INTRACEREBROVENTRICULAR INJECTION OF BETA AMYLOID PEPTIDE (1-42) MODIFIESTHE TEMPORAL ORGANIZATION OF ANTIOXIDANT DEFENSES AND OXIDATIVE STRESS IN THE PREFRONTAL CORTEX

LEDESMA CARINA; DELGADO S.M; CORIA LUCERO CINTHIA; DELSOUC BELEN; CASAIS MARILINA; DELLA VEDOBA CECILIA; RAMIREZ DARIO; ANZULOVICH, ANA C.; NAVIGATORE FONZO LORENA

Las Vegas

Congreso; 26th Annual Conference of the Society for Redox Biology and Medicine,; 2019

Accumulation of amyloid peptides in the brain plays a key role in the pathogenesis of Alzheimer´sdisease (AD). Aggregated beta-amyloid (Aβ) peptide increases intracellular reactive oxygen speciesassociated with a deficient antioxidant defense system. The prefrontal cortex plays a key role inmemory and learning and is especially susceptible to oxidative stress. The objective of this work wasto investigate the effects of an intracerebroventricular (i.c.v.) injection of Aβ (1-42) on 24h patternsof oxidative stress parameters and antioxidant defenses in the rat prefrontal cortex. Four-month-oldmale Holtzman rats were divided into two groups defined as control (CO) and Aβ-injected (Aβ).Rats were maintained under12h-light:12h-dark conditions and received water and food ad libitum.Tissues samples were isolated every 6 h during a 24h 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 oscillatingcatalase and glutathione peroxidase specific activity. Thus, elevated levels of Aβ aggregates-apathogenic hallmark of AD caused altered temporal patterns of the cellular redox state in prefrontalcortex rat. These findings might contribute, at least in part, to the understanding of the molecular andbiochemical basis of redox changes caused by circadian rhythms alterations observed in AD patients