Next Article in Journal
Chemometric Analysis of the Amino Acid Requirements of Antioxidant Food Protein Hydrolysates
Next Article in Special Issue
p66Shc Aging Protein in Control of Fibroblasts Cell Fate
Previous Article in Journal
Inflammation, Oxidative Stress, and Obesity
Int. J. Mol. Sci. 2011, 12(5), 3133-3147; doi:10.3390/ijms12053133

Impaired Mitochondrial Respiratory Functions and Oxidative Stress in Streptozotocin-Induced Diabetic Rats

1,* , 2
1 Department of Biochemistry, Faculty of Medicine and Health Sciences, UAE University, Al Ain, United Arab Emirates 2 Department of Animal Biology, School of Veterinary Medicine, 3800 Spruce Street, University of Pennsylvania, Philadelphia, PA 19104, USA
* Authors to whom correspondence should be addressed.
Received: 14 March 2011 / Revised: 11 April 2011 / Accepted: 29 April 2011 / Published: 13 May 2011
(This article belongs to the Special Issue Oxidative Stress and Mitochondria)
View Full-Text   |   Download PDF [430 KB, 19 June 2014; original version 19 June 2014]   |   Browse Figures


We have previously shown a tissue-specific increase in oxidative stress in the early stages of streptozotocin (STZ)-induced diabetic rats. In this study, we investigated oxidative stress-related long-term complications and mitochondrial dysfunctions in the different tissues of STZ-induced diabetic rats (>15 mM blood glucose for 8 weeks). These animals showed a persistent increase in reactive oxygen and nitrogen species (ROS and RNS, respectively) production. Oxidative protein carbonylation was also increased with the maximum effect observed in the pancreas of diabetic rats. The activities of mitochondrial respiratory enzymes ubiquinol: cytochrome c oxidoreductase (Complex III) and cytochrome c oxidase (Complex IV) were significantly decreased while that of NADH:ubiquinone oxidoreductase (Complex I) and succinate:ubiquinone oxidoreductase (Complex II) were moderately increased in diabetic rats, which was confirmed by the increased expression of the 70 kDa Complex II sub-unit. Mitochondrial matrix aconitase, a ROS sensitive enzyme, was markedly inhibited in the diabetic rat tissues. Increased expression of oxidative stress marker proteins Hsp-70 and HO-1 was also observed along with increased expression of nitric oxide synthase. These results suggest that mitochondrial respiratory complexes may play a critical role in ROS/RNS homeostasis and oxidative stress related changes in type 1 diabetes and may have implications in the etiology of diabetes and its complications.
Keywords: diabetes; oxidative stress; ROS; NO; mitochondrial respiration diabetes; oxidative stress; ROS; NO; mitochondrial respiration
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Share & Cite This Article

Further Mendeley | CiteULike
Export to BibTeX |
MDPI and ACS Style

Raza, H.; Prabu, S.K.; John, A.; Avadhani, N.G. Impaired Mitochondrial Respiratory Functions and Oxidative Stress in Streptozotocin-Induced Diabetic Rats. Int. J. Mol. Sci. 2011, 12, 3133-3147.

View more citation formats

Related Articles

Article Metrics

For more information on the journal, click here


Cited By

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert