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In the first case NO would take over functions of the antioxidant system and thereby prevent its activation, like e.g

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Cardiac-specific deletion of mitochondrial complex I subunit NDUFS4 protein resulted in accumulation of NADH in mitochondria and elevation in NADH/NAD + in rodent heart, which correlated with the accelerated development of heart failure induced by pathological pressure overload or isoproterenol (42, 47)

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