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10.1016/j.tox.2014.02.013 http://scihub22266oqcxt.onion/10.1016/j.tox.2014.02.013 C4019690!4019690 !24631667     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24631667 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\24631667 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Toxicology 2014 ; 320 (ä): 25-33 Nephropedia Template TP {{tp|p=24631667 |t=2014. Myeloperoxidase deficiency attenuates nitrogen mustard-induced skin injuries |pdf=|usr=}}{{24631667 }} gab.com Text Myeloperoxidase deficiency attenuates nitrogen mustard-induced skin injuries JO: Toxicology http://www.kidney.de/pget.php?&tw=1&pmid=24631667 #FOAvip The pathologic mechanisms of skin injuries, following the acute inflammatory response induced by vesicating agents sulfur mustard (SM) and nitrogen mustard (NM) exposure, are poorly understood. Neutrophils which accumulate at the site of injury, abundantly express myeloperoxidase (MPO), a heme protein that is implicated in oxidant-related antimicrobial and cytotoxic responses. Our previous studies have shown that exposure to SM analog 2-chloroethyl ethyl sulfide (CEES) or NM results in an inflammatory response including increased neutrophilic infiltration and MPO activity. To further define the role of neutrophil-derived MPO in NM-induced skin injury, here we used a genetic approach and examined the effect of NM exposure (12h and 24h) on previously established injury endpoints in C57BL/6J wild type (WT) and B6.129X1-MPOtm1Lus/J mice (MPO KO), homozygous null for MPO gene. NM exposure caused a significant increase in skin bi-fold thickness, epidermal thickness, microvesication, DNA damage and apoptosis in WT mice compared to MPO KO mice. MPO KO mice showed relatively insignificant effect. Similarly, NM induced increases in the expression of inflammatory and proteolytic mediators, including COX-2, iNOS and MMP-9 in WT mice, while having a significantly lower effect in MPO KO mice. Collectively, these results show that MPO, which generates microbicidal oxidants, plays an important role in NM-induced skin injuries. This suggests the development of mechanism-based treatments against NM- and SM-induced skin injuries that inhibit MPO activity and attenuate MPO-derived oxidants. Twit Text FOAVip Myeloperoxidase deficiency attenuates nitrogen mustard-induced skin injuries ????Toxicology http://www.kidney.de/pget.php?&tw=1&pmid=24631667 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24631667 #FOAvip English Wikipedia <ref>{{Cite pmid|24631667 }}</ref> Myeloperoxidase deficiency attenuates nitrogen mustard-induced skin injuries #MMPMID24631667 Jain AK ; Tewari-Singh N ; Inturi S ; Orlicky DJ ; White CW ; Agarwal R Toxicology 2014[Jun]; 320 (ä): 25-33 PMID24631667 show ga The pathologic mechanisms of skin injuries, following the acute inflammatory response induced by vesicating agents sulfur mustard (SM) and nitrogen mustard (NM) exposure, are poorly understood. Neutrophils which accumulate at the site of injury, abundantly express myeloperoxidase (MPO), a heme protein that is implicated in oxidant-related antimicrobial and cytotoxic responses. Our previous studies have shown that exposure to SM analog 2-chloroethyl ethyl sulfide (CEES) or NM results in an inflammatory response including increased neutrophilic infiltration and MPO activity. To further define the role of neutrophil-derived MPO in NM-induced skin injury, here we used a genetic approach and examined the effect of NM exposure (12h and 24h) on previously established injury endpoints in C57BL/6J wild type (WT) and B6.129X1-MPOtm1Lus/J mice (MPO KO), homozygous null for MPO gene. NM exposure caused a significant increase in skin bi-fold thickness, epidermal thickness, microvesication, DNA damage and apoptosis in WT mice compared to MPO KO mice. MPO KO mice showed relatively insignificant effect. Similarly, NM induced increases in the expression of inflammatory and proteolytic mediators, including COX-2, iNOS and MMP-9 in WT mice, while having a significantly lower effect in MPO KO mice. Collectively, these results show that MPO, which generates microbicidal oxidants, plays an important role in NM-induced skin injuries. This suggests the development of mechanism-based treatments against NM- and SM-induced skin injuries that inhibit MPO activity and attenuate MPO-derived oxidants. |Animals [MESH] |Apoptosis/*drug effects [MESH] |Blister/chemically induced/pathology [MESH] |Chemical Warfare Agents/*toxicity [MESH] |Cyclooxygenase 2/metabolism [MESH] |DNA Damage/drug effects [MESH] |Male [MESH] |Matrix Metalloproteinase 9/metabolism [MESH] |Mechlorethamine/administration & dosage/*toxicity [MESH] |Metabolism, Inborn Errors/*metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Nitric Oxide Synthase Type II/metabolism [MESH] |Peroxidase/genetics [MESH] |Skin/*drug effects/pathology [MESH]Myeloperoxidase deficiency attenuates nitrogen mustard-induced skin in(epmc).pdf DeepDyve Pubget Overpricing