In Vivo Pharmacodynamic Evaluation of APAP Induced Acute Liver Injury Model (CAT#: STEM-AE-0664-LGZ)

Introduction

Metabolic diseases are diseases caused by the accumulation or deficiency of certain metabolic substances such as sugars, fats, proteins (amino acids), purines, pyrimidines, and copper when biochemical processes in the body are disrupted. Symptoms vary in severity and diagnosis depends on clinical manifestations and blood, urine and other biochemical tests. There is no effective cure, the main is to eliminate the cause and symptomatic treatment. The prognosis depends on the etiology, severity of symptoms and treatment effect.

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Principle Applications Procedure Materials Notes Related Products

Principle

APAP is taken up in the intestine within the first 2 hours after oral administration, metabolized in the liver via glucoronidation and sulfonation, and excreted in the urine. A small fraction (10-15%) is metabolized in hepatocytes by cytochrome P450 isomers to the alkylated, highly toxic metabolite N-acetyl-p-benzoquinoneimine (NAPQI). Antioxidant glutathione (GSH) converts NAPQI to the less harmful reduced form, which is then excreted via bile. When glutathione is depleted, increasing amounts of NAPQI bind to mitochondrial proteins and leading to hepatocyte necrosis.

Applications

Metabolic Disease

Procedure

1. Disease model construction.
2. Mice dosing.
3. Efficacy monitoring.
4. Biochemical detection of tissue samples.

Materials

• Sample Type: liquid or powder

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