Effect of an Intracerebroventricular Injection of Aggregated Beta-amyloid (1-42) on Daily Rhythms of Oxidative Stress Parameters in the Prefrontal Cortex
Autor: | María Belén Delsouc, Cinthia Coria-Lucero, Cristina Devia, Marilina Casais, Cecilia Della Vedova, Dario C. Ramirez, Lorena S. Navigatore-Fonzo, Carina Ledezma, Silvia Marcela Delgado, Ana Cecilia Anzulovich |
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Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Male medicine.medical_specialty Antioxidant Amyloid medicine.medical_treatment Prefrontal Cortex medicine.disease_cause Hippocampus 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Alzheimer Disease Internal medicine medicine Animals Humans Circadian rhythm Prefrontal cortex chemistry.chemical_classification Amyloid beta-Peptides biology General Neuroscience Glutathione peroxidase Glutathione Peptide Fragments Rats Oxidative Stress 030104 developmental biology Endocrinology chemistry Catalase biology.protein 030217 neurology & neurosurgery Oxidative stress |
Zdroj: | Neuroscience. 458 |
ISSN: | 1873-7544 |
Popis: | Accumulation of amyloid peptides in the brain plays a key role in the pathogenesis of Alzheimer's disease (AD). Aggregated beta-amyloid (Aβ) peptide increases intracellular reactive oxygen species associated to a deficient antioxidant defense system. Prefrontal cortex plays a key role in memory and learning and is especially susceptible to oxidative stress. The objective of this work was to investigate the effects of an intracerebroventricular (i.c.v.) injection of Aβ (1–42) on 24 h patterns of oxidative stress parameters and antioxidant defenses in the rat prefrontal cortex. Four-month-old male Holtzman rats were divided into two groups defined as: control (CO) and Aβ-injected (Aβ). Rats were maintained under12 h-light:12 h-dark conditions and received water and food ad libitum. Tissues samples were isolated every 6 h during a 24 h period. Interestingly, we found that an i.c.v. injection of Aβ(1–42) increased lipid peroxidation, reduced total antioxidant capacity level, phase-shifted the daily peak of reduced glutathione, and had a differential effect on the oscillating catalase and glutathione peroxidase specific activity. Thus, elevated levels of Aβ aggregates-a pathogenic hallmark of AD, caused altered temporal patterns of the cellular redox state in prefrontal cortex rat. These findings might contribute, at least in part, to the understanding of the molecular and biochemical basis of redox changes caused by circadian rhythms alterations observed in AD patients. |
Databáze: | OpenAIRE |
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