Vitamin E (alpha-tocopherol) is a lipid-soluble vitamin found within a variety of oils, nuts, and leafy greens. In a balanced diet, individuals receive approximately 10mg of Vitamin E a day. Over the counter supplements contain approximately 180mg to 450mg of synthetic Vitamin E, with no toxicity effects. Vitamin E is a common antioxidant that inhibits inflammation and increases protection of the plasma membranes. Recently, Vitamin E has been proposed to protect DNA and certain proteins against antioxidant activity. Vitamin E also protects against beta amyloid plaque formation and hyperglycemia in vitro. Since vitamin E is beneficial to cell survival, Vitamin E supplementation has the potential to influence cell culture growth. However, no studies have yet been conducted that examine the effects that Vitamin E may have on the initial growth stage of hippocampal neurons. In this study, we evaluated the effects of Vitamin E on NE-4C hippocampal neuronal cells, in vitro. NE-4C cell lines were incubated under normal glycemic conditions (5mM). Vitamin E was added to NE-4C cells at either 20M, 30M, or 40M concentrations. Control groups consisted of either untreated cells or cells treated with 5mM glucose. The experiments were run in triplicate with consistent placement using a microplate reader. The cells were examined for their cell growth and concentration of reactive oxygen species, using an XTT Assay and MitoSOX Assay, respectively. Data was analyzed using a single-factor ANOVA and 2-Tailed T-test. The results of this study concluded that hippocampal cells treated with either 20M or 40M Vitamin E in 5mM glucose possessed significantly less reactive oxygen species than cells treated with 5 mM glucose or 30M Vitamin E and 5mM glucose. The cell growth analysis showed no significant difference in cell growth between treatment conditions. These results suggest that although additions of Vitamin E may not affect initial cell growth, treatments of 20M and 40M Vitamin E decrease mitochondrial reactive oxygen species production allowing for the prolongment of hippocampal neuronal function.