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Oxidation of tocotrienol enriched corn oil was measured for primary oxidative products, lipid hydroperoxides and quantified by peroxide value (PV). Oxidative Stability Index (OSI) was used to determine the induction period (hrs) by indirect measurement of volatile secondary oxidation products, mainly formic acid. Vitamin E stripped corn oil samples were spiked with individual tocotrienols or tocopherols (collectively, tocols) at concentrations between 100 and 5,000 ppm. A positive relationship was observed between the concentration of all tocols and inhibition of the formation of secondary products. Gamma tocotrienol (γ-T3) provided the most protection, with delta tocopherol (δ-T) and delta tocotrienol (δ-T3) providing similar protection. Alpha tocotrienol (α-T3) and alpha tocopherol (α-T) followed a similar trend but with diminishing capacity at concentrations higher than 700 ppm. The change in mean daily peroxide value increased as αtocopherol and αtocotrienol concentrations increased. When compared against the non-spiked, stripped control oil, both αtocopherol and αtocotrienol demonstrated better antioxidant effects at lower concentrations and actually promoted oxidation at concentrations at 700 ppm and above. These effects were not observed with the γand δtocols. Crude oils from corn kernels, both control and that expressing a homogentisate geranylgeranyl transferase (HGGT) gene, were tested for oxidative stability. No pro-oxidant effects were observed in the modified crude corn oil containing up to 5,000 ppm tocotrienols (6,200 ppm total tocotrienols and tocopherols) when compared to the control crude corn oil containing 300 ppm tocotrienols (1,500 ppm total tocols).

To explore possible food applications, the oxidative stability, antioxidants contents (tocopherols and tocotrienols), thermal properties, and solid fat content of winged bean oil were investigated along with soybean oil for comparison. Results showed that winged bean oil was significantly (p < 0.05) resistant to oxidation (27 h) compared to soybean oil (9 h) heated at 110oC for 32 h, due presumably to the presence of alpha tocotrienol and the high behemic acid content. The high content of tocopherols, 230 mg/100 g in soybean oil did not contribute much to its oxidation stability. At around 25oC, winged bean oil contained about 15% solid fat content with

A growing body of research supports that members of the vitamin E family are not redundant with respect to their biological function. Palm oil derived from Elaeis guineensis represents the richest source of the lesser characterized vitamin E, alpha-tocotrienol. One of 8 naturally occurring and chemically distinct vitamin E analogs, alpha-tocotrienol possesses unique biological activity that is independent of its potent antioxidant capacity. Current developments in alpha-tocotrienol research demonstrate neuroprotective properties for the lipid-soluble vitamin in brain tissue rich in polyunsaturated fatty acids (PUFAs). Arachidonic acid (AA), one of the most abundant PUFAs of the central nervous system, is highly susceptible to oxidative metabolism under pathologic conditions. Cleaved from the membrane phospholipid bilayer by cytosolic phospholipase A(2), AA is metabolized by both enzymatic and nonenzymatic pathways. A number of neurodegenerative conditions in the human brain are associated with disturbed PUFA metabolism of AA, including acute ischemic stroke. Palm oil-derived alpha-tocotrienol at nanomolar concentrations has been shown to attenuate both enzymatic and nonenzymatic mediators of AA metabolism and neurodegeneration. On a concentration basis, this represents the most potent of all biological functions exhibited by any natural vitamin E molecule. Despite such therapeutic potential, the scientific literature on tocotrienols accounts for roughly 1% of the total literature on vitamin E, thus warranting further investment and investigation.

Our previous works have elucidated that the 12-lipoxygenase pathway is directly implicated in glutamate-induced neural cell death, and that such that toxicity is prevented by nM concentrations of the natural vitamin E alpha-tocotrienol (TCT). In the current study we tested the hypothesis that phospholipase A(2) (PLA(2)) activity is sensitive to glutamate and mobilizes arachidonic acid (AA), a substrate for 12-lipoxygenase. Furthermore, we examined whether TCT regulates glutamate-inducible PLA(2) activity in neural cells. Glutamate challenge induced the release of [(3)H]AA from HT4 neural cells. Such response was attenuated by calcium chelators (EGTA and BAPTA), cytosolic PLA(2) (cPLA(2))-specific inhibitor (AACOCF(3)) as well as TCT at 250 nM. Glutamate also caused the elevation of free polyunsaturated fatty acid (AA and docosahexaenoic acid) levels and disappearance of phospholipid-esterified AA in neural cells. Furthermore, glutamate induced a time-dependent translocation and enhanced serine phosphorylation of cPLA(2) in the cells. These effects of glutamate on fatty acid levels and on cPLA(2) were significantly attenuated by nM TCT. The observations that AACOCF(3), transient knock-down of cPLA(2) as well as TCT significantly protected against the glutamate-induced death of neural cells implicate cPLA(2) as a TCT-sensitive mediator of glutamate induced neural cell death. This work presents first evidence recognizing glutamate-induced changes in cPLA(2) as a novel mechanism responsible for neuroprotection observed in response to nanomolar concentrations of TCT.

Following model studies, the detection of palm mid-fraction (PMF) added to cocoa butter (CB) in chocolate formulations was investigated. Different levels of PMF (0–25%, CB basis) were added to CB in chocolate. High performance liquid chromatography was then used to detect the presence of PMF in chocolate using α-tocotrienol as an indicator. The results, in line with the model studying indicated that increasing the amount of PMF added to CB resulted in a significant (P

Vitamin E, such as alpha-tocopherol (ATPH) and alpha-tocotrienol (ATTN), is a chain-breaking antioxidant that prevents the chain propagation step during lipid peroxidation. In the present study, we investigated the effects of ATTN on KA-induced neuronal death using organotypic hippocampal slice culture (OHSC) and compared the neuroprotective effects of ATTN and ATPH. After 15 h KA (5 µM) treatment, delayed neuronal death was detected in the CA3 region and reactive oxygen species (ROS) formation and lipid peroxidation were also increased. Both co-treatment and post-treatment of ATPH (100 µM) or ATTN (100 µM) significantly increased the cell survival and reduced the number of TUNEL-positive cells in the CA3 region. Increased dichlorofluorescein (DCF) fluorescence and levels of thiobarbiturate reactive substances (TBARS) were decreased by ATPH and ATTN treatment. These data suggest that ATPH and ATTN treatment have protective effects on KA-induced cell death in OHSC. ATTN treatment tended to be more effective than ATPH treatment, even though there was no significant difference between ATPH and ATTN in co-treatment or post-treatment.

Background Tocotrienols (T3) and tocopherols (T), both members of the natural vitamin E family have unique biological functions in humans. T3 are detected in circulating human plasma and lipoproteins, although at concentrations significantly lower than α-tocopherol (α-T). T3, especially α-T3 is known to be neuropotective at nanomolar concentrations and this study evaluated the postprandial fate of T3 and α-T in plasma and lipoproteins. Methods Ten healthy volunteers (5 males and 5 females) were administered a single dose of vitamin E [526 mg palm tocotrienol-rich fraction (TRF) or 537 mg α-T] after 7-d pre-conditioning on a T3-free diet. Blood was sampled at baseline (fasted) and 2, 4, 5, 6, 8, and 24 h after supplementation. Concentrations of T and T3 isomers in plasma, triacylglycerol-rich particles (TRP), LDL, and HDL were measured at each postprandial interval. Results After TRF supplementation, plasma α-T3 and γ-T3 peaked at 5 h (α-T3: 4.74 ± 1.69 μM; γ-T3: 2.73 ± 1.27 μM). δ-T3 peaked earlier at 4 h (0.53 ± 0.25 μM). In contrast, α-T peaked at 6 h (30.13 ± 2.91 μM) and 8 h (37.80 ± 3.59 μM) following supplementation with TRF and α-T, respectively. α-T was the major vitamin E isomer detected in plasma, TRP, LDL, and HDL even after supplementation with TRF (composed of 70% T3). No T3 were detected during fasted states. T3 are detected postprandially only after TRF supplementation and concentrations were significantly lower than α-T. Conclusions Bio-discrimination between vitamin E isomers in humans reduces the rate of T3 absorption and affects their incorporation into lipoproteins. Although low absorption of T3 into circulation may impact some of their physiological functions in humans, T3 have biological functions well below concentration noted in this study.