Effect of mitochondrial L-arginine availability on isolated ventricular cardiomyocytes during mitochondrial stress.

NVCMs were either untreated, or infected with either CAT1-YFP-MTS AAV6 or YFP-MTS AAV6. Cells were then subjected to 3 hr hypoxia-2 hr reoxygenation or treated with antimycin A for 5 hr. ROS generation and mitochondrial membrane potential were measured in these cells using the fluorescent probes H2DCF-DA and JC-1 respectively. LDH release was also measured as a marker of cell death (n = 3 individual experiments with 4 replicates per experiment for fluorescent probes, or n = 3 for LDH). Data represents mean ± SEM (*p<0.05, **p<0.01 and ***p<0.001 vs. normoxic untreated controls; †p<0.01 and ††p<0.001 vs. antimycin A; and #p<0.01 and §p<0.001 vs. untreated cells after 3 hr hypoxia-2 hr reoxygenation).