Non-steroidal anti-inflammatory agents and hepatic lipid peroxidation in normal- and carrageenin-treated rats

A single oral dose of indomethacin (3 mg/kg b.w.) and phenylbutazone (200 mg/kg b.w.) induces an enhancement of thio-barbituric acid reacting substances (TBArs) formation by total liver homogenate of male rats. On the contrary, treatment with ibuprofen (200 mg/kg b.w., os) does not influence the susceptibility of hepatic tissue to "in vitro" lipid peroxidation. The former two chemicals do not interfere with the pro-oxidant action of carbon tetrachloride (1.0 ml/kg b.w., os) whereas ibuprofen limits the extension of TBArs production provoked by the haloalkane. Further, ibuprofen does not affect the level of glutathione in liver tissue, while indomethacin and phenylbutazone do. Similar results fatty acids was studied "in vivo" by monitoring conjugated diene absorption spectrum of hepatic microsomal lipids. Oedema produced acutely by injection of carrageenin into the plantar region of rat hind paw does not influence the peroxidative decomposition of hepatic lipids as found "in vitro" and/or "in vivo" neither in the presence nor in the absence of all the mentioned chemicals. Carbon tetrachloride administered orally (1.0 ml/kg b.w.) appears to be able to depress significantly the paw oedema induced by carrageenin but does not potentiate the anti-inflammatory effect of the tested non-steroid agents.