Production of Reactive Oxygen Species by Mitochondria
- Qun Chen, Edwin J. Vazquez, S. Moghaddas, C. Hoppel, E. Lesnefsky
- BiologyJournal of Biological Chemistry
- 19 September 2003
Limitation of electron transport by the inhibitor rotenone immediately before ischemia decreases the production of ROS in cardiac myocytes and reduces damage to mitochondria, and blockade of complex I with roten one markedly increased H2O2 production from submitochondrial particles oxidizing the complex I substrate NADH.
Biochemical properties of subsarcolemmal and interfibrillar mitochondria isolated from rat cardiac muscle.
Fatty acid import into mitochondria.
Plasma acylcarnitine profiles suggest incomplete long-chain fatty acid beta-oxidation and altered tricarboxylic acid cycle activity in type 2 diabetic African-American women.
Results are consistent with the working hypothesis that inefficient tissue LCFA beta-oxidation, due in part to a relatively low tricarboxylic acid cycle capacity, increases tissue accumulation of acetyl-CoA and generates chain-shortened acylcarnitine molecules that activate proinflammatory pathways implicated in insulin resistance.
Mitochondrial dysfunction in cardiac disease: ischemia--reperfusion, aging, and heart failure.
- E. Lesnefsky, S. Moghaddas, B. Tandler, J. Kerner, C. Hoppel
- Biology, MedicineJournal of Molecular and Cellular Cardiology
- 1 June 2001
Mechanisms of mitochondrial-derived myocyte injury and the involvement of mitochondria in the pathogenesis of specific cardiac disease states (ischemia, reperfusion, aging, ischemic preconditioning, and cardiomyopathy) are addressed.
Ischemic defects in the electron transport chain increase the production of reactive oxygen species from isolated rat heart mitochondria.
- Qun Chen, S. Moghaddas, C. Hoppel, E. Lesnefsky
- BiologyAmerican Journal of Physiology - Cell Physiology
- 1 February 2008
Findings support that mitochondrial damage occurs during ischemia and contributes to myocardial injury during reperfusion and sets the stage for an increase in ROS production during reperFusion as a mechanism of cardiac injury.
Plasma Metabolomic Profiles Reflective of Glucose Homeostasis in Non-Diabetic and Type 2 Diabetic Obese African-American Women
This work examined differences in plasma concentrations of >350 metabolites in fasted obese T2DM vs. obese non-diabetic African-American women, and utilized principal components analysis to identify 158 metabolite components that strongly correlated with fasting HbA1c over a broad range of the latter.
Carnitine: a nutritional, biosynthetic, and functional perspective.
Cardiac mitochondria in heart failure: decrease in respirasomes and oxidative phosphorylation
It is proposed that the mitochondrial defect lies in the supermolecular assembly rather than in the individual components of the ETC, the major form of respirasome considered essential for oxidative phosphorylation.
A mitochondrial enzyme degrades carotenoids and protects against oxidative stress
The studies in BCDO2‐deficient mice and human cell cultures indicate that carotenoids can impair respiration and induce oxidative stress, and Mammalian cells thus express a mitochondrial carOTenoid‐oxygenase that degrades carotanoids to protect these vital organelles.