Premium
Hyperglycemia compromises mitochondrial function
Author(s) -
Edwards John G.,
Medikayala Sushma,
Zhao Xiangmin
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1226.50
Subject(s) - mitochondrion , oxidative stress , medicine , endocrinology , cytochrome c , oxidative phosphorylation , myocyte , extracellular , chemistry , biology , microbiology and biotechnology , biochemistry
Mitochondrial dysfunction has a significant role in the development and complications of diabetic cardiomyopathy. Hyperglycemia‐induced mitochondrial oxidative stress has been suggested as one contributing factor. The impact of hyperglycemia was studied using H9c2 myotubes (a cardiac‐derived cell line) and Cyt C‐ cells (an embryonic cell line having reduced levels of cytochrome C). Cells were maintained in the presence of 5.5, 16.5, or 35.0 mM glucose for up to 13 days. Hyperglycemia significantly increased protein levels in the Cyt C‐ cells but not the H9c2 cells. Functional tests of mitochondria (succinate dehydrogenase and ATP generation) suggested that although the H9c2 myotubes were sensitive to hyperglycemia, the Cyt C‐ cells were not. Hyperglycemia did not significantly alter generation of extracellular H 2 O 2 in either cell line. However, intramitochondrial superoxide (mtSO) levels (detected using MitoSox) was increased in the H9c2 cells following 13 days of hyperglycemia. Conversely, up to13 days of hyperglycemia did not significantly altered mtSO levels in the Cyt C‐ cells. Hyperglycemia increased H9c2 caspase 3/7 activity that appeared to track mtSO levels. These results suggest that mitochondrial function may be compromised by hyperglycemia as a consequence of altered intramitochondrial oxidative stress. Supported in part by the New York Medical College Research Endowment Fund.