Abstract
Oxidative stress is known to produce tissue injury and to activate various signaling pathways. To investigate the molecular events linked to acute oxidative stress in mouse liver, we injected a toxic dose of paraquat. Liver necrosis was first observed, followed by histological marks of cell proliferation. Concomitantly, activation of the MAP kinase pathway and increased levels of the anti-apoptotic protein Bcl-XL were observed. Gene expression profiles revealed that the differentially expressed genes were potentially involved in cell proliferation. These data suggest that paraquat-induced acute oxidative stress triggers the activation of regeneration-related events in the liver.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alanine Transaminase / blood
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Animals
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Bromodeoxyuridine
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Cell Proliferation
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Cyclic AMP Response Element-Binding Protein / metabolism
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DNA / biosynthesis
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Extracellular Signal-Regulated MAP Kinases / metabolism
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Genes / genetics
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Liver / cytology*
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Liver / drug effects
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Liver / metabolism*
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Liver Regeneration / drug effects
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Mice
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Mice, Inbred C57BL
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Necrosis
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Oligonucleotide Array Sequence Analysis
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Oxidative Stress*
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Paraquat / pharmacology
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Phosphorylation
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Time Factors
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Up-Regulation / genetics
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bcl-X Protein / metabolism
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p38 Mitogen-Activated Protein Kinases / metabolism
Substances
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Cyclic AMP Response Element-Binding Protein
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bcl-X Protein
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DNA
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Alanine Transaminase
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Extracellular Signal-Regulated MAP Kinases
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p38 Mitogen-Activated Protein Kinases
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Bromodeoxyuridine
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Paraquat