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Evan D. Kharasch – One of the best experts on this subject based on the ideXlab platform.

Thomas A Baillie – One of the best experts on this subject based on the ideXlab platform.

  • identification in rat bile of glutathione conjugates of Fluoromethyl 2 2 diFluoro 1 triFluoromethyl vinyl ether a nephrotoxic degradate of the anesthetic agent sevoflurane
    Chemical Research in Toxicology, 1996
    Co-Authors: Margaret R Davis, Evan D. Kharasch, George A Doss, Thomas A Baillie
    Abstract:

    Recent studies have indicated that the nephrotoxicity of Fluoromethyl 2,2-diFluoro1-(triFluoromethyl)vinyl ether (“Compound A”), a breakdown product of the inhaled anesthetic sevoflurane, may be mediated by a reactive intermediate(s) generated via the cysteine conjugate β-lyase pathway. In order to gain a better understanding of glutathione (GSH)-dependent metabolism of Compound A, the present study was carried out with the primary goal of detecting and characterizing Compound A−GSH conjugates. By means of ionspray LC-MS/MS and NMR spectroscopy, a total of four GSH conjugates (“A1−A4”) were identified from the bile of rats dosed intraperitoneally with Compound A. A1 and A2 were identified as two diastereomers of S-[1,1-diFluoro2-(Fluoromethoxy)-2-(triFluoromethyl)ethyl]glutathione, while A3 and A4 were identified as (E)- and (Z)-S-[1Fluoro2-(Fluoromethoxy)-2-(triFluoromethyl)vinyl]glutathione, respectively. Quantitative analyses indicated that approximately 29% of the administered dose of Compound A w…

Bruno Miguel Neves – One of the best experts on this subject based on the ideXlab platform.

  • oxidative stress dependent activation of the eif2α atfr unfolded protein response branch by skin sensitizer 1 Fluoro 2 4 dinitrobenzene modulates dendritic like cell maturation and inflammatory status in a biphasic manner
    Free Radical Biology and Medicine, 2014
    Co-Authors: Andreia Luis, Bruno Miguel Neves, Joao D Martins, Ana Maria Silva, Isabel C F R Ferreira, Maria Teresa Cruz
    Abstract:

    Abstract The pathogenesis of allergic contact dermatitis, the most common manifestation of immunotoxicity in humans, is intimately connected to hapten-induced maturation of dendritic cells (DC). The molecular mechanisms driving this maturational program are not completely known; however, initial danger signals such as the generation of reactive oxygen species (ROS) were shown to play a critical role. Recent evidence linking ROS production, endoplasmic retireticulum (ER) stress, and the pathogenesis of several inflammatory diseases led us to analyze, in the present work, the ability of the skin sensitizer 1Fluoro2,4-dinitrobenzene (DNFB) to evoke ER stress in DC-like THP-1 cells and the concomitant consequences to their immunobiology. We found that DNFB triggers a ROS-dependent activation of the PERK–eIFα–ATF4 unfolded protein response (UPR) branch conferring cytoprotection and modulating the maturation/proinflammatory cell status in a biphasic manner. Early DNFB induction of ATF4 positively modulates autophagy-related genes MAP 1 LC 3 B and ATG 3 and stabilizes the transcription factor Nrf2, causing a strong induction of the HMOX 1-detoxifying gene. Moreover, we observed that in a first phase, DNFB-induced ATF4 upregulates IL 8 mRNA levels while blocking CD 86, IL 1 B , IL 12 B , and CXL 10 transcription. Later, following ATF4 decay, HMOX 1 and IL 8 transcription drastically decrease and CD 86, IL 1 B , and Il 12 B are upregulated. Overall, our results evidence a connection between sensitizer-induced redox imbalance and the establishment of ER stress in DC-like cells and provide new insights into the role of UPR effectors such as ATF4 to the complex DC maturational program.

Margaret R Davis – One of the best experts on this subject based on the ideXlab platform.

  • identification in rat bile of glutathione conjugates of Fluoromethyl 2 2 diFluoro 1 triFluoromethyl vinyl ether a nephrotoxic degradate of the anesthetic agent sevoflurane
    Chemical Research in Toxicology, 1996
    Co-Authors: Margaret R Davis, Evan D. Kharasch, George A Doss, Thomas A Baillie
    Abstract:

    Recent studies have indicated that the nephrotoxicity of Fluoromethyl 2,2-diFluoro1-(triFluoromethyl)vinyl ether (“Compound A”), a breakdown product of the inhaled anesthetic sevoflurane, may be mediated by a reactive intermediate(s) generated via the cysteine conjugate β-lyase pathway. In order to gain a better understanding of glutathione (GSH)-dependent metabolism of Compound A, the present study was carried out with the primary goal of detecting and characterizing Compound A−GSH conjugates. By means of ionspray LC-MS/MS and NMR spectroscopy, a total of four GSH conjugates (“A1−A4”) were identified from the bile of rats dosed intraperitoneally with Compound A. A1 and A2 were identified as two diastereomers of S-[1,1-diFluoro2-(Fluoromethoxy)-2-(triFluoromethyl)ethyl]glutathione, while A3 and A4 were identified as (E)- and (Z)-S-[1Fluoro2-(Fluoromethoxy)-2-(triFluoromethyl)vinyl]glutathione, respectively. Quantitative analyses indicated that approximately 29% of the administered dose of Compound A w…

T. Gul Altuntas – One of the best experts on this subject based on the ideXlab platform.

  • Sulfoxidation of Cysteine and Mercapturic Acid Conjugates of the Sevoflurane Degradation Product Fluoromethyl-2,2-diFluoro1-(triFluoromethyl)vinyl Ether (Compound A)
    Chemical Research in Toxicology, 2004
    Co-Authors: T. Gul Altuntas, Sang B. Park, Evan D. Kharasch
    Abstract:

    The volatile anesthetic sevoflurane is degraded in anesthesia machines to the haloalkene Fluoromethyl-2,2-diFluoro1-(triFluoromethyl)vinyl ether (FDVE), which can cause renal and hepatic toxicity in rats. FDVE is metabolized to S-[1,1-diFluoro2Fluoromethoxy-2-(triFluoromethyl)ethyl]-l-cysteine (DFEC) and (E) and (Z)-S-[1Fluoro2Fluoromethoxy-2-(triFluoromethyl)vinyl]-l-cysteine [(E,Z)-FFVC], which are N-acetylated to N-Ac-DFEC and (E,Z)-N-Ac-FFVC S-conjugates. Some haloalkene S-conjugates undergo sulfoxidation. This investigation tested the hypothesis that FDVE S-conjugates can also undergo sulfoxidation, by evaluating sulfoxide formation by human and rat liver and kidney microsomes and expressed P450s and flavin monooxygenases. Rat, and at lower rates human, liver microsomes oxidized (Z)-N-Ac-FFVC and N-Ac-DFEC to the corresponding sulfoxides. Much lower rates of (Z)-N-Ac-FFVC, but not N-Ac-DFEC, sulfoxidation occurred with rat and human kidney microsomes. In human liver microsomes, the P450 inhibit…