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

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...

Full description

Saved in:
Bibliographic Details
Published in:Experimental gerontology 2017-10, Vol.96, p.89-98
Main Authors: Silva-Palacios, A., Ostolga-Chavarría, M., Buelna-Chontal, M., Garibay, C., Hernández-Reséndiz, S., Roldán, F.J., Flores, P.L., Luna-López, A., Königsberg, M., Zazueta, C.
Format: Article
Language:English
Subjects:
3-Nitropropionic acid
Aging
Animals
Antihypertensive Agents
Antioxidants - pharmacology
Cardiac function
Female
Heart Diseases - chemically induced
Hormesis
Huntington Disease - chemically induced
Hydroquinones - pharmacology
Neuroprotective Agents - pharmacology
NF-E2-Related Factor 2 - drug effects
NF-E2-Related Factor 2 - metabolism
Nitro Compounds - toxicity
Nrf2 signaling
Oxidative Stress - physiology
Propionates - toxicity
Rats, Wistar
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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. [Display omitted] •Chronic oxidative stress induces an hormetic response in heart tissue from old rats.•3-NP exerts differential effects in cardiac tissue depending on age.•The antioxidant response mediated by NRF2 is compromised in old animals.
ISSN:0531-5565
1873-6815
DOI:10.1016/j.exger.2017.06.009