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The proportion of AST to ALT in hepatocytes is about 2.5:1, but because AST is removed from serum by the liver sinusoidal cells twice as quickly (serum half-life t 1/2 = 18 hr) compared to ALT (t 1/2 = 36 hr), so the resulting serum levels of AST and ALT are about equal in healthy individuals, resulting in a normal AST/ALT ratio around 1.
Muscle sources of the enzymes, such as intense exercise, are unrelated to liver function and can markedly increase AST and ALT. [5] Cirrhosis of the liver or fulminant liver failure secondary to hepatitis commonly reach values for both ALT and AST in the >1000 U/L range; however, many people with liver disease have normal transaminases.
An increase of mitochondrial AST in bloods is highly suggestive of tissue necrosis in myocardial infarction and chronic liver disease. More than 80% of the liver AST activity are contributed by mitochondrial form of the isoenzymes, while the circulating AST in blood are contributed by cytoplasmic form of AST.
Aspartate transaminase (AST) or aspartate aminotransferase, also known as AspAT/ASAT/AAT or (serum) glutamic oxaloacetic transaminase (GOT, SGOT), is a pyridoxal phosphate (PLP)-dependent transaminase enzyme (EC 2.6.1.1) that was first described by Arthur Karmen and colleagues in 1954.
Alanine transaminase (ALT), also known as alanine aminotransferase (ALT or ALAT), formerly serum glutamate-pyruvate transaminase (GPT) or serum glutamic-pyruvic transaminase (SGPT), is a transaminase enzyme (EC 2.6.1.2) that was first characterized in the mid-1950s by Arthur Karmen and colleagues. [1]
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Hy's law is a rule of thumb that a patient is at high risk of a fatal drug-induced liver injury if given a medication that causes hepatocellular injury (not Hepatobiliary injury) with jaundice. [1] The law is based on observations by Hy Zimmerman, a major scholar of drug-induced liver injury.