EFFECT OF AN I.C.V. INJECTION OF AMYLOID BETA PEPTIDE (1-42) ON ON THE 24h RHYTHMS OF LIPID PEROXIDATION AND GSH IN THE RAT HIPPOCAMPUS

NAVIGATORE FONZO LS; DEYURKA NA; GARRAZA, M; ANZULOVICH AC

TUCUMAN

Congreso; 3ER REUNION CONJUNTA DE LAS SOCIEDADES DE BIOLOGIA DE LA REP. ARGENTINA; 2015

SOCIEDADES DE BIOLOGIA

Alzheimer's disease (AD) is a neurodegenerative disorder that leads to memory loss, dementia, and death. Accumulation of Aβ peptide causes an increase in intracellular reactive oxygen species (ROS) and free radicals associated to a deficient antioxidant defense system. Besides oxidative stress and cognitive deficit, AD patients show alterations in their circadian rhythms. Previously, we showed that injection of Aβ(1-42) phase shifts CAT and GPx daily rhythms in the rat hippocampus. Continuing with that study, the objective of this work was to investigate the effects of an i.c.v. injection of Aβ(1-42) peptide on temporal patterns of lipid peroxidation and glutathione (GSH) levels, as well as on Aβ protein levels, in the rat hippocampus. Four-month-old males Holtzman rats were divided into two groups defined as: control (CO) and Aβ-injected (Aβ). Rats were maintained under 12h-light:12h-dark conditions and received water and food ad libitum. Hippocampus samples were isolated every 4 h during a 24h period. Lipid peroxidation and GSH levels were determined by colorimetric assays. Aβ protein levels were analyzed by immunoblotting. We found that i.c.v. injection of Aβ(1-42) increased Aβ peptide content in the hippocampus and phase shifted Aβ, lipid peroxidation and GSH daily rhythms. These changes follow the previously observed changes in daily patterns of antioxidant enzymes activity. Thus, elevated Aβ peptide levels alter temporal patterns of oxidative stress-related parameters and, consequently, would negatively affect cellular clock activity in the hippocampus.