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Oxidative stress response in iron-induced acute nephrotoxicity: enhanced expression of heat shock protein 90.
Biochem Biophys Res Commun. 1996 Feb 06; 219(1):76-81.BB

Abstract

Iron overload with ferric nitrilotriacetate (Fe-NTA) induces acute renal proximal tubular necrosis, a consequence of oxidative tissue damage, that leads to a high incidence of renal adenocarcinoma in rodents. In the present study, we determined the proteins preferentially produced in response to the Fe-NTA-induced oxidative injury. A single intraperitoneal Fe-NTA treatment led to the enhanced production of a number of proteins with molecular masses of 85-95 kDa. These included heat shock protein 90 (HSP90) as determined by immunoprecipitation. The enhanced production of HSP90 was prominent in the renal tubular cells. Steady accumulation of HSP90 was observed in the subacute toxicity experiments with multiple injections of Fe-NTA, suggesting that the enhanced production of HSP90 is important in increasing resistance to subsequent injury caused by the Fe-NTA-induced oxidative stress.

Authors+Show Affiliations

Laboratory of Food and Biodynamics, Nagoya University School of Agriculture, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

8619831

Citation

Fukuda, A, et al. "Oxidative Stress Response in Iron-induced Acute Nephrotoxicity: Enhanced Expression of Heat Shock Protein 90." Biochemical and Biophysical Research Communications, vol. 219, no. 1, 1996, pp. 76-81.
Fukuda A, Osawa T, Oda H, et al. Oxidative stress response in iron-induced acute nephrotoxicity: enhanced expression of heat shock protein 90. Biochem Biophys Res Commun. 1996;219(1):76-81.
Fukuda, A., Osawa, T., Oda, H., Tanaka, T., Toyokuni, S., & Uchida, K. (1996). Oxidative stress response in iron-induced acute nephrotoxicity: enhanced expression of heat shock protein 90. Biochemical and Biophysical Research Communications, 219(1), 76-81.
Fukuda A, et al. Oxidative Stress Response in Iron-induced Acute Nephrotoxicity: Enhanced Expression of Heat Shock Protein 90. Biochem Biophys Res Commun. 1996 Feb 6;219(1):76-81. PubMed PMID: 8619831.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidative stress response in iron-induced acute nephrotoxicity: enhanced expression of heat shock protein 90. AU - Fukuda,A, AU - Osawa,T, AU - Oda,H, AU - Tanaka,T, AU - Toyokuni,S, AU - Uchida,K, PY - 1996/2/6/pubmed PY - 1996/2/6/medline PY - 1996/2/6/entrez SP - 76 EP - 81 JF - Biochemical and biophysical research communications JO - Biochem Biophys Res Commun VL - 219 IS - 1 N2 - Iron overload with ferric nitrilotriacetate (Fe-NTA) induces acute renal proximal tubular necrosis, a consequence of oxidative tissue damage, that leads to a high incidence of renal adenocarcinoma in rodents. In the present study, we determined the proteins preferentially produced in response to the Fe-NTA-induced oxidative injury. A single intraperitoneal Fe-NTA treatment led to the enhanced production of a number of proteins with molecular masses of 85-95 kDa. These included heat shock protein 90 (HSP90) as determined by immunoprecipitation. The enhanced production of HSP90 was prominent in the renal tubular cells. Steady accumulation of HSP90 was observed in the subacute toxicity experiments with multiple injections of Fe-NTA, suggesting that the enhanced production of HSP90 is important in increasing resistance to subsequent injury caused by the Fe-NTA-induced oxidative stress. SN - 0006-291X UR - https://www.unboundmedicine.com/medline/citation/8619831/Oxidative_stress_response_in_iron_induced_acute_nephrotoxicity:_enhanced_expression_of_heat_shock_protein_90_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-291X(96)90184-9 DB - PRIME DP - Unbound Medicine ER -