Overexpression of tumor necrosis factor-α increases production of hydroxyl radical in murine myocardium

Abstract

. Overexpression of tumor necrosis factor-␣ increases production of hydroxyl radical in murine myocardium.

Tumor Necrosis Factor Receptors 1 and 2 Differentially Regulate Survival, Cardiac Dysfunction, and Remodeling in Transgenic Mice With Tumor Necrosis Factor-α–Induced Cardiomyopathy

“…23 Moreover, TNFR2 is expressed broadly in a number of cells, including macrophages and CD4-positive lymphocytes, which constitute most of the infiltrating cells in TG myocardium. 24 However, this increase in cardiac TNFR2 levels is in contrast to the observation that myocardial TNF receptor proteins are downregulated in patients with advanced heart failure. 16 This discrepancy may be explained by differences of species, etiology of heart failure, or severity of myocardial infiltrates.…”

TNF-α dilates cerebral arteries via NAD(P)H oxidase-dependent Ca2+ spark activation

“…In cardiac and endothelial cells, signaling mechanisms for TNF-␣ involve mitochondria (20, 23-25, 35, 36). TNF-␣ disrupted the mitochondrial electron transport chain, caused release of cytochrome c, induced mitochondrial ROS generation, and triggered apoptosis (14,28,30,41,52). Although the downstream intramitochondrial target for TNF-␣ is unclear, PTP involvement was proposed in endothelial cells (52).…”

“…TNF-␣-induced intracellular signaling may involve mitochondrial PTP activation and ceramide generation (14,22,28,30,39,41,52). However, ceramide did not alter transient K Ca currents, indicating that it is unlikely to mediate TNF-␣-induced activation of these events (Fig.…”

“…Because RyR channels are redox sensitive (42), we tested the hypothesis that TNF-␣ regulates local Ca 2ϩ signaling by elevating intracellular ROS. Several enzymes generate ROS including NAD(P)H oxidase, xanthine oxidase, cytochrome P450, and mitochondrial electron transport chain complexes (13,28,41,49). The DCF and DHE fluorescence methods were used to determine the pathways through which TNF-␣ elevates ROS in the smooth muscle cells of small cerebral arteries.…”

Cardioprotective effects of Hypericum triquetrifolium Turra. against cyclophosphamide related cardiotoxicity in rats

“…Reduced GSH has low molecule weight scavenger for free radicals and a significant agent to inhibit the formation free radicals (Figure 7, table 1). The results obtained in the research of Machida et al [35] showed that high dose CYP (200 mg/kg)-caused cardiac toxicity was associated with increment in the reactive species of oxygen while there was a decline in the antioxidative defense systems in myocardium that antioxidative compounds lightened CYP-caused cardiac toxicity. The GSH level was found significantly increased in the 25, 50, 100 mg/kg HT-administered groups compared with group of CYP.…”