liu.seSearch for publications in DiVA
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
3-Aminopropanal is a lysosomotropic aldehyde that causes oxidative stress and apoptosis by rupturing lysosomes.
Linköping University, Department of Neuroscience and Locomotion. Linköping University, Faculty of Health Sciences. (Neurokirurgi & Patologi II)
Linköping University, Department of Neuroscience and Locomotion. Linköping University, Faculty of Health Sciences. (Neurokirurgi & Patologi II)
Linköping University, Department of Neuroscience and Locomotion. Linköping University, Faculty of Health Sciences. (Neurokirurgi & Patologi II)
2003 (English)In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 111, no 6, p. 643-652Article in journal (Refereed) Published
Abstract [en]

During cerebral ischemia and following trauma, potent cytotoxic polyamine-derived aminoaldehydes form, diffuse, and damage adjacent tissues not directly subjected to the initial insult. One such aldehyde is 3-aminopropanal (3-AP). The mechanisms by which such a small aldehydic compound is excessively cytotoxic have been unclear until recently when we showed that 3-AP, having the structure of a weak lysosomotropic base, concentrates within the acidic vacuolar compartment and causes lysosomal rupture that, in turn, induces caspase activation and apoptotic cell death. Here, using cultured J774 cells and 3-AP as a way to selectively burst lysosomes, we show that moderate lysosomal rupture induces a transient wave of oxidative stress. The start of this oxidative stress period is concomitant with a short period of enhanced mitochondrial membrane potential that later fades and is replaced by a decreased potential before the oxidative stress diminishes. The result of the study suggests that oxidative stress, which has often been described during apoptosis induced by agonists other than oxidative stress per se, may be a consequence of lysosomal rupture with direct and/or indirect effects on mitochondrial respiration and electron transport causing a period of passing enhanced formation of reactive oxygen species.

Place, publisher, year, edition, pages
Linköping: Wiley-Blackwell Publishing Inc., 2003. Vol. 111, no 6, p. 643-652
National Category
Medical Biotechnology
Identifiers
URN: urn:nbn:se:liu:diva-157127DOI: 10.1034/j.1600-0463.2003.1110607.xISI: 000185478100007PubMedID: 12969020Scopus ID: 2-s2.0-0141853870OAI: oai:DiVA.org:liu-157127DiVA, id: diva2:1318855
Available from: 2019-05-28 Created: 2019-05-28 Last updated: 2019-06-05Bibliographically approved

Open Access in DiVA

No full text in DiVA

Other links

Publisher's full textPubMedScopus

Authority records BETA

Zhengquan, YuLi, WeiBrunk, Ulf

Search in DiVA

By author/editor
Zhengquan, YuLi, WeiBrunk, Ulf
By organisation
Department of Neuroscience and LocomotionFaculty of Health Sciences
In the same journal
Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS)
Medical Biotechnology

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 1 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf