Mitochondrial ATPase: a target for paracetamol-induced hepatotoxicity

We examined the effect of paracetamol treatment (650 mg/kg) on the function of the ATPase from rat hepatic mitochondria. The drug treatment caused an overall 35% decrease in ATPase activity, with a complete loss of the high affinity component as determined by substrate kinetic studies. The K m for t...

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Bibliographic Details
Published in:European journal of pharmacology. Environmental toxicology and pharmacology section 1995-10, Vol.293 (3), p.225-229
Main Authors: parmar, Dipak V., Ahmed, Gazala, Khandkar, Milind A., Katyare, Surendra S.
Format: Article
Language:English
Subjects:
Arrhenius kinetics
Hepatotoxicity
Mitochondrial ATPase
Mitochondrial particle, sonic
Paracetamol
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Summary:We examined the effect of paracetamol treatment (650 mg/kg) on the function of the ATPase from rat hepatic mitochondria. The drug treatment caused an overall 35% decrease in ATPase activity, with a complete loss of the high affinity component as determined by substrate kinetic studies. The K m for the intermediate and low affinity components decreased by about 30% without change in V max, which may represent a compensatory mechanism. The drug treatment also resulted in a dramatic decrease in the phase transition temperature by about 19°C without affecting the energies of activation of the enzyme. Mitochondrial total phospholipid content increased significantly with a reciprocal decrease in the cholesterol content. The total phopholipid/cholesterol molar ratio increased by 50% after paracetamol treatment. However, phospholipid composition (as % of total) of the mitochondria was unaltered.
ISSN:0926-6917
DOI:10.1016/0926-6917(95)00021-6