Research article

Xenon prevents cellular damage in differentiated PC-12 cells exposed to hypoxia

Christian Petzelt¹ , Per Blom² , Wolfgang Schmehl² , Jana Müller¹ and Wolfgang J Kox¹

¹  University Hospital Charité, Clinic for Anesthesiology and Intensive Care, Experimental Anesthesiology, 14050 Berlin, Germany

²  Linde Gas Therapeutics, 18181-Lidingö, Sweden

author email corresponding author email

BMC Neuroscience 2004, 5:55doi:10.1186/1471-2202-5-55

Published:	8 December 2004

Abstract

Background

The neuroprotective effect of xenon has been demonstrated for glutamatergic neurons. In the present study it is investigated if dopaminergic neurons, i.e. nerve-growth-factor differentiated PC-12 cells, are protected as well against hypoxia-induced cell damage in the presence of xenon.

Results

Pheochromocytoma cells differentiated by addition of nerve growth factor were placed in a N₂-saturated atmosphere, a treatment that induced release of dopamine, reaching a maximum after 30 min. By determining extracellular lactate dehydrogenase concentration as marker for concomitant cellular damage, a substantial increase of enzymatic activity was found for N₂-treated cells. Replacement of N₂ by xenon in such a hypoxic atmosphere resulted in complete protection against cellular damage and prevention of hypoxia-induced dopamine release. Intracellular buffering of Ca²⁺ using the Ca-chelator 1, 2-bis(2-Aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis(acetoxymethyl) ester (BAPTA) reduced the neuroprotective effect of xenon indicating the essential participation of intracellular Ca²⁺-ions in the process of xenon-induced neuroprotection.

Conclusions

The results presented demonstrate the outstanding property of xenon to protect neuron-like cells in a hypoxic situation.