Portal de Periódicos da CAPES

3-NP-induced Huntington's-like disease impairs Nrf2 activation without loss of cardiac function in aged rats

2017; Elsevier BV; Volume: 96; Linguagem: Inglês

10.1016/j.exger.2017.06.009

1873-6815

Alejandro Silva‐Palacios, M. Ostolga-Chavarría, Mabel Buelna‐Chontal, Carlos Sánchez-Garibay, Sauri Hernández‐Reséndiz, Francisco‐Javier Roldán, Pedro Flores, Armando Luna–López, Mina Königsberg, Cecilia Zazueta,

Coenzyme Q10 studies and effects

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.