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Production of Reactive Oxygen Species by Mitochondria
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.
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.
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.
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.
Ischemic defects in the electron transport chain increase the production of reactive oxygen species from isolated rat heart mitochondria.
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.
Carnitine: a nutritional, biosynthetic, and functional perspective.
Direct Inhibition of Mitochondrial Respiratory Chain Complex III by Cell-permeable Ceramide*
It is demonstrated that ceramide can directly inhibit mitochondrial respiratory chain function in isolated mitochondria, and suggested that these in vitro observations may set the stage for identifying a novel mechanism of regulation of mitochondrial function in vivo.
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.