Vitamin C Decreases the Toxicity of Aβ42 in SH-SY5Y Cell Culture Assay

Alzheimer’s disease (AD) is an age-related neurodegenerative disease marked by a progressive cognitive decline. Progressive impairments in memory, cognition, and behavior are symptoms of the disease. The histopathological changes in AD include neuronal and synaptic loss, formation of extracellular senile plaques and intracellular neurofibrillary tangles in brain. In addition to the factors mentioned before, there is evidence that environmental risk factors, such as air quality, toxic heavy metals and occupational-related exposures, may also contribute to the development of AD. Multiple lines of evidence indicate that oxidative stress not only strongly participates in an early stage of AD prior to cytopathology, but plays an important role in inducing and activating multiple cell signaling pathways that contribute to the formation of lesions by toxic substances and promotion of disease. Production and accumulation of amyloid beta peptides (Aβ) is one of the important hallmarks of AD which can lead to the production of reactive oxygen species (ROS) and death of neurons. The present study evaluates the impact of an antioxidant (vitamin C) on cell viability in a neuroblastoma cell culture model (SH-SY5Y) to assess the viability of cells in its presence and absence with different concentrations in cultures containing Aβ42. We showed that vitamin C can perform as an antioxidant and increased the viability of cells at low concentrations (0.01, 0.05 and 0.1 µM). Our results indicated that vitamin C showed no protective effect against Aβ42 at high concentrations (0.5 and 1 µM). These findings could be considered as another support to the neuroprotective effect of vitamin C as an antioxidant in AD and would help to open avenues in the development of therapeutic regimens in AD.