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Inhibition of serum aspartate aminotransferase induced by isoniazid administration in mice
Intraperitoneal administration of isoniazid (IN), an antituberculous drug, to mice at a dose of 100 mg/kg body weight induced significant inhibition of serum aspartate aminotransferase (AAT) in several hours. The original activity was not restored readily by in vitro treatment of the sera with pyridoxal phosphate (PLP), in contrast to the rapid activation, by the same treatment, of apoAAT in the sera from control mice. Prolonged incubation with PLP prior to the assay was required to restore most of the lost activity. Serum AAT activity enhanced by experimental and the reversal of the inhibition similarly required prolonged incubation with PLP. The results suggest the possibility that human serum AAT activity measured for clinical diagnosis may be underestimated in cases of IN overdose even if the conditions for in vitro PLP treatment of samples are sufficient for conversion of the apoenzyme to the holoenzyme.
Intraperitoneal administration of isoniazid (IN), an antituberculous drug, to mice at a dose of 100 mg/kg body weight induced significant inhibition of serum aspartate aminotransferase (AAT) in several hours. The original activity was not restored readily by in vitro treatment of the sera with pyridoxal phosphate (PLP), in contrast to the rapid activation, by the same treatment, of apoAAT in the sera from control mice. Prolonged incubation with PLP prior to the assay was required to restore most of the lost activity. Serum AAT activity enhanced by experimental and the reversal of the inhibition similarly required prolonged incubation with PLP. The results suggest the possibility that human serum AAT activity measured for clinical diagnosis may be underestimated in cases of IN overdose even if the conditions for in vitro PLP treatment of samples are sufficient for conversion of the apoenzyme to the holoenzyme.