Abstract
The apoptotic cell death of Jurkat cells due to Cd(2+) toxicity was studied by fluorescence microscopic observation and DNA fragmentation assaying. It was suggested that the apoptotic response to Cd(2+) was less clear than that to a typical apoptosis inducer, ultraviolet light (254 nm). Examination of MAP kinase phosphorylation (p38, JNKs, and c-Jun) due to Cd(2+) toxicity indicated that the phosphorylation was very slowly activated (4 h after stimulation), while UV light could activate the phosphorylation immediately. Therefore, it was suggested that Cd(2+) may not be a typical apoptosis inducer. Antioxidants [glutathione (GSH) and N-acetylcysteine (NAC)] could detoxify Cd(2+), indicating that the toxicity is a kind of oxidative stress. The detoxification effect of antioxidants showed cooperation with Bcl-2, suggesting that Cd(2+)-treatment causes diversified toxic signals including oxidative stress. On the addition of a plant-specific peptide, phytochelatin [PC(7), (gammaGlu-Cys)(7)-Gly], to the medium, the detoxification of Cd(2+) and cooperation with Bcl-2 were more intense than in the cases of GSH and NAC. Using an appropriate vector, a PC synthase gene was transferred from Arabidopsis thaliana to the Jurkat cell. The transfectant exhibited resistance to Cd(2+) and production of plant-specific PC (PC(2-6)).
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetylcysteine / metabolism
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Aminoacyltransferases / genetics
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Aminoacyltransferases / metabolism
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Aminoacyltransferases / pharmacology
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Apoptosis / drug effects*
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Blotting, Western
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Cadmium / toxicity*
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Cell Nucleus / metabolism
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Cells, Cultured / drug effects
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Cells, Cultured / metabolism
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Chelating Agents / metabolism
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Chelating Agents / pharmacology*
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DNA Primers / chemistry
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Drug Resistance
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Free Radical Scavengers / metabolism
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Glutathione / metabolism
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Humans
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Inactivation, Metabolic
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JNK Mitogen-Activated Protein Kinases
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Jurkat Cells / drug effects*
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MAP Kinase Kinase 4
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Metalloproteins / metabolism
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Metalloproteins / pharmacology*
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Mitogen-Activated Protein Kinase Kinases / metabolism
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Mitogen-Activated Protein Kinases / metabolism
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Oxidative Stress
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Phytochelatins
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Plants / chemistry
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Plasmids
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Polymerase Chain Reaction
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Proto-Oncogene Proteins c-bcl-2 / biosynthesis
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Time Factors
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Transfection
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p38 Mitogen-Activated Protein Kinases
Substances
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Chelating Agents
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DNA Primers
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Free Radical Scavengers
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Metalloproteins
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Proto-Oncogene Proteins c-bcl-2
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Cadmium
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Phytochelatins
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Aminoacyltransferases
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glutathione gamma-glutamylcysteinyltransferase
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JNK Mitogen-Activated Protein Kinases
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Mitogen-Activated Protein Kinases
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p38 Mitogen-Activated Protein Kinases
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MAP Kinase Kinase 4
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Mitogen-Activated Protein Kinase Kinases
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Glutathione
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Acetylcysteine