3-NP-induced Huntington's-like disease impairs Nrf2 activation without loss of cardiac function in aged rats.
Exp Gerontol
; 96: 89-98, 2017 10 01.
Article
en En
| MEDLINE
| ID: mdl-28624355
Cardiovascular diseases (CVDs) are one of the leading causes of death in patients over 60years 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.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Propionatos
/
Enfermedad de Huntington
/
Fármacos Neuroprotectores
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Factor 2 Relacionado con NF-E2
/
Nitrocompuestos
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
Exp Gerontol
Año:
2017
Tipo del documento:
Article
Pais de publicación:
Reino Unido