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Mitochondrial membrane fluidity, potential, and calcium transients in the myocardium from acute diabetic rats
I Waczulikova, D Habodaszova, M Cagalinec, M Ferko, O Ulicna, A Mateasik, L Sikurova, A Ziegelhoffer
Language English Country Canada
NLK
ProQuest Central
from 1998-01-01 to 2007-05-31
Medline Complete (EBSCOhost)
from 2001-01-01 to 1 year ago
Nursing & Allied Health Database (ProQuest)
from 1998-01-01 to 2007-05-31
Health & Medicine (ProQuest)
from 1998-01-01 to 2007-05-31
- MeSH
- Diabetes Mellitus, Experimental metabolism physiopathology MeSH
- Financing, Organized MeSH
- Membrane Fluidity MeSH
- Myocytes, Cardiac metabolism MeSH
- Rats MeSH
- Cells, Cultured MeSH
- Membrane Potential, Mitochondrial MeSH
- Mitochondrial Membranes physiology MeSH
- Myocardium metabolism MeSH
- Oxidative Phosphorylation MeSH
- Rats, Wistar MeSH
- Oxygen Consumption MeSH
- Heart physiopathology MeSH
- Heart Ventricles cytology MeSH
- Mitochondria, Heart physiology MeSH
- Calcium physiology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
In this study, we report for the first time concurrent measurements of membrane potential and dynamics and respiratory chain activities in rat heart mitochondria, as well as calcium transients in the hearts of rats in an early phase of streptozotocin diabetes, not yet accompanied with diabetes-induced complications. Quantitative relationships among these variables were assessed. The mitochondria from diabetic rats exhibited decreased fluorescence anisotropy values of diphenylhexatriene. This indicates that hydrophobic core of the membranes was more fluid compared with controls (p<0.05). We discuss the changes in fluidity as having been associated with augmented energy transduction through the diabetic membranes. Reduced ratio of JC-1 fluorescence (aggregates to monomers) in the mitochondria from diabetic hearts reflected descendent transmembrane potential. A significant negative association between membrane fluidity and potential in the diabetic group was found (p<0.05; r=0.67). Further, we observed an increase in calcium transient amplitude (CTA) in the diabetic cardiomyocytes (p=0.048). We conclude that some of the calcium-induced regulatory events that dictate fuel selection and capacity for ATP production in diabetic heart occur at the membrane level. Our findings offer new insight into acute diabetes-induced changes in cardiac mitochondria.
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- $a Mitochondrial membrane fluidity, potential, and calcium transients in the myocardium from acute diabetic rats / $c I Waczulikova, D Habodaszova, M Cagalinec, M Ferko, O Ulicna, A Mateasik, L Sikurova, A Ziegelhoffer
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- $a Department of Nuclear Physics and Biophysics, Division of Biomedical Physics, Faculty of Mathematics, Physics, and Informatics, Comenius University, Mlynska dolina F1, 842 48 Bratislava, Slovak Republic. waczulikova@fmph.uniba.sk
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- $a In this study, we report for the first time concurrent measurements of membrane potential and dynamics and respiratory chain activities in rat heart mitochondria, as well as calcium transients in the hearts of rats in an early phase of streptozotocin diabetes, not yet accompanied with diabetes-induced complications. Quantitative relationships among these variables were assessed. The mitochondria from diabetic rats exhibited decreased fluorescence anisotropy values of diphenylhexatriene. This indicates that hydrophobic core of the membranes was more fluid compared with controls (p<0.05). We discuss the changes in fluidity as having been associated with augmented energy transduction through the diabetic membranes. Reduced ratio of JC-1 fluorescence (aggregates to monomers) in the mitochondria from diabetic hearts reflected descendent transmembrane potential. A significant negative association between membrane fluidity and potential in the diabetic group was found (p<0.05; r=0.67). Further, we observed an increase in calcium transient amplitude (CTA) in the diabetic cardiomyocytes (p=0.048). We conclude that some of the calcium-induced regulatory events that dictate fuel selection and capacity for ATP production in diabetic heart occur at the membrane level. Our findings offer new insight into acute diabetes-induced changes in cardiac mitochondria.
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