Gene/Protein
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Drug
Enzyme
Compound
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Target Concepts:
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Query: EC:4.1.1.32 (
phosphoenolpyruvate carboxykinase
)
4,204
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
These studies were undertaken to determine the mechanism by which intravenously administered lead salts inhibit hepatic gluconeogenesis. Within 1 h after the intravenous administration of lead acetate (10 mg), there is 97% inhibition of CO2 fixation in isolated rat liver mitochondria. This effect is concentration-dependent. The induction of
phosphoenolpyruvate carboxykinase
activity observed with starvation was also inhibited by intravenously administered lead acetate, but the activities of pyruvate kinase, glucose 6-phosphate dehydrogenase and pyruvate carboxylase were unaffected, as was the oxidation of palmitate and palmitoyl-CoA by mitochondria from
Pb2+
-treated animals. The addition of reduced glutathione to mitochondria from
Pb2+
-treated animals had no effect on the inhibited CO2 fixation. ATP concentrations in mitochondria from
Pb2+
-treated animals are decreased and the dose-response relationships for the effect of
Pb2+
on CO2 fixation and ATP concentrations correspond. We conclude that the decrease in mitochondrial ATP in
Pb2+
-treated animals is probably responsible for the marked inhibition ov CO2 fixation, and hence the impairment of gluconeogenesis from alanine, lactate and pyruvate observed by others.
...
PMID:Inhibition of carbon dioxide fixation by lead acetate in rat liver mitochondria. 90 20
