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Oxidative stress promotes the regression of fetal liver hemopoiesis.

Authors
  • Sato, E F1
  • Nakagawa, E
  • Hiramoto, K
  • Yamamasu, S
  • Moriyama-Shimamoto, I
  • Inoue, M
  • 1 Department of Biochemistry and Molecular Pathology, Osaka City University Medical School, Osaka, 545-8585, Japan. [email protected] , (Japan)
Type
Published Article
Journal
Biochemistry. Biokhimiia
Publication Date
Jan 01, 2004
Volume
69
Issue
1
Identifiers
PMID: 14972013
Source
Medline
Language
English
License
Unknown

Abstract

Although apoptosis is believed to play an important role in the ontogenetic development of animals, the molecular mechanism that triggers the regression of liver hemopoiesis during the perinatal period is not known. Apoptosis is induced by many factors such as a decrease in growth factors and increased oxygen stress. Since hepatic gamma-glutamyl transferase (GT) levels change markedly during the perinatal period in rodents, the metabolism of glutathione (GSH), a naturally occurring major antioxidant, might change significantly in and around liver cells. Hemopoietic cells but not hepatocytes exhibit significant apoptosis in thiol-free medium and the hemopoietic apoptosis can be inhibited by various thiols, such as L-cysteine, N-acetyl-L-cysteine, and GSH. The contribution of GSH levels in and around fetal liver cells in the triggering of apoptosis in hemopoietic cells is discussed.

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