V Dyachenko1, U Rueckschloss, G Isenberg. 1. Department of Physiology, Martin-Luther-University, Magdeburger Street 6, 06097 Halle, Germany.
Abstract
RATIONALE: Heterogeneity of ventricular myocytes from old murine hearts was tested in regard to cell volume and tolerance to stress induced by ROS generated by photoactivation of tetramethylrhodamine methylester. RESULTS: During repetitive linescans, ROS generated 'scars' of depolarized mitochondria. All young and 60% of old myocytes had type1 scars that were small and remained stable with time. Forty percent cells from old hearts responded with type2 scars that were wide and expanded with time. Depolarization of individual mitochondria was characterized by its half decay time. HDT was 6.9s in young mice (type1 mitochondria). HDT was 5.6s in old mice due to a 30% population of mitochondria with reduced ROS-tolerance (type2, HDT=3.0 s). Type1 and type2 mitochondria did not coexist in the same cell, however, in the same old heart (different myocytes). In a different set of myocytes the volumes were measured to be larger (83+/-29 pl) and more heterogeneous than in young myocytes (49+/-13 pl). CONCLUSION: Hearts of old mice contain a subpopulation of myocytes with reduced mitochondrial stress-tolerance that is attributed to an age-dependent reduction of cellular ROS defence capacity. We discuss how heterogeneities in stress-tolerance and cell volume could be causally linked.
RATIONALE: Heterogeneity of ventricular myocytes from old murine hearts was tested in regard to cell volume and tolerance to stress induced by ROS generated by photoactivation of tetramethylrhodamine methylester. RESULTS: During repetitive linescans, ROS generated 'scars' of depolarized mitochondria. All young and 60% of old myocytes had type1 scars that were small and remained stable with time. Forty percent cells from old hearts responded with type2 scars that were wide and expanded with time. Depolarization of individual mitochondria was characterized by its half decay time. HDT was 6.9s in young mice (type1 mitochondria). HDT was 5.6s in old mice due to a 30% population of mitochondria with reduced ROS-tolerance (type2, HDT=3.0 s). Type1 and type2 mitochondria did not coexist in the same cell, however, in the same old heart (different myocytes). In a different set of myocytes the volumes were measured to be larger (83+/-29 pl) and more heterogeneous than in young myocytes (49+/-13 pl). CONCLUSION: Hearts of old mice contain a subpopulation of myocytes with reduced mitochondrial stress-tolerance that is attributed to an age-dependent reduction of cellular ROS defence capacity. We discuss how heterogeneities in stress-tolerance and cell volume could be causally linked.