The effects of Cerebrolysin on isolated chicken cortical neurons in an iron induced oxidative stress model and in a combined iron-glutamate model have been examined. In a first part of experiments it has been shown that under low serum conditions exposure of neurons to different concentrations of ammonium-iron (III)citrate (1, 5 microM AC-Fe3+) for 8 days caused a significant reduction in neuronal survival. Cerebrolysin not only prevented iron induced neurodegeneration, demonstrating that ionic iron was responsible for the cell damage, moreover, it increased the neuronal viability up to tenfold with respect to the controls. In the second part of the study neurons pre-incubated for 8 days with AC-Fe3+ were additionally lesioned with 1 mM L-glutamate and allowed to recover for another 48 h. Under these conditions cerebrolysin again clearly counteracted the in vitro destructive effects of glutamate. Besides consequences on the viability and survival of neurons Cerebrolysin increased abundance of the microtubule-associated protein MAP2, which is known to play a an important role in maintaining normal neuronal function.