Acute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm

Abstract N-acetyl-para-amino phenol (APAP, usually named paracetamol), which is commonly used for its analgesic and antipyretic properties may lead to hepatotoxicity and acute liver damage in case of overdoses. Released cytokines and oxidative stress following acute liver damage may affect other org...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	C. S. Bruells, P. Duschner, G. Marx, G. Gayan-Ramirez, N. Frank, T. Breuer, O. Krenkel, F. Tacke, J. C. Mossanen
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/66c0b5c7766142aeacee1b9d270bf2f5
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:66c0b5c7766142aeacee1b9d270bf2f5
record_format	dspace
spelling	oai:doaj.org-article:66c0b5c7766142aeacee1b9d270bf2f52021-12-02T11:39:27ZAcute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm10.1038/s41598-021-85859-22045-2322https://doaj.org/article/66c0b5c7766142aeacee1b9d270bf2f52021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-85859-2https://doaj.org/toc/2045-2322Abstract N-acetyl-para-amino phenol (APAP, usually named paracetamol), which is commonly used for its analgesic and antipyretic properties may lead to hepatotoxicity and acute liver damage in case of overdoses. Released cytokines and oxidative stress following acute liver damage may affect other organs’ function notably the diaphragm, which is particularly sensitive to oxidative stress and circulating cytokines. We addressed this issue in a mouse model of acute liver injury induced by administration of APAP. C57BL/6J mice (each n = 8) were treated with N-acetyl-para-amino phenol (APAP) to induce acute drug caused liver injury and sacrificed 12 or 24 h afterwards. An untreated group served as controls. Key markers of inflammation, proteolysis, autophagy and oxidative stress were measured in diaphragm samples. In APAP treated animals, liver damage was proven by the enhanced serum levels of alanine aminotransferase and aspartate aminotransferase. In the diaphragm, besides a significant increase in IL 6 and lipid peroxidation, no changes were observed in key markers of the proteolytic, and autophagy signaling pathways, other inflammatory markers and fiber dimensions. The first 24 h of acute liver damage did not impair diaphragm atrophic pathways although it slightly enhanced IL-6 and lipid peroxidation. Whether longer exposure might affect the diaphragm needs to be addressed in future experiments.C. S. BruellsP. DuschnerG. MarxG. Gayan-RamirezN. FrankT. BreuerO. KrenkelF. TackeJ. C. MossanenNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-9 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q C. S. Bruells P. Duschner G. Marx G. Gayan-Ramirez N. Frank T. Breuer O. Krenkel F. Tacke J. C. Mossanen Acute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm
description	Abstract N-acetyl-para-amino phenol (APAP, usually named paracetamol), which is commonly used for its analgesic and antipyretic properties may lead to hepatotoxicity and acute liver damage in case of overdoses. Released cytokines and oxidative stress following acute liver damage may affect other organs’ function notably the diaphragm, which is particularly sensitive to oxidative stress and circulating cytokines. We addressed this issue in a mouse model of acute liver injury induced by administration of APAP. C57BL/6J mice (each n = 8) were treated with N-acetyl-para-amino phenol (APAP) to induce acute drug caused liver injury and sacrificed 12 or 24 h afterwards. An untreated group served as controls. Key markers of inflammation, proteolysis, autophagy and oxidative stress were measured in diaphragm samples. In APAP treated animals, liver damage was proven by the enhanced serum levels of alanine aminotransferase and aspartate aminotransferase. In the diaphragm, besides a significant increase in IL 6 and lipid peroxidation, no changes were observed in key markers of the proteolytic, and autophagy signaling pathways, other inflammatory markers and fiber dimensions. The first 24 h of acute liver damage did not impair diaphragm atrophic pathways although it slightly enhanced IL-6 and lipid peroxidation. Whether longer exposure might affect the diaphragm needs to be addressed in future experiments.
format	article
author	C. S. Bruells P. Duschner G. Marx G. Gayan-Ramirez N. Frank T. Breuer O. Krenkel F. Tacke J. C. Mossanen
author_facet	C. S. Bruells P. Duschner G. Marx G. Gayan-Ramirez N. Frank T. Breuer O. Krenkel F. Tacke J. C. Mossanen
author_sort	C. S. Bruells
title	Acute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm
title_short	Acute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm
title_full	Acute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm
title_fullStr	Acute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm
title_full_unstemmed	Acute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm
title_sort	acute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/66c0b5c7766142aeacee1b9d270bf2f5
work_keys_str_mv	AT csbruells acuteliverinjuryfollowingacetaminophenadministrationdoesnotactivateatrophicpathwaysinthemousediaphragm AT pduschner acuteliverinjuryfollowingacetaminophenadministrationdoesnotactivateatrophicpathwaysinthemousediaphragm AT gmarx acuteliverinjuryfollowingacetaminophenadministrationdoesnotactivateatrophicpathwaysinthemousediaphragm AT ggayanramirez acuteliverinjuryfollowingacetaminophenadministrationdoesnotactivateatrophicpathwaysinthemousediaphragm AT nfrank acuteliverinjuryfollowingacetaminophenadministrationdoesnotactivateatrophicpathwaysinthemousediaphragm AT tbreuer acuteliverinjuryfollowingacetaminophenadministrationdoesnotactivateatrophicpathwaysinthemousediaphragm AT okrenkel acuteliverinjuryfollowingacetaminophenadministrationdoesnotactivateatrophicpathwaysinthemousediaphragm AT ftacke acuteliverinjuryfollowingacetaminophenadministrationdoesnotactivateatrophicpathwaysinthemousediaphragm AT jcmossanen acuteliverinjuryfollowingacetaminophenadministrationdoesnotactivateatrophicpathwaysinthemousediaphragm
_version_	1718395704061198336

Acute liver injury following acetaminophen administration does not activate atrophic pathways in the mouse diaphragm

Ejemplares similares