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Decreased complex II respiration and HNE-modified SDH subunit in diabetic heart.

Authors: Lashin, OM  Szweda, PA  Szweda, LI  Romani, AM 
Citation: Lashin OM, etal., Free Radic Biol Med. 2006 Mar 1;40(5):886-96. Epub 2005 Nov 2.
Pubmed: (View Article at PubMed) PMID:16520240
DOI: Full-text: DOI:10.1016/j.freeradbiomed.2005.10.040

Several lines of research suggest that mitochondria play a role in the etiopathogenesis of diabetic cardiomyopathy, although the mechanisms involved are still debated. In the present study, we report that State 3 oxygen consumption decreases by approximately 35% with glutamate and by approximately 30% with succinate in mitochondria from diabetic rat hearts compared to controls. In these mitochondria the enzymatic activities of complex I and complex II are also decreased to a comparable extent. Western blot analysis of mitochondrial protein pattern using antibodies recognizing proteins modified by the lipid peroxidation product 4-hydroxynonenal indicates the FAD-containing subunit of succinate dehydrogenase as one of the targets of this highly reactive aldehyde. In rats diabetic for 6 or 12 weeks, insulin supplementation for 2 weeks decreases the level of protein modified by 4-hydroxynonenal and restores mitochondrial respiration and enzyme activity to control level. Taken together, these results: (1) indicate that 4-hydroxynonenal is endogenously produced within diabetic mitochondria and forms an adduct with selective mitochondrial proteins, (2) identify one of these proteins as a subunit of succinate dehydrogenase, and (3) provide strong evidence that insulin treatment can reverse and ameliorate free radical damage and mitochondrial function under diabetic conditions.


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CRRD Object Information
CRRD ID: 2306906
Created: 2009-05-12
Species: All species
Last Modified: 2009-05-12
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.