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Possible involvement of reactive oxygen species in D-galactosamine-induced sensitization against tumor necrosis factor-alpha-induced hepatocyte apoptosis.
J Cell Physiol 2001; 187(3):374-85JC

Abstract

Intravenous administration of tumor necrosis factor-alpha (TNF-alpha) (0.5 microg/mouse) caused hepatocyte apoptosis in BALB/c mice when they were sensitized with D-galactosamine (GalN, 20 mg/mouse). Activation of nuclear factor kappa B (NF-kappa B) and expression of apoptotic Bcl-2 family members were not significantly different between livers of mice treated with TNF-alpha alone and GalN + TNF-alpha, indicating that neither activation of NF-kappa B nor expression of Bcl-2 family is involved in the sensitization by GalN against TNF-alpha-induced hepatocyte apoptosis. To identify differentially expressed genes implicated in GalN-induced hepatocyte sensitization, we adopted mRNA fingerprinting using an arbitrarily primed polymerase chain reaction. The present analysis revealed that mRNA expression of extracellular antioxidant, selenoprotein P, was up-regulated in the livers after GalN administration. GalN-induced increase in its protein level was confirmed by Western blotting. Increased expression of this gene was also observed in the liver of mice treated with concanavalin A, but not anti-Fas antibody. mRNA of another antioxidant, glutathione peroxidase-1, was also up-regulated, and lipid peroxides were produced in the liver after GalN administration. Selenoprotein P mRNA level also increased in Huh-7 human hepatoma cells incubated with GalN (5 or 10 mM). Accordingly, formation of reactive oxygen species (ROS) was observed in GalN-treated Huh-7 cells. H(2)O(2) induced up-regulation of selenoprotein P mRNA and sensitized Huh-7 cells to TNF-alpha-induced apoptosis. These results suggest that ROS produced by GalN may play a pivotal role in hepatocyte sensitization toward TNF-alpha-induced apoptosis.

Authors+Show Affiliations

First Department of Internal Medicine, Gifu University School of Medicine, Gifu, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11319761

Citation

Osawa, Y, et al. "Possible Involvement of Reactive Oxygen Species in D-galactosamine-induced Sensitization Against Tumor Necrosis Factor-alpha-induced Hepatocyte Apoptosis." Journal of Cellular Physiology, vol. 187, no. 3, 2001, pp. 374-85.
Osawa Y, Nagaki M, Banno Y, et al. Possible involvement of reactive oxygen species in D-galactosamine-induced sensitization against tumor necrosis factor-alpha-induced hepatocyte apoptosis. J Cell Physiol. 2001;187(3):374-85.
Osawa, Y., Nagaki, M., Banno, Y., Yamada, Y., Imose, M., Nozawa, Y., ... Nakashima, S. (2001). Possible involvement of reactive oxygen species in D-galactosamine-induced sensitization against tumor necrosis factor-alpha-induced hepatocyte apoptosis. Journal of Cellular Physiology, 187(3), pp. 374-85.
Osawa Y, et al. Possible Involvement of Reactive Oxygen Species in D-galactosamine-induced Sensitization Against Tumor Necrosis Factor-alpha-induced Hepatocyte Apoptosis. J Cell Physiol. 2001;187(3):374-85. PubMed PMID: 11319761.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Possible involvement of reactive oxygen species in D-galactosamine-induced sensitization against tumor necrosis factor-alpha-induced hepatocyte apoptosis. AU - Osawa,Y, AU - Nagaki,M, AU - Banno,Y, AU - Yamada,Y, AU - Imose,M, AU - Nozawa,Y, AU - Moriwaki,H, AU - Nakashima,S, PY - 2001/4/25/pubmed PY - 2001/5/25/medline PY - 2001/4/25/entrez SP - 374 EP - 85 JF - Journal of cellular physiology JO - J. Cell. Physiol. VL - 187 IS - 3 N2 - Intravenous administration of tumor necrosis factor-alpha (TNF-alpha) (0.5 microg/mouse) caused hepatocyte apoptosis in BALB/c mice when they were sensitized with D-galactosamine (GalN, 20 mg/mouse). Activation of nuclear factor kappa B (NF-kappa B) and expression of apoptotic Bcl-2 family members were not significantly different between livers of mice treated with TNF-alpha alone and GalN + TNF-alpha, indicating that neither activation of NF-kappa B nor expression of Bcl-2 family is involved in the sensitization by GalN against TNF-alpha-induced hepatocyte apoptosis. To identify differentially expressed genes implicated in GalN-induced hepatocyte sensitization, we adopted mRNA fingerprinting using an arbitrarily primed polymerase chain reaction. The present analysis revealed that mRNA expression of extracellular antioxidant, selenoprotein P, was up-regulated in the livers after GalN administration. GalN-induced increase in its protein level was confirmed by Western blotting. Increased expression of this gene was also observed in the liver of mice treated with concanavalin A, but not anti-Fas antibody. mRNA of another antioxidant, glutathione peroxidase-1, was also up-regulated, and lipid peroxides were produced in the liver after GalN administration. Selenoprotein P mRNA level also increased in Huh-7 human hepatoma cells incubated with GalN (5 or 10 mM). Accordingly, formation of reactive oxygen species (ROS) was observed in GalN-treated Huh-7 cells. H(2)O(2) induced up-regulation of selenoprotein P mRNA and sensitized Huh-7 cells to TNF-alpha-induced apoptosis. These results suggest that ROS produced by GalN may play a pivotal role in hepatocyte sensitization toward TNF-alpha-induced apoptosis. SN - 0021-9541 UR - https://www.unboundmedicine.com/medline/citation/11319761/Possible_involvement_of_reactive_oxygen_species_in_D_galactosamine_induced_sensitization_against_tumor_necrosis_factor_alpha_induced_hepatocyte_apoptosis_ L2 - https://doi.org/10.1002/jcp.1088 DB - PRIME DP - Unbound Medicine ER -