Gutenberg Open Science: High membrane protein oxidation in the human cerebral cortex

Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-8056

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DC Field	Value	Language
dc.contributor.author	Granold, Matthias	-
dc.contributor.author	Moosmann, Bernd	-
dc.contributor.author	Staib-Lasarzik, Irina	-
dc.contributor.author	Arendt, Thomas	-
dc.contributor.author	del Rey, Adriana	-
dc.contributor.author	Engelhard, Kristin	-
dc.contributor.author	Behl, Christian	-
dc.contributor.author	Hajieva, Parvana	-
dc.date.accessioned	2022-10-17T07:36:30Z	-
dc.date.available	2022-10-17T07:36:30Z	-
dc.date.issued	2015	-
dc.identifier.uri	https://openscience.ub.uni-mainz.de/handle/20.500.12030/8071	-
dc.description.abstract	Oxidative stress is thought to be one of the main mediators of neuronal damage in human neurodegenerative disease. Still, the dissection of causal relationships has turned out to be remarkably difficult. Here, we have analyzed global protein oxidation in terms of carbonylation of membrane proteins and cytoplasmic proteins in three different mammalian species: aged human cortex and cerebellum from patients with or without Alzheimer's disease, mouse cortex and cerebellum from young and old animals, and adult rat hippocampus and cortex subjected or not subjected to cerebral ischemia. Most tissues showed relatively similar levels of protein oxidation. However, human cortex was affected by severe membrane protein oxidation, while exhibiting lower than average cytoplasmic protein oxidation. In contrast, ex vivo autooxidation of murine cortical tissue primarily induced aqueous protein oxidation, while in vivo biological aging or cerebral ischemia had no major effect on brain protein oxidation. The unusually high levels of membrane protein oxidation in the human cortex were also not predicted by lipid peroxidation, as the levels of isoprostane immunoreactivity in human samples were considerably lower than in rodent tissues. Our results indicate that the aged human cortex is under steady pressure from specific and potentially detrimental membrane protein oxidation. The pronounced difference between humans, mice and rats regarding the primary site of cortical oxidation might have contributed to the unresolved difficulties in translating into therapies the wealth of data describing successful antioxidant neuroprotection in rodents.	en_GB
dc.description.sponsorship	DFG, Open Access-Publizieren Universität Mainz / Universitätsmedizin	de
dc.language.iso	eng	de
dc.rights	CC BY-NC-ND	*
dc.rights.uri	https://creativecommons.org/licenses/by-nc-d/4.0/	*
dc.subject.ddc	610 Medizin	de_DE
dc.subject.ddc	610 Medical sciences	en_GB
dc.title	High membrane protein oxidation in the human cerebral cortex	en_GB
dc.type	Zeitschriftenaufsatz	de
dc.identifier.doi	http://doi.org/10.25358/openscience-8056	-
jgu.type.dinitype	article	en_GB
jgu.type.version	Published version	de
jgu.type.resource	Text	de
jgu.organisation.department	FB 04 Medizin	de
jgu.organisation.number	2700	-
jgu.organisation.name	Johannes Gutenberg-Universität Mainz	-
jgu.rights.accessrights	openAccess	-
jgu.journal.title	Redox Biology	de
jgu.journal.volume	4	de
jgu.pages.start	200	de
jgu.pages.end	207	de
jgu.publisher.year	2015	-
jgu.publisher.name	Elsevier	de
jgu.publisher.place	Amsterdam	de
jgu.publisher.uri	http://dx.doi.org/10.1016/j.redox.2014.12.013	de
jgu.publisher.issn	2213-2317	de
jgu.organisation.place	Mainz	-
jgu.subject.ddccode	610	de
opus.date.modified	2017-04-25T13:17:29Z	-
opus.subject.dfgcode	00-000	-
opus.organisation.string	FB 04: Medizin: Institut für Physiologische Chemie und Pathobiochemie	de_DE
opus.organisation.string	FB 04: Medizin: Klinik für Anästhesiologie	de_DE
opus.identifier.opusid	53363	-
opus.institute.number	0404	-
opus.institute.number	0418	-
opus.metadataonly	false	-
opus.type.contenttype	Keine	de_DE
opus.type.contenttype	None	en_EN
opus.affiliated	Moosmann, Bernd	-
opus.affiliated	Staib-Lasarzik, Irina	-
opus.affiliated	Engelhard, Kristin	-
opus.affiliated	Behl, Christian	-
opus.affiliated	Hajieva, Parvana	-
jgu.publisher.doi	10.1016/j.redox.2014.12.013	de
jgu.organisation.ror	https://ror.org/023b0x485	-
Appears in collections:	DFG-OA-Publizieren (2012 - 2017)

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