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A Mechanistic Study Of S-Adenosyl-L-Methionine Protection Against Acetaminophen Hepatotoxicity, James Michael Brown
A Mechanistic Study Of S-Adenosyl-L-Methionine Protection Against Acetaminophen Hepatotoxicity, James Michael Brown
Theses, Dissertations and Capstones
Acetaminophen (APAP) toxicity remains the leading cause of drug induced liver failure in the United States. The current therapy for APAP toxicity is N-acetylcysteine (NAC). NAC must be administered within eight hours of APAP overdose for maximum efficacy. That, coupled with the fact that APAP toxicity may not be overtly evident, makes an alternative therapeutic intervention worth exploring. Previous work by our laboratory has demonstrated that S-adenosyl-L-methionine (SAMe) prevents APAP toxicity when given following APAP overdose in C57Bl/6 mice at a level comparable to NAC. The focus of the current work was to examine the mechanistic aspects of this protection …
A Mechanistic Study Of The Protective Effects Of S-Adenosyl-L-Methionine Against Hepatotoxicity Of Acetaminophen, Marcus V. Terneus Jr.
A Mechanistic Study Of The Protective Effects Of S-Adenosyl-L-Methionine Against Hepatotoxicity Of Acetaminophen, Marcus V. Terneus Jr.
Theses, Dissertations and Capstones
Hepatic toxicity is known to be associated with excessive doses of the over-the-counter analgesic, acetaminophen (APAP). APAP overdose is the leading cause of drug-induced liver failure in the United States. APAP hepatotoxicity is dependent on the biotransformation of APAP by cytochrome P450 to the toxic metabolite, N-acetyl-p-benzoquinone imine (NAPQI). APAP, when taken in excessive doses, can lead to severe liver damage with the potential to progress to liver failure. Despite substantial efforts in past studies, the mechanism by which APAP induces such damaging effects is not completely understood. Recent discoveries suggest that glutathione (GSH) depletion, protein alkylation and reactive metabolite …