Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
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 ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (30)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Kawabata, T.
Right arrow Articles by Okada, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kawabata, T.
Right arrow Articles by Okada, S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Carcinogenesis, Vol 18, 1389-1394, Copyright © 1997 by Oxford University Press

ARTICLES

Iron-induced apoptosis in mouse renal proximal tubules after an injection of a renal carcinogen, iron-nitrilotriacetate

T Kawabata, Y Ma, I Yamador and S Okada
Department of Pathology, Okayama University Medical School, Shikata- cho, Japan.

Redox-active iron was demonstrated in mouse kidney by Timm's sulphide- silver staining after an injection of a renal carcinogen, iron- nitrilotriacetate (Fe-NTA). The iron was on the apical site of tubular epithelia of the renal proximal convoluted portion and in the tubules of the straight portion 30 min after the Fe-NTA injection. As the epithelial cells of the proximal tubules died, the iron disappeared in the dead cells and was stored in the cytoplasm of the more distal tubular epithelia. Biochemically, redox-active iron in the kidney rapidly increased to four times higher than the control 30 min after the Fe-NTA injection, then decreased to a plateau which was still higher than the control. Iron tightly stored in iron-storage proteins increased gradually by 3 h after the injection and then decreased at 5 h. The iron-induced free radical injuries, such as lipid peroxidation and protein oxidation, were demonstrated in the renal proximal tubules by histochemistry. The nuclei of the proximal tubular epithelia shrank and fragmented with the free radical injuries, and were positive for terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling. DNA ladder was demonstrated in the mice renal cortexes by agarose gel electrophoresis. It was elucidated that redox-active iron caused free radical injuries in the proximal tubules of mice kidneys after the injection of a renal carcinogenic iron (Fe-NTA) and induced the apoptosis of the proximal tubular epithelial cells.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Toxicol PatholHome page
K. Kanki, T. Umemura, Y. Kitamura, Y. Ishii, Y. Kuroiwa, Y. Kodama, K. Itoh, M. Yamamoto, A. Nishikawa, and M. Hirose
A Possible Role of Nrf2 in Prevention of Renal Oxidative Damage by Ferric Nitrilotriacetate
Toxicol Pathol, February 1, 2008; 36(2): 353 - 361.
[Abstract] [Full Text] [PDF]

Home page
 J. Pharmacol. Exp. Ther.Home page
S.-y. Chen and K. K. Sulik
Iron-Mediated Free Radical Injury in Ethanol-Exposed Mouse Neural Crest Cells
J. Pharmacol. Exp. Ther., July 1, 2000; 294(1): 134 - 140.
[Abstract] [Full Text]

Home page
 CarcinogenesisHome page
S. Ansar, M. Iqbal, and M. Athar
Nordihydroguairetic acid is a potent inhibitor of ferric-nitrilotriacetate-mediated hepatic and renal toxicity, and renal tumour promotion, in mice
Carcinogenesis, April 1, 1999; 20(4): 599 - 606.
[Abstract] [Full Text] [PDF]

Home page
 StrokeHome page
E. H. Lo, P. Bosque-Hamilton, W. Meng, and N. Panahian
Inhibition of Poly(ADP-Ribose) Polymerase : Reduction of Ischemic Injury and Attenuation of N-Methyl-D-Aspartate–Induced Neurotransmitter Dysregulation • Editorial Comment: Reduction of Ischemic Injury and Attenuation of N-Methyl-D-Aspartate–Induced Neurotransmitter Dysregulation
Stroke, April 1, 1998; 29(4): 830 - 836.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.