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Please use this identifier to cite or link to this item: http://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17349
Title: 3-NP-induced Huntington's-like disease impairs Nrf2 activation without loss of cardiac function in aged rats
metadata.dc.creator: ALEJANDRO SILVA PALACIOS
MARCOS OSTOLGA CHAVARRIA
MABEL BUELNA CHONTAL
CARLOS SANCHEZ GARIBAY
Sauri Hernández Resédiz
FRANCISCO JAVIER ROLDAN GOMEZ
Pedro Lorenzo Flores Chavez
ARMANDO LUNA LOPEZ
MINA KONIGSBERG FAINSTEIN
ANA CECILIA ZAZUETA MENDIZABAL
Keywords: MEDICINA Y CIENCIAS DE LA SALUD;Ciencias médicas;Ciencias clínicas;Geriatría;Envejecimiento;Aging;Envejecido;Aged;Función cardiaca;Cardiac function;Hormesis
metadata.dc.date: 2017
Publisher: Elsevier
Description: Cardiovascular diseases (CVDs) are one of the leading causes of death in patients over 60 years with Huntington's disease (HD). Here, we investigated if age-related oxidative stress (OS) is a relevant factor to develop cardiac damage in an in vivo model of striatal neurodegeneration induced by 3-nitropropionic acid (3-NP). We also evaluated the potential effect of tert-butylhydroquinone (tBHQ) to increase the Nrf2-regulated antioxidant response in hearts from adult and aged rats intoxicated with 3-NP. Our results showed that 3-NP-treatment did not induce cardiac dysfunction, neither in adult nor in aged rats. However, at the cellular level, adult animals showed higher susceptibility to 3-NP-induced damage than aged rats, which suggest that chronic oxidative stress ongoing during aging might have induced an hormetic response that probably prevented from further 3-NP damage. We also found that the oxidative unbalance concurs with unresponsiveness of the Nrf2-mediated antioxidant response in old animals.
URI: https://hdl.handle.net/20.500.12100/17349
Appears in Collections:1. Artículos

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