Abstract
Endoplasmic reticulum (ER) stress-responsive alkaline phosphatase (ES-TRAP) serves as a sensitive indicator for ER stress. In response to heavy metals including cadmium, nickel and cobalt, hepatocytes and renal tubular cells expressing ES-TRAP exhibited ER stress and decreased ES-TRAP activity. In ES-TRAP transgenic mice, acute exposure to cadmium showed rapid, transient decreases in the activity of serum ES-TRAP. It was inversely correlated with the induction of endogenous ER stress markers in the liver and kidney. Our result provides first evidence for the acute, reversible induction of ER stress in vivo after exposure to heavy metal.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alkaline Phosphatase / blood
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Animals
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Cell Line
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Endoplasmic Reticulum / drug effects*
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Endoplasmic Reticulum / pathology*
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Endoplasmic Reticulum Chaperone BiP
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Heat-Shock Proteins
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Kidney / drug effects*
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Kidney / enzymology
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Kinetics
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Liver / drug effects*
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Liver / enzymology
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Metals, Heavy / administration & dosage*
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Metals, Heavy / toxicity*
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Mice
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Mice, Transgenic
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Molecular Chaperones
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Organ Specificity / drug effects
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Rats
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Thapsigargin / pharmacology
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Time Factors
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Toxicity Tests, Acute
Substances
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Endoplasmic Reticulum Chaperone BiP
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Heat-Shock Proteins
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Metals, Heavy
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Molecular Chaperones
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Thapsigargin
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Alkaline Phosphatase