Abstract
The effects of cadmium (Cd) on phytohemoagglutinin or phorbol myristate acetate-induced lymphocyte activation were investigated and a dose-dependent inhibition of cell proliferation was found. Kinetic studies revealed that the Cd-sensitive step is an early event of T cell stimulation. Failure of IL2 secretion and reduction of IL2 receptor expression in the Cd-treated cells are also reported. Regardless of which mechanism is responsible for Cd effects, our studies show that the inhibition of lymphocyte activation is associated with reduced [3H]phorbol dibutyrate binding to Ca2+-phospholipid-dependent protein kinase and altered breakdown of phosphatidylinositols. Thus, Cd interferes with two biochemical events which play a critical role in lymphocyte signal transduction and activation.
MeSH terms
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Adult
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Cadmium / pharmacology*
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Cadmium Chloride
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Cadmium Radioisotopes
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Calcium / pharmacology
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Cell Division / drug effects
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Cell Membrane / metabolism
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Dose-Response Relationship, Drug
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Humans
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Interleukins / metabolism
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Kinetics
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Lymphocyte Activation / drug effects*
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Lymphocytes / cytology
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Lymphocytes / drug effects
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Lymphocytes / physiology
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Phorbol 12,13-Dibutyrate / metabolism
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Phosphatidylinositols / metabolism
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Phospholipids / pharmacology
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Phytohemagglutinins / pharmacology
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Protein Kinases / metabolism
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Receptors, Interleukin-2 / metabolism
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Tetradecanoylphorbol Acetate / pharmacology
Substances
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Cadmium Radioisotopes
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Interleukins
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Phosphatidylinositols
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Phospholipids
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Phytohemagglutinins
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Receptors, Interleukin-2
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Cadmium
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Phorbol 12,13-Dibutyrate
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Protein Kinases
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Cadmium Chloride
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Tetradecanoylphorbol Acetate
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Calcium