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Published on: July 3, 2013
Stress proteins in experimental nephrotoxicity: a ten year experience
Alessandra Stacchiotti1, Francesca Bonomini, Gaia Favero
1Division of Human Anatomy, Department of Biomedical Sciences and Biotechnology, School of Medicine, University of Brescia. stacchio@med.unibs.it
Summary
Kidney stress proteins (heat shock and glucose-regulated proteins) defend against chemical damage. Modulating these proteins with antioxidants or inducers shows promise for reducing drug-induced kidney injury.
Area of Science:
- Nephrology
- Cellular Biology
- Toxicology
Background:
- Heat shock proteins (HSPs) and glucose-regulated proteins (GRPs) are crucial defense mechanisms in the kidney against chemical and drug-induced damage.
- These stress proteins play a vital role in cellular survival and maintaining kidney function under toxic conditions.
Purpose of the Study:
- To investigate the presence and regulation of stress proteins in acute and chronic nephrotoxic models in rodents and in vitro.
- To explore the potential of modulating stress protein expression as a therapeutic strategy against kidney toxicity.
Main Methods:
- Induction of acute renal damage in rats using inorganic mercury, followed by treatment with melatonin or bimoclomol.
- Induction of ischemia-reperfusion injury in rats treated with stannous chloride.
- Administration of cyclosporine A and aluminum to induce chronic nephrotoxicity in rats.
- In vitro studies using rat tubular proximal cells exposed to heavy metals.
Main Results:
- In acute mercury-induced nephrotoxicity, stress proteins increased dose-dependently to aid recovery of cytoskeleton and mitochondria.
- Pre-treatment with melatonin or bimoclomol modulated stress protein expression and improved tubular recovery.
- Ischemia-reperfusion injury studies showed cytoprotection with stannous chloride via heme oxygenase induction.
- Chronic cyclosporine A toxicity showed stress protein overexpression correlated with oxidative stress and cell death, reduced by antioxidants.
- Aluminum intoxication induced a time-dependent, organ-specific stress response in rat kidneys.
- In vitro studies revealed metal-specific mechanisms influencing stress protein expression in tubular cells.
Conclusions:
- Experimental studies on renal chaperones enhance understanding of their protective roles in nephrotoxicity.
- Agents that modulate stress protein responses represent promising therapeutic avenues for mitigating kidney damage caused by chemicals and drugs.
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