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The results obtained in the animal model of HHcy were then corroborated in primary cultures of neonatal rat cardiomyocytes, where incubation of NaHS (80 µM) for 3 days reduced mitochondrial ROS production, restored the expression of the mitochondrial NOX4 protein—a major source of oxidative stress in mitochondria—and cytochrome c in both cytoplasm and mitochondria, and preserved mitochondrial membrane potential in cells treated with Hcy (100 µM)

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