Pharmacology, Toxicology and Therapeutics : Faculty & Graduate Students : Chiek Saito
When I was in undergraduate school, I studied the regulatory mechanisms for fibrinolysis factors by inflammatory cytokine. After I graduated, I came to the united state in 2004.
Research Interests
Now I am working on Acetaminophen hepatotoxicity in Dr. Jaeschke's lab.
Acetaminophen (AAP) is a widely used analgesic and is eliminated as nontoxic conjugates with glucuronic acid and sulfate. Only a small portion of AAP is metabolized by P-450 isoenzymes and forms the reactive metabolite N-acetyl-p-benzoquinone imine (NAPQI). NAPQI can react with sulfhydryl groups such as GSH.
After taking an AAP overdose, hepatic GSH is dramatically reduced. After GSH depletion, NAPQI starts to bind cellular proteins including mitochondrial proteins, which results in mitochondrial dysfunction and reactive oxygen formation. These chains of events eventually lead to necrotic cell death in hepatocytes.
Our goal of this research is to investigate the mechanisms and signaling pathways of cell necrosis caused by AAP in the liver and to identify therapeutic approaches to prevent liver failure
Chieko Saito
Department of Pharmacology, Toxicology, and Therapeutics
The University of Kansas Medical Center
MS1018
3901 Rainbow Boulevard
Kansas City, KS 66160
Phone: (913) 588-9183
Fax: (913) 588-7501
E-Mail: csaito@kumc.edu
Updated 9/5/08
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The University of Kansas Medical Center