Aspartate aminotransferase - AST|
Glutamic oxaloacetic transaminase, GOT
Aspartate amino transferase catalyzes the transfer of the alpha amino
group of aspartic acid to alpha-ketoglutaric acid, resulting in the formation
of oxaloacetic acid and glutamic acid. Both aminotransferases (ALT and
AST) require pyridoxal 5' phosphate (P5P) as an essential cofactor for
maximum enzyme activity. P5P is the active metabolite of vitamin B6, therefore
reduced vitamin B6 (as occurs rarely in animal patients with liver disease
or on certain drugs) can result in decreased aminotransferase activity,
unless P5P is included in the assay system for the aminotransferases (as
done here at Cornell). AST is useful as an indicator of liver and/or muscle
injury in large and small animals.
AST is not organ specific. Skeletal muscle contains the highest
concentration, followed by liver and cardiac muscle. Erythrocytes contain enough to raise levels when
hemolysis occurs. AST is also found in renal epithelial cells and brain tissue. It is located in the cytoplasm and mitochondria as different isoenzymes. Elevations in the cytoplasmic AST isoenzyme requires only mild hepatocellular injury (and compared to ALT, AST levels
may increase less in relatively mild hepatocellular injury), whereas release of the mitochondrial isoenzyme requires (and indicates) more severe cellular injury. Isoenzyme differentiation is not performed in veterinary medicine.
The enzyme half life is about 22 hours in the dog, 77 minutes in the cat
and 2 or more days in large animals.
Causes of increased AST
- Artifact: Hemolysis or leakage from
cells can cause erroneously high values (enzyme is present in RBC).
- Drug effects: Anticonvulsants may cause
an increase in AST, which is thought to be secondary to hepatocellular
injury in dogs. Corticosteroids generally do not result in increased
AST levels, unless they result in a steroid hepatopathy (in dogs).
- Physiologic effects: In horses, exercise
can increase serum activity as much as 30%. In early training, resting
levels are 50-100% greater than resting levels of horses not in training.
- Disease effects
1) Myopathies: Muscle trauma (including "down" animals), rhabdomyolysis,
white muscle disease (vitamin E-selenium deficiency), and infectious
myositis (black leg or Clostridial myositis), and muscular dystrophy
may result in marked increases. Serum CK activity will also increased.
Note that as AST has a longer half life than CK, increases in AST
persist for longer than increases in CK. Therefore, in chronic muscle
disease, AST may be elevated, whilst CK levels may be normal. When
there is active muscle disease, both CK and AST are elevated (and
CK will decline more rapidly as the injury resolves).
2) Liver disease: AST will increase in liver disease with
the same causes as for ALT. Increased levels seen with hepatocellular
injury often aren't as high as those seen with muscle damage. CK levels
are normal unless there is concomitant muscle disease. Other liver
specific enzymes (SDH) would also be increased. In cats, AST appears
to be a more sensitive marker of liver injury (values are often mildly
increased with normal ALT in conditions such as pyogranulomatous hepatitis
secondary to feline infectious peritonitis virus infection).