PMID: 9538944Apr 16, 1998Paper

Carbon monoxide induces murine thymocyte apoptosis by a free radical-mediated mechanism

Cell Biology and Toxicology
V TurcanuP Poindron

Abstract

Carbon monoxide (CO) induces acute or chronic toxicity, according to the level and duration of the exposure. Since chronic CO exposure was shown to have immunosuppressive effects (as it decreases the frequency of rat splenic immunocompetent cells and immunoglobulin production), we investigated the effect of CO on thymocytes, since these are the most sensitive cells to oxidative damage from the lymphoid lineage. We exposed thymocytes to CO, then determined their apoptotic index after 6 h of incubation at 37 degrees C using the fluorochrome Hoechst 33342 and electron microscopy and found an increase of apoptosis in CO-exposed thymocytes. Trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid), an antioxidant vitamin E analog, decreased CO-induced thymocyte apoptosis unlike methylene blue, L-nitroarginine methyl ester or pyrrolidine dithiocarbamate. We also observed that lipid peroxidation was increased in the CO-exposed thymocytes and that it was inhibited by Trolox. Our results suggest that CO induces thymocyte apoptosis by a free radical-mediated mechanism which can be inhibited by Trolox but which does not involve the activation of the guanylyl cyclase-cGMP pathway.

Citations

Jul 9, 2009·Acta Veterinaria Hungarica·Sándor György FeketeRóbert Glávits
May 16, 2012·European Journal of Immunology·Zsuzsa SzondyKrisztina Köröskényi
Apr 24, 2003·Experimental Biology and Medicine·Xiao-Ming LiuWilliam Durante
Aug 19, 2007·American Journal of Respiratory and Critical Care Medicine·Ramona O HopkinsJohn Carlquist
Jan 22, 2008·Free Radical Biology & Medicine·Laura Conde de la RosaHan Moshage

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