AAT Activity Research Articles

Impeded cerebellar development and reduced serum thyroxine levels associated with fetal alcohol intoxication

Pregnant albino rats were placed on a complete liquid diet (Ensure) containing either 9% ethanol or an isocaloric amount of sucrose between the third and twentieth day of gestation. The pups born to these rats were sacrificed either day 11 or day 14 postnatum and morphometrical, histological and biochemical analyses were done on their cerebellums and cerebrums. Pups that were exposed to ethanol in utero had significantly smaller body weights, cerebrums and cerebellums than pair-fed controls. The cerebellar mass was reduced by 10% and the cerebral weight by 3% in the pups exposed to alcohol when body weights were normalized to that of pair-fed controls. Cerebellar aspartyl aminotransferase (EC 2.6.1.1) activity was reduced at day 11 and 14 in ethanol treated pups compared with controls. Serum T4 levels were also reduced in the ethanol treated group. Histological analyses revealed that the external granule cell (EGC) layer of ethanol treated pups was significantly thicker at 11 and 14 days postnatum than that of pair-fed control pups. Cerebellar ornithine decarboxylase (ODC, EC 4.1.1.17) activity was higher at day 11 in the ethanol treated pups than in controls. The reduced mass, AAT activity, T4 serum levels and the increased thickness of the ECG layer indicate a delayed or impeded maturation of cerebellum in ethanol treated pups. These data are considered from the viewpoint that ethanol, other drugs such as methadone and prenatal stress (malnutrition) may cause delayed cerebellar maturation by reducing serum T4 levels in the early postnatal period (day 5-14).

Aspartate aminotransferase activity in dog heart lymph after myocardial infarction.

Heart lymph aspartate aminotransferase activity (AAT=GOT) was measured before and after myocardial infarctions of different sizes in 7 dogs. In all dogs the AAT activity of heart lymph rose with maximum values around 8 hours after infarction, ranging from 390 to 9700 mU/ml. In blood serum the peak AAT activity appeared about 4 hours later than in lymph, ranging from 21 to 148 mU/ml. A significant amount of the enzyme released from the infarcted myocardial cells was calculated to reach the blood via heart lymph. In 5 control dogs without myocardial infarction, the heart lymph AAT remained unchanged, ranging from 18 to 82 mU/ml during 17 hours of corresponding experimental observation.

Effects of boranes upon tissues of the rat. I. Aspartate aminotransferase and lactic dehydrogenase.

SummaryBoron hydrides inhibit AAT in the liver, heart, brain, and kidneys of normal rats. Decaborane does not cause a significant loss in activity in the tissues of pyridoxal-deficient rats. The AAT activity, when assayed with sufficient exogenous pyridoxal, is greater in the tissues from the pyridoxal-deficient animals than in the tissues from the normal animals. LDH, an enzyme that does not require pyridoxal, is moderately inhibited in the heart and kidney of both normal and pyridoxal-deficient animals, and in the brain of normal animals.