English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

A striking correlation between lethal activity and apoptotic DNA fragmentation of liver in response of D-galactosamine- sensitized mice to a non-lethal amount of lipopolysaccharide

MPS-Authors
/persons/resource/persons191079

Gumenscheimer,  Marina
Metchnikoff Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons191059

Freudenberg,  Marina
Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

/persons/resource/persons191064

Galanos,  Chris
Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

External Resource
No external resources are shared
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Zhou, B.-R., Gumenscheimer, M., Freudenberg, M., & Galanos, C. (2003). A striking correlation between lethal activity and apoptotic DNA fragmentation of liver in response of D-galactosamine- sensitized mice to a non-lethal amount of lipopolysaccharide. Acta Pharmacologica Sinica, 24(3), 193-198.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002B-9558-8
Abstract
AIM: To observe whether challenge of bacterial lipopolysaccharide (LPS) with D-galactosamine (D-GalN) in mice will result in apoptotic characteristic of vital organs. METHODS: The experimental group of mice was challenged directly with bacterial LPS (0.05 μg) in the presence of D-GalN (20 mg), and the control group of mice was challenged either with bacterial LPS or with D-GalN alone. The organs including brain, kidney, heart, spleen, lung, and liver were removed at an indicated time point under ether anethesia, and immediately homogenized, from which DNA was extracted. The DNA obtained from these organs was analyzed by agarose gel electrophoresis to determine whether the DNA laddering phenomenon existed. The amount of plasma LDH and GOT was detected in mice challenged with bacterial LPS in the presence of D-GalN, and either bacterial LPS or D-GalN alone. RESULTS: Apoptotic DNA fragmentation was initially seen at 4 h after challenge only in the livers of mice challenged with bacterial LPS and D-GalN, all mice in this group challenged with bacterial LPS and D-GalN died at 7 h after challenge; in contrast, the animals in the control group were all alive and the DNA was integral. CONCLUSION: The liver is the only specific target organ where apoptotic DNA fragmentation was present in mice treated with D- GalN and challenged with bacterial LPS and the liver impairment might be the critical cause of the lethality of mice elicited by bacterial LPS.