Biologia, Bratislava 54/Suppl. 6: 103-108, 1999.

ISSN 0006-3088 (Biologia). ISSN 1335-6399 (Biologia. Section Cellular and Molecular Biology).

 

Full paper

Effect of stobadine on the inhibition of translation induced by ischemia and subsequent reperfusion in the rat brain.

 

Jozef Burda* & Miroslava Nemethova

Institute of Neurobiology, Slovak Academy of Sciences, Soltesovej 4, SK-04001 Kosice, Slovakia; fax: ++421 95 765074, e-mail: burda@saske.sk

* corresponding author

Received: January 5, 1999 / Accepted: October 5, 1999

 

Abstract

The ability of stobadine to prevent inhibition of proteosynthesis was examined in incomplete forebrain ischemia that was induced by a 4-vessel occlusion model and subsequent reperfusion. The extent of inhibition was determined by the measurement of labelled leucine incorporation into polypeptide chains in the cell free system and the activity of eukaryotic initiation factor 2 (eIF-2). Both labelled leucine incorporation into proteins and the activity of eIF-2 were significantly inhibited in brain cortex samples from animals subjected to ischemia followed by reoxygenation in comparison with ischemic samples without reperfusion, or control samples from sham operated animals. Whereas the effect of therapeutic doses of stobadine, (5 mg/kg) administered i.p. 15 min before ischemia, on leucine incorporation was low in samples from ischemia without reperfusion, stobadine significantly prevented inhibition occuring in the first minutes of reperfusion. Favourable impact of stobadine was higher in the assay of ternary complex formation (activity of eIF-2) than in the leucine incorporation into polypeptides. It may be concluded that: 1) free oxygen radicals probably play a significant role in postischemic inhibition of translation; 2) stobadine very effectively prevents deprivation of the reinitiation ability of the proteosynthetic machinery and the activity of eIF-2.

 

Key words: stobadine, translation, transient cerebral ischemia, initiation factors, free oxygen radicals.