Lyso-phosphatidylcholine is implicated in thioacetamide-induced liver necrosis

Biochem Biophys Res Commun. 1988 Jul 29;154(2):803-8. doi: 10.1016/0006-291x(88)90211-2.


Thioacetamide is a weak hepatocarcinogen. To determine whether alterations in lysophosphatidylcholine are implicated in thioacetamide-induced hepatic necrosis, rats were injected i.p. with this agent (50 mg/Kg body weight per day) or diluent for 1, 3, 8 and 30 days. Serum catalytic activities of aminotransferases were determined. Incorporation of (32P)-orthophosphate into hepatic lysophosphatidylcholine was also evaluated in animals killed 75 minutes or 13 hours after isotope administration. Results demonstrate that: A significant increase in hepatic lysolecithin concentration occurs when a maximum level of serum aminotransferases is present. An increase of (32P)-orthophosphate radioactive incorporation in lysolecithin was observed at the two assayed labelling periods, which suggest an activation of phospholipase A. The radioactivity present in lysolecithin after 13 h isotope injection showed a close correlation with serum level of aminotransferases. From these results it can be deduced that lysolecithin is implicated in TAA-induced necrosis and may be generated by increase in either phospholipase A activity and/or synthesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetamides / toxicity*
  • Animals
  • Liver / drug effects*
  • Liver / pathology
  • Lysophosphatidylcholines / metabolism*
  • Male
  • Necrosis
  • Rats
  • Rats, Inbred Strains
  • Thioacetamide / toxicity*


  • Acetamides
  • Lysophosphatidylcholines
  • Thioacetamide