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Adriamycin-induced oxidative mitochondrial cardiotoxicity
The anticancer agent Adriamycin (ADR) has long been recognized to induce a dose-limiting cardiotoxicity. Numerous studies have attempted to characterize and elucidate the mechanism(s) behind itsExpand
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Perfluorooctanoate, perflourooctanesulfonate, and N-ethyl perfluorooctanesulfonamido ethanol; peroxisome proliferation and mitochondrial biogenesis.
Compounds that cause peroxisome proliferation in rats and mice have been reported to interfere with mitochondrial (mt) bioenergetics and possibly biogenesis. The purpose of this investigation was toExpand
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Persistent Alterations to the Gene Expression Profile of the Heart Subsequent to Chronic Doxorubicin Treatment
Doxorubicin (DOX, Adriamycin®) is a potent antineoplastic agent used to treat a number of cancers. Despite its utility, DOX causes a cumulative, irreversible cardiomyopathy that may become apparentExpand
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Hyperglycemia decreases mitochondrial function: the regulatory role of mitochondrial biogenesis.
Increased generation of reactive oxygen species (ROS) is implicated in "glucose toxicity" in diabetes. However, little is known about the action of glucose on the expression of transcription factorsExpand
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Role of Receptor Protein Tyrosine Phosphatase γ in Sensing Extracellular CO2 and HCO3.
Regulation of blood pH-critical for virtually every facet of life-requires that the renal proximal tubule (PT) adjust its rate of H(+) secretion (nearly the same as the rate of HCO3 (-) reabsorption,Expand
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Lymphocyte mitochondrial biomarkers in asymptomatic HIV-1-infected individuals treated with nucleoside reverse transcriptase inhibitors.
Mitochondrial toxicity was evaluated in peripheral lymphocytes obtained from a cohort of 10 subjects with extensive exposure to nucleoside reverse transcriptase inhibitors (NRTI) and matchedExpand
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Dietary vitamin E decreases doxorubicin-induced oxidative stress without preventing mitochondrial dysfunction
Doxorubicin (DOX) is a widely prescribed antineoplastic and although the precise mechanism(s) have yet to be identified, DOX-induced oxidative stress to mitochondrial membranes is implicated in theExpand
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Mitochondrial NAD+/NADH Redox State and Diabetic Cardiomyopathy
Abstract Significance: Diabetic cardiomyopathy (DCM) is a frequent complication occurring even in well-controlled asymptomatic diabetic patients, and it may advance to heart failure (HF). RecentExpand
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Changes in myofilament proteins, but not Ca²⁺ regulation, are associated with a high-fat diet-induced improvement in contractile function in heart failure.
Pathological conditions such as diabetes, insulin resistance, and obesity are characterized by elevated plasma and myocardial lipid levels and have been reported to exacerbate the progression ofExpand
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4-Hydroxy-2(E)-nonenal (HNE) catabolism and formation of HNE adducts are modulated by β oxidation of fatty acids in the isolated rat heart.
We previously reported that a novel metabolic pathway functionally catabolizes 4-hydroxy-2(E)-nonenal (HNE) via two parallel pathways, which rely heavily on β-oxidation pathways. The hypothesisExpand
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