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Unidad de Investigacion B, Hospital Universitario Vall d'Hebron, Pg. Vall d'Hebron 119–129, 08035 Barcelona, Spain
Post-ischaemic reperfusion may precipitate cardiomyocyte death upon correction of intracellular acidosis due in part to mitochondrial permeability transition. We investigated whether glycine, an amino acid with poorly understood cytoprotective properties, may interfere with this mechanism. In cardiomyocyte cultures, addition of glycine during re-energization following 1 h of simulated ischaemia (NaCN/2-deoxyglucose, pH 6.4) completely prevented necrotic cell death associated with pH normalization. Glycine also protected against cell death associated with pH normalization in reoxygenated rat hearts. Glycine prevented cyclosporin-sensitive swelling and calcein release associated with re-energization in rat heart mitochondria submitted to simulated ischaemia or to Ca2+ stress under normoxia. NMR spectroscopy revealed a marked glycine depletion in re-energized cardiomyocytes that was reversed by exposure to 3 mM glycine. These results suggest that intracellular glycine exerts a previously unrecognized inhibition on mitochondrial permeability transition in cardiac myocytes, and that intracellular glycine depletion during myocardial hypoxia/reoxygenation makes the cell more vulnerable to necrotic death.
(Received 18 May 2004;
accepted after revision 17 June 2004;
first published online 24 June 2004)
Corresponding author D. Garcia-Dorado: Unidad de Investigacion B, Hospital Universitario Vall d'Hebron, Pg. Vall d'Hebron 119–129, 08035 Barcelona, Spain. Email: dgdorado{at}vhebron.net
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