AJP - Renal AJP: Lung Cellular and Molecular Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol 250: F991-F998, 1986;
0363-6127/86 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gordon, J. A.
Right arrow Articles by Gattone, V. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gordon, J. A.
Right arrow Articles by Gattone, V. H., 2nd

AJP - Renal Physiology, Vol 250, Issue 6 991-F998, Copyright © 1986 by American Physiological Society

ARTICLES

Mitochondrial alterations in cisplatin-induced acute renal failure

J. A. Gordon and V. H. Gattone 2nd

The mild reversible nonoliguric form of acute renal failure is perhaps the most common of many nephrotoxic side effects that occur secondary to cisplatin administration. The present studies were undertaken to gain insight into mitochondria alterations and morphological abnormalities underlying this form of renal failure. Following a single intraperitoneal injection of 5.5 mg/kg body wt of cisplatin changes in renal function, mitochondrial respiration, and calcium accumulation were measured serially over a 9-day period. Results indicate that reversible functional changes secondary to cisplatin are accompanied by changes in mitochondrial respiration and calcium accumulation. A decline in state 3 mitochondrial respiration precedes mitochondrial calcium accumulation. However, calcium accumulation begins to recover before mitochondrial respiration. At the peak of functional and biochemical injury morphological damage is extensive, and mitochondria are strikingly aberrant. The results demonstrate that changes in mitochondrial respiration and calcium accumulation occur secondary to cisplatin administration. Both of these effects may play a role in the renal cellular injury induced by cisplatin.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
F. Yu, J. Megyesi, and P. M. Price
Cytoplasmic initiation of cisplatin cytotoxicity
Am J Physiol Renal Physiol, July 1, 2008; 295(1): F44 - F52.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
F. Yu, J. Megyesi, R. L. Safirstein, and P. M. Price
Involvement of the CDK2-E2F1 pathway in cisplatin cytotoxicity in vitro and in vivo
Am J Physiol Renal Physiol, July 1, 2007; 293(1): F52 - F59.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
C. Yang, V. Kaushal, S. V. Shah, and G. P. Kaushal
Mcl-1 is downregulated in cisplatin-induced apoptosis, and proteasome inhibitors restore Mcl-1 and promote survival in renal tubular epithelial cells
Am J Physiol Renal Physiol, June 1, 2007; 292(6): F1710 - F1717.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
W. Qian, M. Nishikawa, A. Md. Haque, M. Hirose, M. Mashimo, E. Sato, and M. Inoue
Mitochondrial density determines the cellular sensitivity to cisplatin-induced cell death
Am J Physiol Cell Physiol, December 1, 2005; 289(6): C1466 - C1475.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online