Tocopherols and tocotrienols have been shown in previous studies to protect neurons from oxidative injuries, especially from hydrogen peroxide (H2O2) and buthionine sulfoximine (BSO) induced oxidative stress. In this study, we compared two vitamin E isomers, γ-tocotrienol (GTT) and α-tocopherol (ATF) in their neuroprotective effects against H2O2-induced apoptosis in primary rat cortical neurons and human neuroblastoma cell line SH-SY5Y. Cytotoxicity screening of H2O2, GTT and ATF was done to determine the IC50 levels. To screen for neuroprotective effects, cortical neurons and SH-SY5Y cell cultures were pre-incubated with GTT or ATF, respectively at different concentrations for 1 hour before concurrent treatment of H2O2 at IC50. Results of these treatments were compared to cells treated with H2O2 only and control cells. Cytotoxicology screening showed that IC50 of H2O2 for cortical neuron is at 50 μM while SH-SY5Y have higher IC50 of 100 μM. GTT is cytotoxic to cortical neurons at ≥50 μM and SH-SY5Y at ≥100 μM while ATF did not show any toxicity within the range of concentration tested (1-750 μM). Results from neuroprotection screening showed that GTT and ATF were able to protect both cortical neurons and SH-SY5Y from H2O2-induced oxidative stress at concetration of ≤10 μM. Cellular uptake of GTT is higher in both cortical neurons and SH-SY5Y as compared to ATF when both cortical neuron and SH-SY5Y were incubated with 10 μM GTT or ATF, respectively for 24 hour. Although primary rat cortical neurons and human neuroblastoma SH-SY5Y were different culture system, the effects of GTT and ATF are similar in both H2O2 –induced culture which strongly suggest that both GTT and ATF act as free radical scavenger to exert their neuroprotective effects.
Vitamin E is composed of various subfamilies that include tocopherols and tocotrienols. These compounds have antioxidant properties but differ in structure, dietary source and potency. In this study we evaluated the efficacy of alpha-tocopherol as an antioxidant and its role in wound closure in normal and streptozotocin-induced diabetic rats. The healing of 6 cm linear incisions created on the back of each male Sprague-Dawley rat (250-300 g) was monitored by measuring the length of the wounds daily. The rats were divided into two categories; normal and streptozotocin-induced diabetic rats. For each category, the animals were further divided into two groups; those untreated and those receiving 200 mg/kg bodyweight alpha-tocopherols daily by oral gavage. All rats were fed standard food and water ad libitum. Blood samples were taken at 0, 5 and 10 days after the wounds were created for the determination of malondialdehyde levels and red cell superoxide dismutase, catalase and glutathione peroxidase activities. The results showed that alpha-tocopherol reduced plasma malondialdehyde levels, increased glutathione peroxidase activity and accelerated the rate of wound closure in treated rats.