On the Release and Elimination
of Liver Glutamic-Oxalacetic-Transferase
A. FISCHER, and L. TAKACS
With 2 Figures
Abstract
The activity of serum enzymes depends on their rates of entrance as well of
elimination (or inactivation). Since previous observations were contradictory,
we investigated G.O.T. in the blood of rats following ligature of the left liver
lobe and after recirculation; an increase in S.G.O.T. occurred. Following i.v.
injection ofG.O.T., its excretion via the bile is considerably enhanced; however,
only a small fraction of injected G.O. T. can be recovered. Addition of lung
slices in vitro greatly increases G.O.T. inactivation. Some implications for the
interpretation of S.G.O.T. increase are discussed.
Increased activity of serum glutamic-oxalacetic-transferase (S.G.O.T.)
in liver disease is correctly ascribed to damage of liver cells; it is doubtful,
however, whether cell necrosis is necessary for an increase of enzyme
release. Experiments wit CCl 4 -intoxication [5] failed to prove unequivocal
relations between the toxic dose applied and the enzyme level in the blood.
In our experiments with rats the serum level of G.O.T. remains unchanged although the left liver lobe has been ligatured for 10 min., also the
enzyme activity in the ligatured lobe is the same as in the non-ligatured one.
Special experimental equipment allows recirculation of the ligatured lobe
without additional laparatomy; then a ligature of 10 min and subsequent
recirculation of 2 hrs brings about a definite increase in the serum activity
and a prompt decrease of the G.O.T. activity in the previously ligatured
lobe (Fig. 1). No necrosis in the liver can be detected. Thus, interruption
of the liver circulation for 10 min is followed by a significant release of
G.O.T. without gross morphological alteration of the liver cells.
The problem of S.G.O.T. elimination is still open [2]; some observations suggest elimination through the bile [1], but this mechanism has
been questioned [3]. For the duodenal fluid a daily excretion of 20000 units
G.O.T. has been reported [4]; this value is, however, only approximate,
since we observed a rapid decrease of G.O.T. activity in the bile at 37°C,
probably due to trypsin digestion. An i.v. injection of large amounts of
G.O.T. (400000--1 million units) increases the excretion through a
of Liver Glutamic-Oxalacetic-Transferase
A. FISCHER, and L. TAKACS
With 2 Figures
Abstract
The activity of serum enzymes depends on their rates of entrance as well of
elimination (or inactivation). Since previous observations were contradictory,
we investigated G.O.T. in the blood of rats following ligature of the left liver
lobe and after recirculation; an increase in S.G.O.T. occurred. Following i.v.
injection ofG.O.T., its excretion via the bile is considerably enhanced; however,
only a small fraction of injected G.O. T. can be recovered. Addition of lung
slices in vitro greatly increases G.O.T. inactivation. Some implications for the
interpretation of S.G.O.T. increase are discussed.
Increased activity of serum glutamic-oxalacetic-transferase (S.G.O.T.)
in liver disease is correctly ascribed to damage of liver cells; it is doubtful,
however, whether cell necrosis is necessary for an increase of enzyme
release. Experiments wit CCl 4 -intoxication [5] failed to prove unequivocal
relations between the toxic dose applied and the enzyme level in the blood.
In our experiments with rats the serum level of G.O.T. remains unchanged although the left liver lobe has been ligatured for 10 min., also the
enzyme activity in the ligatured lobe is the same as in the non-ligatured one.
Special experimental equipment allows recirculation of the ligatured lobe
without additional laparatomy; then a ligature of 10 min and subsequent
recirculation of 2 hrs brings about a definite increase in the serum activity
and a prompt decrease of the G.O.T. activity in the previously ligatured
lobe (Fig. 1). No necrosis in the liver can be detected. Thus, interruption
of the liver circulation for 10 min is followed by a significant release of
G.O.T. without gross morphological alteration of the liver cells.
The problem of S.G.O.T. elimination is still open [2]; some observations suggest elimination through the bile [1], but this mechanism has
been questioned [3]. For the duodenal fluid a daily excretion of 20000 units
G.O.T. has been reported [4]; this value is, however, only approximate,
since we observed a rapid decrease of G.O.T. activity in the bile at 37°C,
probably due to trypsin digestion. An i.v. injection of large amounts of
G.O.T. (400000--1 million units) increases the excretion through a