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Keywords:

  • acetaminophen;
  • coronavirus;
  • hepatitis;
  • mice;
  • tumor necrosis factor

Abstract: Previous reports have demonstrated that tumor necrosis factor alpha (TNF-α) plays an important role in the pathogenesis of fulminant hepatic necrosis. The purpose of this experimental study was to measure TNF-α blood activity in paracetamol-induced liver necrosis and in coronavirus (MHV3)-induced fulminant hepatitis in mice. No elevation of TNF-α activity was found in hepatic failure complicating paracetamol poisoning. In contrast, TNF-α activity significantly increased in response to MHV3, reaching 16.3 ± 5.5 U/ml from 24 h post infection (P>0.01). This augmentation was observed even though the virus was not detectable in the liver. Serum alanine aminotransferase levels were low and no histological lesion was observed. In conclusion, our study further supports the implication of TNF-α in virus-induced hepatitis failure and confirms that paracetamol poisoning does not cause increased TNF-α activity in the circulation.