Carvedilol protects against apoptotic cell death induced by cisplatin in renal tubular epithelial cells

Carvalho Rodrigues, M. A., Gobe, G., Santos, N. A. G. and Santos, A. C. (2012) Carvedilol protects against apoptotic cell death induced by cisplatin in renal tubular epithelial cells. Journal of Toxicology and Environmental Health Part A: Current Issues, 75 16-17: 981-990. doi:10.1080/15287394.2012.696512


Author Carvalho Rodrigues, M. A.
Gobe, G.
Santos, N. A. G.
Santos, A. C.
Title Carvedilol protects against apoptotic cell death induced by cisplatin in renal tubular epithelial cells
Journal name Journal of Toxicology and Environmental Health Part A: Current Issues   Check publisher's open access policy
ISSN 1528-7394
1087-2620
Publication date 2012-08-15
Year available 2011
Sub-type Article (original research)
DOI 10.1080/15287394.2012.696512
Open Access Status Not yet assessed
Volume 75
Issue 16-17
Start page 981
End page 990
Total pages 10
Editor Wilma Kempinas
Fernando Barbosa
Place of publication Philadelphia, PA, United States
Publisher Taylor & Francis
Language eng
Subject 2307 Health, Toxicology and Mutagenesis
3005 Toxicology
Abstract Cisplatin is a highly effective chemotherapeutic drug; however, its use is limited by nephrotoxicity. Studies showed that the renal injury produced by cisplatin involves oxidative stress and cell death mediated by apoptosis and necrosis in proximal tubular cells. The use of antioxidants to decrease cisplatin-induced renal cell death was suggested as a potential therapeutic measure. In this study the possible protective effects of carvedilol, a beta blocker with antioxidant activity, was examined against cisplatin-induced apoptosis in HK-2 human kidney proximal tubular cells. The mitochondrial events involved in this protection were also investigated. Four groups were used: controls (C), cisplatin alone at 25 mu M (CIS), cisplatin 25 mu M plus carvedilol 50 mu M (CV + CIS), and carvedilol alone 50 mu M (CV). Cell viability, apoptosis, caspase-9, and caspase-3 were determined. Data demonstrated that carvedilol effectively increased cell viability and minimized caspase activation and apoptosis in HK-2 cells, indicating this may be a promising drug to reduce nephrotoxicity induced by cisplatin.
Formatted abstract
Cisplatin is a highly effective chemotherapeutic drug; however, its use is limited by nephrotoxicity. Studies showed that the renal injury produced by cisplatin involves oxidative stress and cell death mediated by apoptosis and necrosis in proximal tubular cells. The use of antioxidants to decrease cisplatin-induced renal cell death was suggested as a potential therapeutic measure. In this study the possible protective effects of carvedilol, a beta blocker with antioxidant activity, was examined against cisplatin-induced apoptosis in HK-2 human kidney proximal tubular cells. The mitochondrial events involved in this protection were also investigated. Four groups were used: controls (C), cisplatin alone at 25 μM (CIS), cisplatin 25 μM plus carvedilol 50 μM (CV + CIS), and carvedilol alone 50 μM (CV). Cell viability, apoptosis, caspase-9, and caspase-3 were determined. Data demonstrated that carvedilol effectively increased cell viability and minimized caspase activation and apoptosis in HK-2 cells, indicating this may be a promising drug to reduce nephrotoxicity induced by cisplatin.
Keyword Environmental Sciences
Public, Environmental & Occupational Health
Toxicology
Environmental Sciences & Ecology
Public, Environmental & Occupational Health
Toxicology
ENVIRONMENTAL SCIENCES
PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH, SCI
TOXICOLOGY
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ
Additional Notes Special Issue: "Selected papers from the 17th Brazilian Congress of Toxicology, 2011" (XVII Congresso Brasileiro de Toxicologia, Ribeirão Preto, São Paulo, Brazil, 22-25 June, 2011).

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Medicine Publications
 
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