The effect of microwave irradiation on the oxidative stability of tocopherol-enriched corn oil at temperatures of 60 or 100°C was evaluated using the Rancimat assay. Short durations of microwave treatment (1 min) on 10-g oil aliquots were found to increase the induction period of corn oil samples containing 500 and 1000 ppm tocopherol by 7.7% and 9.9%, respectively compared to control oils. The moisture content of tocopherol-enriched corn oil decreased by 15% compared to that of corn oil after 1 min of microwave treatment. At 100°C, 1000 ppm tocopherol-enriched corn oil received 3 min of microwave treatment had 5.8% and 9.9% lower primary and secondary oxidation products than control groups, respectively while this effect was not clearly observed for oils stored at 60°C. However, 15 min of microwave irradiation accelerated the rates of lipid oxidation in corn oils irrespective of the addition of tocopherol. Content of α- and γ-tocopherols in 1 min of microwave irradiated samples remained more by 28.8 and 5.8%, respectively than those of controls after 9 h heat treatment at 100°C. Overall, microwave irradiation within 3 min can increase the oxidative stability of 10 g-corn oils, especially at 100°C, which could be due to the reduced moisture content in the bulk oil matrix. Practical Application: A microwave oven is an irreplaceable home appliance and is widely used in households. Short time exposure to microwave irradiation can remove moisture efficiently from edible oils without the formation of oxidation products, which could increase the oxidative stability of these oils, especially under frying conditions. The results of this study can be utilized to ensure a longer shelf-life of fried products in the food industry by short time treatment of microwave irradiation.

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In evaluating vitamin E (VE) nutritional status of preterm infants, it is essential that any data should be compared with those of healthy term infants, and never with those of adults. Moreover, it should be evaluated in terms of gestational age (GA), not birth weight (BW), because placental transfer of most nutrients from mother to fetus is dependent on GA, not BW. Judging from the limited data during the last 75 years, there was no significant correlation between GA and VE concentrations in circulation or in the red blood cells (RBCs), leukocytes, and buccal mucosal cells. In addition, the oxidizability of polyunsaturated fatty acids (PUFAs) in plasma or RBCs, as targets for protection by VE chain-breaking ability, was lower in preterm infants. However, because of the minimal information available about hepatic VE levels, which is considered a key determinant of whole body VE status, the decision on whether VE status of preterm infants is comparable with that of term infants should be postponed. Clinical trials of VE supplementation in preterm infants were repeatedly undertaken to investigate whether VE reduces severity or inhibits development of several diseases specific to preterm infants, namely retinopathy of prematurity (ROP), bronchopulmonary dysplasia (BPD), and germinal matrix hemorrhage – intraventricular hemorrhage (GMH-IVH). Most of these trials resulted in a misfire, with a few exceptions for IVH prevention. However, almost all these studies were performed from 1980s to early 1990s, in the pre-surfactant era, and the study populations were composed of mid-preterm infants with GAs of approximately 30 weeks (wks). There is considerable difference in ‘preterm infants’ between the pre- and post-surfactant eras; modern neonatal medicine mainly treats preterm infants of 28 wks GA or less. Therefore, these results are difficult to apply in modern neonatal care. Before considering new trials of VE supplementation, we should fully understand modern neonatal medicine, especially the recent method of oxygen supplementation. Additionally, a deeper understanding of recent progress in pathophysiology and therapies for possible target diseases is necessary to decide whether VE administration is still worth re-challenging in modern neonatal intensive care units (NICUs). In this review, we present recent concepts and therapeutic trends in ROP, BPD, and GMH-IVH for those unfamiliar with neonatal medicine. Numerous studies have reported the possible involvement of reactive oxygen species (ROS)-induced damage in relation to supplemental oxygen use, inflammation, and immature antioxidant defense in the development of both BPD and ROP. Various antioxidants effectively prevented the exacerbation of BPD and ROP in animal models. In the future, VE should be re-attempted as a complementary factor in combination with various therapies for BPD, ROP, and GMH-IVH. Because VE is a natural and safe supplement, we are certain that it will attract attention again in preterm medicine.

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Chemical investigation of Allophylus africanus P. Beauv fruits led to the isolation of a new δ-tocotrienol, 3α-hydroxy-δ-tocotrienol (1) together with eight known compounds (2–9). Compound (1) was allylated (1a) and prenylated (1 b and 1c) to give three new semi-synthesized derivatives which were fully characterized as: 6-O-allyl-3α-hydroxy-δ-tocotrienol (1a), 6-O-prenyl-3α-hydroxy-δ-tocotrienol (1 b) and 6-O,5-C-diprenyl-3α-hydroxy-δ-tocotrienol (1c). The structures of compounds were established using comprehensive spectroscopic analysis including UV, MS, 1 D NMR, 2 D NMR and by comparison with the corresponding literature data. Compound (1) and its semi-synthetic derivatives (1a-c) were tested for their antioxydant activity using DPPH radical scavenging assay and also for their cytotoxicity using human cervix carcinoma KB-3-1 cell lines. The results showed that compound (1) exhibited antioxidant activity with an IC₅₀ value of 0.25 μM compared to the reference control trolox (26 µM); and good cytotoxic activity with IC₅₀ values of 97 μM compared to the reference (+)-griseofulvin (IC₅₀ between17-21 μM).

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The early history of vitamin E from its discovery by Herbert M. Evans and Katharine J. S. Bishop in 1922 up to its chemical synthesis by Paul Karrer and coworkers in 1938 and the development of the concept that vitamin E acts as an antioxidant in vivo are recalled. Some more recent results shedding doubt on this hypothesis are reviewed. They comprise influence of vitamin E on enzyme activities, signaling cascades, gene expression and bio-membrane structure. The overall conclusion is that our knowledge of the vitamin’s mechanism of action still remains fragmentary. The metabolism of tocopherols and tocotrienols is presented and discussed in respect to bioactivity of the metabolites, interference with drug metabolism and the future design of clinical trials. Some strategies are recommended how to reach the final goal: the identification of the primary vitamin E target(s) and the analysis of the downstream events up to the physiological phenomena.

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