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

Behonick, George; Novak, Mark J.; Nealley, Eric W.; Baskin, Steven I.

doi:10.1002/jat.793

Cited by 109 publications

(76 citation statements)

References 41 publications

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“…Catecholamines are known to be a major risk factor for hypertension and CVD, because they can increase heart rate, blood pressure and ROS production. [67][68][69][70] Elevated catecholamines may be caused by two factors: (1) an increase in catecholamines release from the sympathetic nervous system and (2) a decrease in their degradation (that is, inactivation). Methylation is a crucial step in the degradation of catecholamines, which involves two methyltransferases: phenylethanolamine N-methyltransferase and catechol O-methyltransferase, where the former catalyzes norepinephrine to epinephrine and the latter converts catecholamines to methylated derivatives.…”

Section: Arsenicmentioning

confidence: 99%

Dietary methyl-consuming compounds and metabolic syndrome

Zhou

et al. 2011

Hypertens Res

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The metabolic syndrome, a major risk factor for type 2 diabetes and cardiovascular disease, is a cluster of metabolic abnormalities including obesity, insulin resistance, hypertension and dyslipidemia. Although systemic oxidative stress and aberrant methylation status are known to have important roles in the development of metabolic syndrome, how they occur remains unclear. The metabolism of methyl-consuming compounds generates reactive oxygen species and consumes labile methyl groups; therefore, a chronic increase in the levels of methyl-consuming compounds in the body can induce not only oxidative stress and subsequent tissue injury, but also methyl-group pool depletion and subsequent aberrant methylation status. In the past few decades, the intake amount of methyl-consuming compounds has substantially increased primarily due to pollution, food additives, niacin fortification and high meat consumption. Thus, increased methyl consumers might have a causal role in the development and prevalence of metabolic syndrome and its related diseases. Moreover, factors that decrease the elimination/ metabolism of methyl-consuming compounds and other xenobiotics (for example, sweat gland inactivity and decreased liver function) or increase the generation of endogenous methyl-consuming compounds (for example, mental stress-induced increase in catecholamine release) may accelerate the progression of metabolic syndrome. Based on current nutrition knowledge and the available evidence from epidemiological, ecological, clinical and laboratory studies on metabolic syndrome and its related diseases, this review outlines the relationship between methyl supply-consumption imbalance and metabolic syndrome, and proposes a novel mechanism for the pathogenesis and prevalence of metabolic syndrome and its related diseases.

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Section: Arsenicmentioning

confidence: 99%

Dietary methyl-consuming compounds and metabolic syndrome

Zhou

et al. 2011

Hypertens Res

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“…La patogenia de esto se ha relacionado con hipoxia miocárdica funcional, espasmo coronario, cambios en la permeabilidad de la membrana para Ca +2 y Mg +2 y cambios metabólicos en la célula miocárdica, todo ello causado por metabolitos oxidativos de las catecolaminas 10 . Los hallazgos ecocardiográficos son variables y van desde la hipertrofia ventricular izquierda, mio-con MIBG es una técnica de imágenes funcional que se basa en la capacidad del MIBG, un análogo de la norepinefrina, de ser captado por el tejido adrenal.…”

Section: Discussionunclassified

Feocromocitoma: presentación como síndrome coronario agudo. Reporte de un caso

Enríquez¹,

Paredes

Tagle

et al. 2014

Rev. méd. Chile

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Refería haber presentado episodio de similares características dos días antes, lo que motivó consulta en otro servicio de urgencias, donde fue evaluada con electrocardiograma (ECG) y enzimas cardiacas; no impresionando cuadro de origen coronario, por lo que se derivó a su domicilio. Dentro de sus antecedentes destacaba historia de hipertensión arterial de data no precisada, en tratamiento con atenolol 50 mg al día, y cáncer de mama tratado 20 años antes con cirugía y radioterapia. La paciente no era fumadora ni tenía antecedentes familiares de cardiopatía coronaria.Al ingreso, la paciente se encontraba sudorosa, pero sin dolor. La presión arterial era 100/60 mmHg y su frecuencia cardiaca 87 lpm. Al examen físico destacaban yugulares colapsables en inspiración, la auscultación cardiaca no reveló soplos ni galope y había sensibilidad a la palpación epigástrica. El resto del examen no era destacable. Al interrogatorio, la paciente refería historia de episodios similares durante los últimos 6 meses, sin clara relación con esfuerzos físicos, que en un principio eran esporádicos pero que durante la última semana se hicieron más frecuentes, casi diarios. El ECG mostró un discreto supradesnivel del segmento ST (SDST) anteroseptal con inversión de la onda T de V1 a V3, que ya era evidente en ECG tomado 2 días antes y que no fue evolutivo (Figura 1). La radiografía de tórax mostró una silueta cardiaca de tamaño normal y no se observaban signos de congestión pulmonar. La paciente fue admitida a la unidad coronaria, con terapia de síndrome coronario agudo sin SDST. La troponina I de ingreso fue de 0,07 pg/ml (valor normal < 0,05) y la CK

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“…31 The later can be further aggravated by metabolic changes, such as the stimulation of lipolysis with deposition of neutral lipid droplets in cardiomyocytes resulting in an uncoupling of oxidative phosphorylation. 32 Changes in membrane permeability leading to various electrolytic imbalances, disturb multiple cellular homeostatic processes fostering additional myocardial toxicity. 33 Finally, Martin and coll.…”

Section: Catecholamine-mediated Myocardial Stunningmentioning

confidence: 99%

Pathogenesis of Takotsubo Syndrome

et al. 2017

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Takotsubo syndrome (TTS) is an enigmatic disease with a multifactorial and still unresolved pathogenesis. Postulated mechanisms include catecholamine excess, coronary artery spasm, and microvascular dysfunction, however catecholamines seem to play a central role in the pathophysiology of TTS. In facts catecholamines have relevant effects on the vasculature and myocardium. Toxic direct effects of catecholamine on myocardium are mediated by multiple pathway including functional hypoxia, metabolic changes and changes in membrane permeability leading to various electrolytic imbalances. Recently report of familial cases has suggested a genetic component. Further research is required to help clarify the proposed hypotheses and to increase our understanding of the cardiovascular responses to acute stress and the pathophysiology underpinning TTS.

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

Cited by 109 publications

References 41 publications

Dietary methyl-consuming compounds and metabolic syndrome

Dietary methyl-consuming compounds and metabolic syndrome

Feocromocitoma: presentación como síndrome coronario agudo. Reporte de un caso

Pathogenesis of Takotsubo Syndrome

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