Selenium’s Role in Neuroprotection Against Stroke-Induced Inflammation

Abstract

Acute ischemic stroke (AIS) incidence across the globe is on the rise, and the deleterious effects have not yet been improved with the use of current pharmaceuticals. Tissue plasminogen activator (tPA) has many risks and time constraints, making it difficult to use even as the standard treatment. Selenium deficiency and stroke incidence have a strong linear correlation among various populations. Using the ADME-Tox software, selenious acid absorption in brain cells, tissue, and interstitium was modeled under ischemic conditions to determine the bioavailability of selenium (Se) in the brain using various IV (intravenous) infusion doses. Additionally, we studied the cytotoxicity of selenious acid and selenourea on human dermal fibroblasts (HDF) and lung carcinoma cells (A549) to determine the overall growth and toxicity of different body cell lines to account for systemic side effects of IV infusion. Our data suggest that selenium can reach a dose-dependent concentration of 1.5µg/L or 250µg/L in brain cells within two hours of a one-time IV infusion, showing the ability to reach brain vasculature. Furthermore, cell viability can be maintained between 95% and 100% using 1nM and 0.5nM concentrations of selenious acid.