3-nitrotyrosine and Ventricular-Dysfunction

3-nitrotyrosine has been researched along with Ventricular-Dysfunction* in 2 studies

Other Studies

2 other study(ies) available for 3-nitrotyrosine and Ventricular-Dysfunction

ArticleYear
Polyphenol-Rich Fraction of Parquetina nigrescens Mitigates Dichlorvos-Induced Cardiorenal Dysfunction Through Reduction in Cardiac Nitrotyrosine and Renal p38 Expressions in Wistar Rats.
    Journal of dietary supplements, 2018, May-04, Volume: 15, Issue:3

    Parquetina nigrescens is commonly used to treat diseases in humans and animals in developing countries, including Nigeria. This study evaluates the effects of its polyphenol-rich fraction (prf) on dichlorvos-induced cardio- and renal toxicity. There were several factors assessed during this study, including cardiac and renal markers, serum myeloperoxidase and xanthine oxidase, and electrocardiograph (ECG) changes. The changes in electrocardiograph (ECG) were recorded. Immunohistochemistry of cardiac and renal p38 and nitrotyrosine was determined. Dichlorvos exposure caused a significant decrease in L-glutathione (reduced glutathione) and other antioxidant enzymes with increases in malondialdehyde, myeloperoxidase, advanced oxidation protein products, and protein carbonyl levels. It also brought about alterations in microanatomy of the heart and kidneys accompanied by increases in serum creatinine and urea levels. Exposure to dichlorvos induced prolonged QRS interval and shortened QT durations in rats. Immunohistochemistry revealed lower expressions of cardiac nitrotyrosine and renal p38 (mitogen-activated protein kinase; MAPK) in rats treated with prf of P. nigrescens. Combining all, prf of P. nigrescens demonstrated antioxidant as well as protective properties in the heart and kidneys of rats exposed to dichlorvos. It ameliorated dichlorvos-induced cardio- and nephrotoxicity giving credence to its use in ethnomedicine.

    Topics: Administration, Oral; Animals; Biomarkers; Cryptolepis; Dichlorvos; Dietary Supplements; Heart Ventricles; Insecticides; Kidney; Male; Nigeria; Organophosphate Poisoning; p38 Mitogen-Activated Protein Kinases; Plant Components, Aerial; Plant Extracts; Polyphenols; Protective Agents; Random Allocation; Rats, Wistar; Renal Insufficiency; Tyrosine; Ventricular Dysfunction

2018
Oxidative stress-mediated cardiac cell death is a major determinant of ventricular dysfunction and failure in dog dilated cardiomyopathy.
    Circulation research, 2001, Aug-03, Volume: 89, Issue:3

    Cell death has been questioned as a mechanism of ventricular failure. In this report, we tested the hypothesis that apoptotic death of myocytes, endothelial cells, and fibroblasts is implicated in the development of the dilated myopathy induced by ventricular pacing. Accumulation of reactive oxygen products such as nitrotyrosine, potentiation of the oxidative stress response by p66(shc) expression, formation of p53 fragments, release of cytochrome c, and caspase activation were examined to establish whether these events were coupled with apoptotic cell death in the paced dog heart. Myocyte, endothelial cell, and fibroblast apoptosis was detected before indices of severe impairment of cardiac function became apparent. Cell death increased with the duration of pacing, and myocyte death exceeded endothelial cell and fibroblast death throughout. Nitrotyrosine formation and p66(shc) levels progressively increased with pacing and were associated with cell apoptosis. Similarly, p50 (DeltaN) fragments augmented paralleling the degree of cell death in the failing heart. Moreover, cytochrome c release and activation of caspase-9 and -3 increased from 1 to 4 weeks of pacing. In conclusion, cardiac cell death precedes ventricular decompensation and correlates with the time-dependent deterioration of function in this model. Oxidative stress may be critical for activation of apoptosis in the overloaded heart.

    Topics: Adaptor Proteins, Signal Transducing; Adaptor Proteins, Vesicular Transport; Animals; Apoptosis; Blotting, Western; Cardiac Pacing, Artificial; Cardiomyopathy, Dilated; Caspase 3; Caspase 9; Caspases; Cytochrome c Group; Disease Models, Animal; Dogs; Enzyme Activation; Hemodynamics; Immunohistochemistry; In Situ Nick-End Labeling; Myocardium; Oxidative Stress; Protein Biosynthesis; Reactive Oxygen Species; Shc Signaling Adaptor Proteins; Tumor Suppressor Protein p53; Tyrosine; Ventricular Dysfunction

2001
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