Anti-TFEC (aa 217-228) polyclonal antibody

Fluorinated carbonates such as fluoroethylene carbonate (FEC) and di-2,2,2-trifluoroethyl carbonate (TFEC) improve cycling performance and decrease parasitic reactions at high potentials. However they also decrease cell life at lower voltage ranges compared to typical organic carbonate solvents. A method of quantifying the parasitic heat flow during open circuit and voltage hold conditions was implemented using isothermal microcalorimetry on Li-ion pouch cells to investigate the effect of additives in FEC: TFEC (3: 7) and the effects of blending ethylene carbonate (EC): ethylmethyl carbonate (EMC) 3: 7 with FEC: TFEC (3: 7) in order to reduce parasitic reactions during operation at 4.2 V, 4.4 V and 4.6 V. Additives were found to lower parasitic heat flow in FEC: TFEC at all operating potentials, however to less of an effect at 4.6 V. Blending EC: EMC and FEC: TFEC resulted in decreased rates of parasitic reactions at all operating potentials compared to EC: EMC alone. Cells with unblended FEC: TFEC exhibited the lowest parasitic heat flow at 4.4 V and 4.6 V, although they produced more gas than EC: EMC containing blends. This work demonstrates the advantage of blending fluorinated carbonates with traditional solvents, particularly during use at low operating potentials, as well as demonstrating some advantages of fluorinated carbonates for high voltage lithium ion battery applications. (C) 2016 The Electrochemical Society. All rights reserved.

S-(1,1,2.2-Tetrafluoroethyl)-L-cysteine (TFEC), a major metabolite of the industrial gas tetrafluoroethylene, has been shown to mediate nephrotoxicity by necrosis. TFEC-induced cell death is associated with an early covalent modification of specific intramitochondrial proteins; including aconitase, alpha-ketoglutarate dehydrogenase (KGDH) subunits, HSP60 and HSP70. Previous studies have indicated that the TAMH line accurately models TFEC-induced in vivo cell death with dose- and time-dependent inhibitions of both KGDH and aconitase activities. Here, we show that the molecular pathway leading to TFEC-mediated cell death is associated with an early cytosolic to mitochondrial translocation of BAX, a pro-apoptotic member of the BCL-2 family. Immunoblot analyses indicated movement of BAX (21 kDa) to the mitochondrial fraction after exposure to a cytotoxic concentration of TFEC (250 muM). Subsequent cytochrome c release from mitochondria was also demonstrated, but only a modest increase in caspase activities was observed, suggesting a degeneration of early apoptotic signals into secondary necrosis. Significantly, TAMH cells overexpressing BCL-xL preserved cell viability even to supratoxicological concentrations of TFEC (less than or equal to600 muM), and this cytoprotection was associated with decreased HSP70i upregulation, indicating suppression of TFEC-induced proteotoxicity. Hence, TFEC-induced necrotic cell death in the TAMH cell line is mediated by BAX and antagonized by the anti-apoptotic BCL-2 family member, BCL-xL. (C) 2004 Elsevier Inc. All rights reserved.