Potential Antioxidative Effects of Folic Acid and Betaine Combination Against to Amyloid beta (1-42) and Homocysteine-induced Oxidative Stress in Synaptosomes

Abstract

Abstract Alzheimer's disease (AD) is a progressive neurodegenerative disease and common type of dementia. Increasing number of death due to the disease has made it an important public health problem to be solved. Extracellular accumulation of amyloid beta (Aβ) peptide and hyperphosphorylated tau proteins in intracellular matrix are two major signs of the AD. In many research high levels of homocysteine (Hcy) were noted in AD. Oxidative stress appears as one of the significant factors in AD pathogenesis. Synaptosomes are substantial physiological membranous structures and can be utilized one of the in vitro models of AD. In this study, synaptosomal fractions were obtain from forebrain of rats and study groups were separated into five: control, Aβ(1–42), Aβ(1–42) + Hcy, Aβ(1–42) + Hcy + Folic Acid + Betaine, Betaine + Folic Acid. Total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), malondialdehyde (MDA) levels and activities of catalase (CAT) and superoxide dismutase (SOD) were evaluated. In Aβ(1–42) + Hcy group the high levels of TOS (0.2 ± 0.05 mol H2O2 eq/L), OSI (34.47 ± 4.41) and MDA (2,29 ± 0.42 nmol/g protein) were remarkable findings compared the control group. Administration of folic acid and betaine in combination recovered the harmful effect of Aβ(1 42) + Hcy by decreasing the TOS, OSI and MDA levels and increasing the TAS (0.41 ± 0.11mmol Trolox eq/L). In conclusion, Hcy and Aβ peptide together can lead to neurodegeneration by increasing the oxidative stress and this detrimental effect can be eliminated by administration of folic acid and betaine.