Skip redundant pieces
Pharmacology, Toxicology & Therapeutics

Chieko Saito

 

B.S. in Agricultural Biological Chemistry, Nihon University, Japan

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

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 binds to cellular proteins including mitochondrial proteins, which results in mitochondrial dysfunction and reactive oxygen formation. This chain of events eventually leads to necrotic cell death in hepatocytes.

Our goal is to investigate the mechanisms and signaling pathways of AAP-induced cell necrosis by AAP in the liver and to identify therapeutic approaches to prevent the liver failure.

Contact Information

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 11/13/08