3-NP-induced Huntington's-like disease impairs Nrf2 activation without loss of cardiac function in aged rats
Autor: | Alejandro Silva-Palacios, Cecilia Zazueta, Armando Luna-López, C. Garibay, Sauri Hernández-Reséndiz, P.L. Flores, Mina Königsberg, Francisco-Javier Roldán, M. Ostolga-Chavarría, Mabel Buelna-Chontal |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Cardiac function curve Aging medicine.medical_specialty Heart Diseases NF-E2-Related Factor 2 Oxidative phosphorylation Disease Biology medicine.disease_cause Biochemistry Antioxidants Nrf2 activation Toxicology 03 medical and health sciences 0302 clinical medicine Endocrinology In vivo Internal medicine Genetics medicine Animals Rats Wistar Molecular Biology Antihypertensive Agents Neurodegeneration Hormesis Cell Biology Nitro Compounds medicine.disease Hydroquinones Oxidative Stress Huntington Disease Neuroprotective Agents 030104 developmental biology Female Propionates 030217 neurology & neurosurgery Oxidative stress |
Zdroj: | Experimental Gerontology. 96:89-98 |
ISSN: | 0531-5565 |
DOI: | 10.1016/j.exger.2017.06.009 |
Popis: | 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. |
Databáze: | OpenAIRE |
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