macula
densa it was at 3.5 mg/kg. HSP60 and GRP75 were
intense in the nucleus and cytoplasm of proximal tubules
but moderate in distal tubules. HSP72 was induced in
distal tubules after low exposures but in proximal
tubules it happened at the highest dose. Moreover, a
significant increase in lysosomal and total mitochondria
(normal and with broken cristae) area and density were
progressively found after HgCl2 treatments. Stress
proteins could represent sensitive biomarkers that
strongly correlate with the degree of oxidative injury
induced by HgCl2 in the rat proximal tubules.
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