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Possible involvement of reactive oxygen species in D-galactosamine-induced sensitization against tumor necrosis factor-alpha-induced hepatocyte apoptosis.

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.

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  • Authors+Show Affiliations

    ,

    First Department of Internal Medicine, Gifu University School of Medicine, Gifu, Japan.

    , , , , , ,

    Source

    Journal of cellular physiology 187:3 2001 Jun pg 374-85

    MeSH

    Animals
    Antibodies
    Apoptosis
    Carcinoma, Hepatocellular
    Cell Line
    Concanavalin A
    Drug Synergism
    Galactosamine
    Gene Expression Profiling
    Glutathione Peroxidase
    Hepatocytes
    Humans
    Hydrogen Peroxide
    JNK Mitogen-Activated Protein Kinases
    Liver
    Liver Neoplasms
    Male
    Mice
    Mice, Inbred BALB C
    Mitogen-Activated Protein Kinases
    NF-kappa B
    Protein Biosynthesis
    Proteins
    Proto-Oncogene Proteins c-bcl-2
    RNA, Messenger
    Reactive Oxygen Species
    Selenoprotein P
    Selenoproteins
    Specific Pathogen-Free Organisms
    Tumor Necrosis Factor-alpha
    fas Receptor

    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 -