REVIEW: Oxidative Stress Promotes the Regression of Fetal Liver Hemopoiesis

E. F. Sato^1*, E. Nakagawa¹, K. Hiramoto¹, S. Yamamasu¹, I. Moriyama-Shimamoto², and M. Inoue¹

¹Department of Biochemistry and Molecular Pathology, Osaka City University Medical School, 1-4-3 Asahimachi, Abeno, Osaka 545-8585, Japan; fax: +81-6-6645-3721; E-mail: sato@med.osaka-cu.ac.jp

²College of Nursing, Nara Medical University, Japan

^* To whom correspondence should be addressed.

Received April 30, 2003

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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 beta-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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KEY WORDS: apoptosis, fetal liver, beta-glutamyl transferase, glutathione, cysteine, hemopoiesis, liver, oxidative stress

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