Ventricular dysfunction and necrosis produced by adrenochrome metabolite of epinephrine: Relation to pathogenesis of catecholamine cardiomyopathy

Grape seed proanthocyanidins ameliorates isoproterenol-induced myocardial injury in rats by stabilizing mitochondrial and lysosomal enzymes: An in vivo study

“…During this reaction, highly toxic oxygen-derived free radicals are generated which are detrimental to extra and intracellular enzymes and proteins (Thompson and Hess, 1986). Adrenochrome and other oxidation metabolites of catecholamines can cause cell necrosis and contractile failure in the rat's heart (Yates et al, 1981). Cohen and Heikkila (1974) have reported that autooxidation of catecholamines results in the generation of highly cytotoxic free radicals.…”

Inactivation of catecholamines by superoxide gives new insights on the pathogenesis of septic shock

“…Although it remains to be tested, it is possible that formation of adrenochromes accounts for the organ dysfunction associated with septic shock. Some evidence already exists to support a role for adrenochromes as specific mediators of cytotoxicity and cell damage, although their mechanism(s) of actions are not known at this stage (38,40,52,53). More pertinent to the cardiovascular abnormalities of septic shock is the fact that adrenochromes have been shown to be cardiotoxic and cause myocardial necrosis (52)(53)(54).…”

“…Some evidence already exists to support a role for adrenochromes as specific mediators of cytotoxicity and cell damage, although their mechanism(s) of actions are not known at this stage (38,40,52,53). More pertinent to the cardiovascular abnormalities of septic shock is the fact that adrenochromes have been shown to be cardiotoxic and cause myocardial necrosis (52)(53)(54). If true, such adrenochrome-mediated cardiotoxicity would have adverse consequences for subjects with preexisting compromise of ventricular function and systemic O 2 delivery after coronary artery disease, hypertension, and other conditions.…”

Toxicology update: the cardiotoxicity of the oxidative stress metabolites of catecholamines (aminochromes)

“…Ascorbic acid and diththiothreitol accelerated the rate of failure of the heart due to AC Singal et al 57 Langendorff perfused rat heart using E (10 filaments and contracture with swelling of mitochondria and sarcoplasmic reticulum. 51 The post-myocardial infarction interval of 6-7 months is crucial to patients surviving a first myocardial infarction (MI) because mortality can be as much as 15%; moreover, sudden cardiac death is believed to account for 60-80% of this loss of life following an initial MI. 52 -54 In an in vivo experiment using rats, a single intravenous injection of adrenochrome (10-50 mg kg cause death in a dose-dependent manner.…”