Saadane A, Delautier D, Lestriez V, Feldmann G, Lardeux B, Bleiberg-Daniel F
Laboratoire de Biologie Cellulaire, U 327 de l'Institut National de la Santé de la Recherche Médicale (INSERM), Faculté de Médecine Xavier Bichat, Université Paris 7, France.
Inflamm Res. 1999 Apr;48(4):210-7. doi: 10.1007/s000110050448.
To determine whether the inhibition of RNA breakdown observed in ad libitum fed rats 24 h after turpentine administration still occurs in inflamed rats fasted for 24 h and to examine the mechanism and factors involved.
RNA breakdown was measured during cyclic in situ perfusion of livers by the accumulation of [14C] cytidine after in vivo RNA labelling. Autophagic activity was determined by the morphometric analysis of lysosomal structures.
The decrease in RNA breakdown (53%) observed in the inflamed rats was accompanied by a 38% drop in the fractional cytoplasmic volume of initial and digestive autophagic vacuoles. Among amino acids, only the portal levels of glutamate were significantly enhanced by 83%. In vivo suppression of glucocorticoid activity using RU 38486 in inflamed rats did not affect the inhibition of RNA breakdown.
The results show that turpentine-induced inflammation in fasted rats inhibits RNA degradation as well as autophagy and that glucocorticoids do not seem to be involved.
