Effect of pyridoxine deficiency on serum and liver transaminases in experimental liver injury in the rat

Abstract

We fed rats either a pyridoxine-deficient or normal rat chow diet for 8 wk and then determined transaminase activity in serum and liver with and without exposure to a known hepatotoxin, bromobenzene. Preincubation of serum and liver cytosol with pyridoxal phosphate in vitro resulted in a significantly greater increment of glutamic oxalacetic transaminase activity in the pyridoxine-deficient animals compared with controls. However, this effect was significantly reduced during liver necrosis. Total activities for both glutamic oxalacetic transaminase and glutamic pyruvic transaminase measured in the presence of excess pyridoxal phosphate were decreased significantly in serum and liver of the pyridoxine-deficient rats compared with controls. The magnitude of the fall in glutamic pyruvic transaminase in both serum and liver cytosol was significantly greater than that for glutamic oxalacetic transaminase. In the presence of bromobenzene-induced hepatocellular necrosis, there was a striking and nearly identical increase in serum glutamic oxalacetic transaminase in the pyridoxine-deficient rats and controls. In contrast, the concurrent increase in serum glutamic pyruvic transaminase was significantly less in the pyridoxinedeficient rats compared with controls. Therefore, the serum glutamic oxalacetic transaminase/glutamic pyruvic transaminase ratio was significantly greater in the pyridoxine-deficient vs. control rats. There was a parallel increased glutamic oxalacetic transaminase/ glutamic pyruvic transaminase ratio in liver cytosol of the pyridoxine-deficient compared with control animals, suggesting that the serum ratio in response to chemical hepatotoxicity reflects release of these enzymes from damaged hepatocytes in their existing proportions in liver.