Effects Of Tocotrienol-rich Fraction Research Articles

EFFECTS OF PALM OIL DERIVED TOCOTRIENOL RICH FRACTION AND VITAMIN E ISOMERS ON BIOMARKERS OF EARLY ATHEROGENESIS IN STIMULATED HUMAN UMBILICAL VEIN ENDOTHELIAL CELLS

This study was conducted to investigate the effects of tocotrienol rich fraction (TRF), α-TOC, and pure TCT isomers (α-. γ- & δ-TCT) on inflammation, endothelial activation, nuclear factor kappa B (NFκB), endothelial nitric oxide synthase (eNOS) and monocyte binding activity (MBA) in vitro. Human umbilical vein endothelial cells (HUVECs) were incubated with various concentrations of α-TOC, pure TCT isomers and TRF (0.3-10 µM) together with lipopolysaccharides (LPS) for 16 h. Culture medium and cells were collected and measured for the protein and gene expression of IL-6, TNF-α, NFκB, ICAM-1, VCAM-1, e-selectin, and eNOS. Monocyte binding activity (MBA) was measured by Rose Bengal staining. Area under the curve (AUC) analysis revealed that TRF and pure TCT particularly γ- and δ- isomers, showed better inhibition of inflammation and endothelial activation, MBA and greater eNOS increment than α-TOC. These suggest that TRF and pure TCT isomers have potential as preventive anti-atherogenic agents by attenuating the release of early biomarkers of atherogenesis which is better than α-TOC in LPS-stimulated human endothelial cells.

Tocotrienol-rich Fraction Modulated Genes Responsible for Inflammation in Lipopolysaccharide-stimulated RAW 264.7 Macrophages

Background: Inflammation plays a vital role in the pathogenesis of chronic non-communicable diseases (NCDs), the leading health issue worldwide. An earlier study reported that tocotrienol-rich fraction (TRF) showed better anti-inflammation effects in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages.
 Aim: This study aimed to investigate the anti-inflammatory effects of tocotrienol-rich fraction at the molecular level by looking at the genes that were differentially regulated and pathways affected in LPS-stimulated macrophages exposed to TRF using the microarray approach.
 Methods: A microarray study was carried out in LPS-stimulated RAW 264.7 macrophages. Total ribonucleic acid (RNA) was extracted from the RAW 264.7 cells treated with TRF (10µg/mL), alpha-tocopherol (10 µg/mL) or LPS (10 ng/mL). Untreated cells served as control. Enrichment analyses, such as Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway (KEGG), were conducted for genes listed in the differentially expressed genes (DEGs). 
 Results: The microarray analysis showed that the expression of five genes [Hamp, Interleukin-1a (IL-1a), IL-b, C-X-C motif chemokine ligand 2 (CXCL2) and colony-stimulating factor 3 (CSF3)] and one gene (SLC1A4), an amino acid transporter, was modulated (fold change 2, P< 0.05) in the TRF-treated cells. With a more stringent analysis (fold change 3, P < 0.05), only one gene (CSF3) was downregulated in the TRF-treated in RAW 264.7 cells. Analysis using the GO and KEGG pathways revealed interactions between pro-inflammatory agents such as tumor necrosis factor-alpha (TNFα) and nuclear factor kappa-light-chain-enhancer of activated B-cells (NF-B), as well as signaling pathways of interleukin (IL)-1 and IL-17.
 Conclusion: TRF modulated the expression of genes responsible for acute and chronic inflammation that were part of the lipoxygenase (LOX) and cyclooxygenase (COX) inflammatory pathways. Further investigation on the effects of TRF in different cell lines and in vivo studies should be conducted in the future.

Effect of Tocotrienol-Rich Fraction on Superoxide Dismutase 3 Expression in Mice Liver

Effect of Tocotrienol-Rich Fraction on Superoxide Dismutase 3 Expression in Mice Liver

The effects of royal jelly and tocotrienol-rich fraction on impaired glycemic control and inflammation through irisin in obese rats.

The effects of royal jelly (RJ) and tocotrienol-rich fraction (TRF) on obesity-induced glucose intolerance and inflammation were assessed in the current study. Regarding irisin as an important adipomyokine that attenuates obesity-induced disorders, we evaluated whether RJ and TRF could exert their metabolism regulatory effects through irisin. Obese rats were fed a high-fat diet (HFD) with or without supplementation of RJ, TRF, or both, for 8weeks. At the end of the intervention, weight, irisin, glycemic, and inflammatory indices were measured. The weight of the rats did not remarkably reduce in any of the groups. Glucose homeostasis and inflammation were improved when we added RJ and TRF to HFD. RJ elevated irisin concentration, but the effect of TRF on irisin was not noticeable. Our results indicated that, despite the lack of significant weight loss, RJ and TRF promoted healthy obesity. This improvement was mediated by irisin in RJ consuming rats. PRACTICAL APPLICATIONS: Obesity is a public health concern associated with several chronic disorders. The beneficial effects of irisin on obesity-related disorders are well-established. It is the first study assessing the effect of RJ and TRF as functional foods, with pharmacological and nutritional activities on obesity complications, through irisin mediation. Our study demonstrated that RJ exerts its metabolic regulatory effects by irisin as a mediator. Our investigation makes a remarkable contribution to the literature, because it suggests a new mechanism for the anti-obesity properties of RJ and TRF.

Zebrafish parkinson's model: The effects of tocotrienol rich fraction towards rotenone induced zebrafish

Zebrafish parkinson's model: The effects of tocotrienol rich fraction towards rotenone induced zebrafish

Tocotrienol-Rich Fraction Modulates Genes Expression in Oxidative Stress-induced Caenorhabditis e legans

Objective: The study was done to determine the effect of Tocotrienol rich fraction (TRF) on the expression of RNAs in C. elegans under oxidative stress.
 Methods: The nematodes were divided into 4 groups and treated accordingly: control; TRF; hydrogen peroxide (H202); TRF treatment before and after H202-induction (TRF+H202+TRF). Expressions of RNAs were analyzed with Affymetrix Genechip C. elegans Genome Array and Genespring GX11 software where differentially expressed genes were further analyzed using gene ontology (GO). Selected genes (unc-15, cit-1.2, ftn-1, rsks-1, unc-4 and daf-12) were analyzed with RT-qPCR to validate the results.
 Results: TRF modulated the expression of 314 genes involved in determination of adult lifespan, regulation of growth and lipid modification. A total of 440 genes involved in RNA metabolic processes, transcription, growth and differentiation of muscle and nerve cells were differently expressed following H202 induction. TRF treatment before and after H202- induction resulted in 438 differentially expressed genes involved in RNA metabolic processes, transcription, response to xenobiotic stimulus and protein amino acid phosphorylation.
 Conclusion: TRF modulates the expression of genes involved in the regulation of lifespan in C. elegans.
 Bangladesh Journal of Medical Science Vol.18(4) 2019 p.711-721

Tocotrienol-Rich Fraction (TRF) Improves the Viability of Wild-Type Saccharomyces cerevisiae in the Initial Stationary Phase

Palm oil tocotrienol-rich fraction (TRF) containing majorly of αα, β, γ andδδ-tocotrienols and some αα-tocopherols, was reported to have anti-ageing effects in both human and non-human model organisms, but still remains unexplored in the yeast model. It was reported to have the ability to extend the lifespan of several organisms. Chronological lifespan is one of the means to measure ageing in yeasts. The effect of TRF on the viability of three strains of Saccharomyces cerevisiae (wild-type, CTT1ΔΔand GPx2Δ) was studied. Phenotypic growth analysis of all strains was carried out for 15 hours by measuring the absorbance at OD600nm and cell counting. The optimum dose of TRF was optimised by determining the number of colony-forming unit by the wild-type strain at the end of a 24-hour treatment with TRF (ranging from 0μg/ml to 300μg/ml). TRF at 300 μg/mL showed the best result, and selected as a working dose. Treatment of cells with 300 μg/mL of TRF improved the viability of the wild-type strain in the initial stationary phase, but not on the knockout strains. These finding suggests that TRF has a potential in prolonging the chronological lifespan of S. cerevisiae, and perhaps other organisms as well.

The Effect of Tocotrienol-Rich Fraction on the Expression of Glutathione S-Transferase Isoenzymes in Mice Liver

Glutathione S-transferase isoenzymes (GSTs) catalyze the conjugation reaction between glutathione and electrophilic compounds. GSTs are involved in the detoxification of toxic and carcinogenic compounds, thus protecting the body from toxic injuries. Tocotrienols are part of the vitamin E family and is believed to possess potent antioxidant activity. The objective of this study was to determine the effect of increasing doses of tocotrienol rich fraction (TRF) supplementation on liver GSTs gene and protein expression. A total of 30 male ICR white mice were divided into five groups (n=6 for each group) and given treatment for 14 days through oral supplementation. Groups were divided as follows: - three groups administered with TRF at doses of 200, 500 and 1000 mg/kg, respectively, a positive control group administered with 100 mg/kg butylated hydroxyanisole (BHA) and a control group administered with only the vehicle (corn oil). At day 15, the mice were sacrificed and their livers isolated. Total RNA was extracted from the liver and quantitative real-time polymerase chain reaction (qPCR) assays were performed to analyze GSTs gene expression. Total liver protein was also extracted and the protein expression of GSTs was determined by Western blotting. The results showed that TRF oral supplementation caused a significant dose-dependent increase in liver GST isoenzymes gene and protein expression, compared to controls. In conclusion, TRF oral supplementation for 14 days resulted in increased gene and protein expression of GST isoenzymes in mice liver dose-dependently, with the highest expression seen in mice treated with 1000 mg/kg TRF.

Proteomic Profiling of Equine Blastocoel Fluid and Functional Mapping of Embryo Transcriptome

Dyslipidemia is common in patients with diabetes mellitus (DM) and is considered a risk factor for the progression of diabetic nephropathy (DN). Hyperlipidemia and hyperglycemia act synergistically to induce renal injury. The present study was designed to investigate the protective effects of tocotrienols as tocotrienol-rich fraction (TRF) extracted from palm (PO) and rice bran oils (RBO) against lipid induced nephropathy in type-2 diabetic rats and its probable molecular mechanism. Male Wistar rats (175–200 g) were divided into four groups. The first group served as diabetic control, while the second and third groups received PO-TRF and RBO-TRF, respectively by gavage over a period of sixteen weeks post-induction of diabetes. The fourth group comprised of age-matched rats that served as normal control. The effects of TRF on serum lipid profile, oxidative stress markers, expression of TGF-β, fibronectin and collagen type IV were analyzed in the kidney of diabetic rats. Treatment with PO-TRF and RBO-TRF significantly improved glycemic status, serum lipid profile and renal function in type-2 diabetic rats. In addition, TRF supplementation down-regulated the expression of TGF-β, fibronectin and collagen type IV in the kidney of diabetic rats. Transforming growth factor-β (TGF-β) plays a critical role in progression of DN, but its modulation by tocotrienols in DN remains unexplored. TRF ameliorated lipid induced nephropathy in type-2 diabetes by its hypoglycemic, hypolipidemic and antioxidant activities as well as by modulation of TGF-β to prevent increased expression of collagen type IV and fibrinogen. We finally propose a mechanism for the expression of molecular markers that are significant in the events leading to diabetic nephropathy and its modulation by tocotrienols/TRF.

The Effect of Tocotrienol-Rich Fraction on Oxidative Liver Damage Induced by Fenitrothion

Exposure to organophosphate pesticide including fenitrothion (FNT) has led to many adverse effects on human health. However, a potent antioxidant like palm oil tocotrienol-rich fraction (TRF) can reduce oxidative damage in various pathological conditions, could also reduce the adverse effects by FNT. The aim of this study was to evaluate the effect of TRF on oxidative liver damage in FNT induce hepatotoxicity in experimental rats. A total of 40 male Sprague-Dawley rats were randomly divided into four groups of 10, namely control, TRF, FNT and TRF+FNT group. TRF (200 mg/kg body weight) and FNT (20 m/kg body weight) were administered through oral gavage for 28 days. Corn oil which served as vehicle was given orally to the control group. At the end of the study period, liver and blood was taken for oxidative damage and biochemical evaluation and histological observation. TRF supplementation prevents oxidative liver damage by reducing the hepatic malondialdehyde (MDA) and protein carbonyl (PCO) level significantly. Besides, TRF also restored the endogenous antioxidants particularly reduced glutathione (GSH), glutathione peroxidase (GPx) and ferric reducing/antioxidant power (FRAP). TRF also prevent liver damage by reducing the liver enzymes, alanine aminotransferase (ALT) and aspartate aminotransferase (AST). The attenuation of liver damage by TRF was also showed histologically. In conclusion, TRF supplementation showed a potential in preventing oxidative liver damage in FNT-treated rats by reducing the oxidative damage and improving the antioxidant status.

Comparing palm oil tocotrienol rich fraction with α-tocopherol supplementation on oxidative stress in healthy older adults

Vitamin E is a fat-soluble compound and powerful antioxidant that have been shown to protect the cell membranes against damage caused by free radicals. Human vitamin E supplementation studies are usually limited to α-tocopherol but currently tocotrienols are also available. This study aims to compare the effects of tocotrienol rich fraction (TRF) with α-tocopherol (α-TF) supplementation on oxidative stress in healthy male and female older adults aged 50-55 years old. A total of 71 subjects both male and female aged between 50 and 55 years were divided into groups receiving placebo (n=23), α-TF (n=24) and TRF (n=24) for six months. Blood was taken at baseline (month 0), 3 months and 6 months osf supplementation for determination of plasma malondialdehyde (MDA), protein carbonyl, total DNA damage, vitamin D concentration and vitamin E isomers. α-TF supplementation reduced plasma MDA and protein carbonyl in female subjects after 3 and 6 months. TRF supplementation reduced MDA levels in both males and females as early as 3 months while DNA damage was reduced in females only at 6 months. Supplementation with α-TF and TRF increased plasma vitamin D concentration in both males and females after 6 months, but vitamin D concentration in male subjects were significantly higher compared to female subjects in TRF group. Vitamin E isomer determination showed α-TF, α-tocotrienol and γ-tocotrienol were increased in both male and female subjects. In conclusion, TRF supplementation effects were different from α-TF in reducing oxidative stress markers and vitamin D levels with a more pronounced effect in female subjects.

Effect of tocotrienol rich fraction extracted from palm oil on cognitive functions and antioxidant enzymes status in Alzheimer’s disease mouse model

Effect of tocotrienol rich fraction extracted from palm oil on cognitive functions and antioxidant enzymes status in Alzheimer’s disease mouse model

Effect of Tocotrienol Rich Fraction (TRF) on synaptogenic molecules in aging Caenorhabdis elegans

Objective: This study was performed to determine the effect of tocotrienol rich fraction (TRF) on the expression of synaptogenic genes and proteins in aging C.elegans . Method: Age synchronized DP132 strain worms were divided into two groups; control and treatment where worms were grown in nematode growth medium enriched with 50 ?g/ml TRF. The RNA and proteins expressions of syd-2, sad-1 and aex-3 were determined at day 2, 8 and 13 by q-RTPCR and western blot respectively. Results: The RNA and proteins expressions of syd-2, sad-1 and aex-3 decreased significantly with age in C.elegans . Interestingly, TRF treatment successfully increased the expression of these molecules from day 2 to day 8 which is known to be the reproductive phase of C.elegans but showed limited effect on the expression of these proteins at day 13. Conclusion: TRF enhances the expression of molecules involved in synaptic function of young C.elegans .

The neuroprotective effects of tocotrienol rich fraction and alpha tocopherol against glutamate injury in astrocytes.

Tocotrienol rich fraction (TRF) is an extract of palm oil, which consists of 25% alpha tocopherol (α-TCP) and 75% tocotrienols. TRF has been shown to possess potent antioxidant, anti-inflammatory, anticancer, neuroprotection, and cholesterol lowering activities. Glutamate is the main excitatory amino acid neurotransmitter in the central nervous system of mammalian, which can be excitotoxic, and it has been suggested to play a key role in neurodegenerative disorders like Parkinson's and Alzheimer's diseases. In this present study, the effects of vitamin E (TRF and α-TCP) in protecting astrocytes against glutamate injury were elucidated. Astrocytes induced with 180 mM of glutamate lead to significant cell death. However, glutamate mediated cytotoxicity was diminished via pre and post supplementation of TRF and α-TCP. Hence, vitamin E acted as a potent antioxidant agent in recovering mitochondrial injury due to elevated oxidative stress, and enhanced better survivability upon glutamate toxicity.

Tocotrienol rich fraction reverses age-related deficits in spatial learning and memory in aged rats.

Little is known about the effect of vitamin E on brain function. Therefore, in this study we evaluated the effect of tocotrienol rich fraction (TRF) on behavioral impairment and oxidative stress in aged rats. Thirty-six male Wistar rats (young: 3-months-old; aged: 21-months-old) were treated with either the control (olive oil) or TRF (200 mg/kg) for 3 months. Behavioral studies were performed using the open field test and Morris water maze (MWM) task. Blood was taken for assessment of DNA damage, plasma malondialdehyde (MDA) and vitamin E, and erythrocyte antioxidant enzyme activity. Brains were also collected to measure vitamin E levels. Results showed that aged rats exhibited reduced exploratory activity, enhanced anxiety and decreased spatial learning and memory compared with young rats. DNA damage and plasma MDA were increased, and vitamin E levels in plasma and brain were reduced in aged rats. Aged rats supplemented with TRF showed a markedly reduced level of anxiety, improved spatial learning and memory, reduced amount and severity of DNA damage, a reduced level of MDA, and increased levels of antioxidant enzyme activity and plasma/brain vitamin E compared with age-matched controls. In conclusion, TRF supplementation reverses spatial learning and memory decline and decreases oxidative stress in aged rats.

Tocotrienol rich fraction supplementation confers protection on the ovary from cyclophasphamide induced apoptosis

IntroductionCyclophosphamide (CPA) therapy leads to infertility via oxidative stress induced apoptosis of ovarian cells. Tocotrienol, vitamin E isoform, is a much more potent antioxidant compared to tocopherol, the more investigated vitamin E isoform. Tocotrienol rich fraction (TRF) is an affordable and available form of tocotrienol supplementation. The effect of concurrent TRF supplementation with CPA treatment is un-investigated. ObjectiveTo study the ovarian protective effect of tocotrienol rich fraction (TRF) when coadministered with CPA. Methods60 female ICR mice, aged between 8 −10 weeks were divided into 5 treatment groups: CPA, CPA&TRF, normal saline, TRF only, and corn oil (TRF carriage vehicle) only. The treatment was given for 30 consecutive days, after which all animal were euthanized. At dissection, both ovaries were removed, fixed in 10% formalin, processed and embedded in paraffin to form tissue blocks. Terminal deoxynucleotidyl transferase–mediated deoxy-uridine triphosphate nick-end labelling (TUNEL) assay was performed on the tissue blocks. Results & DiscussionThere was a significant reduction of TUNEL positive cells in the combined CPA&TRF group compared to CPA only group (p<0.05). All ovaries in normal control group showed only occasional TUNEL–positive cells, mostly confined to atretic follicles. No increase in TUNEL positive cells were seen in the TRF and oil only control groups. ConclusionCo administration of TRF with CPA confers protection against apoptosis in ovaries. TRF is a potential candidate for ovarian conservation in chemotherapy associated damage.

Protective effects of tocotrienols against lipid-induced nephropathy in experimental type-2 diabetic rats by modulation in TGF-β expression

Dyslipidemia is common in patients with diabetes mellitus (DM) and is considered a risk factor for the progression of diabetic nephropathy (DN). Hyperlipidemia and hyperglycemia act synergistically to induce renal injury. The present study was designed to investigate the protective effects of tocotrienols as tocotrienol-rich fraction (TRF) extracted from palm (PO) and rice bran oils (RBO) against lipid induced nephropathy in type-2 diabetic rats and its probable molecular mechanism. Male Wistar rats (175–200g) were divided into four groups. The first group served as diabetic control, while the second and third groups received PO-TRF and RBO-TRF, respectively by gavage over a period of sixteen weeks post-induction of diabetes. The fourth group comprised of age-matched rats that served as normal control. The effects of TRF on serum lipid profile, oxidative stress markers, expression of TGF-β, fibronectin and collagen type IV were analyzed in the kidney of diabetic rats. Treatment with PO-TRF and RBO-TRF significantly improved glycemic status, serum lipid profile and renal function in type-2 diabetic rats. In addition, TRF supplementation down-regulated the expression of TGF-β, fibronectin and collagen type IV in the kidney of diabetic rats. Transforming growth factor-β (TGF-β) plays a critical role in progression of DN, but its modulation by tocotrienols in DN remains unexplored. TRF ameliorated lipid induced nephropathy in type-2 diabetes by its hypoglycemic, hypolipidemic and antioxidant activities as well as by modulation of TGF-β to prevent increased expression of collagen type IV and fibrinogen. We finally propose a mechanism for the expression of molecular markers that are significant in the events leading to diabetic nephropathy and its modulation by tocotrienols/TRF.

Reversal of Myoblast Aging by Tocotrienol Rich Fraction Posttreatment

Skeletal muscle satellite cells are heavily involved in the regeneration of skeletal muscle in response to the aging-related deterioration of the skeletal muscle mass, strength, and regenerative capacity, termed as sarcopenia. This study focused on the effect of tocotrienol rich fraction (TRF) on regenerative capacity of myoblasts in stress-induced premature senescence (SIPS). The myoblasts was grouped as young control, SIPS-induced, TRF control, TRF pretreatment, and TRF posttreatment. Optimum dose of TRF, morphological observation, activity of senescence-associated β-galactosidase (SA-β-galactosidase), and cell proliferation were determined. 50 μg/mL TRF treatment exhibited the highest cell proliferation capacity. SIPS-induced myoblasts exhibit large flattened cells and prominent intermediate filaments (senescent-like morphology). The activity of SA-β-galactosidase was significantly increased, but the proliferation capacity was significantly reduced as compared to young control. The activity of SA-β-galactosidase was significantly reduced and cell proliferation was significantly increased in the posttreatment group whereas there was no significant difference in SA-β-galactosidase activity and proliferation capacity of pretreatment group as compared to SIPS-induced myoblasts. Based on the data, we hypothesized that TRF may reverse the myoblasts aging through replenishing the regenerative capacity of the cells. However, further investigation on the mechanism of TRF in reversing the myoblast aging is needed.

Palm oil tocotrienol rich fraction reduces extracellular matrix production by inhibiting transforming growth factor-β1 in human intestinal fibroblasts

Extracellular matrix deposition is key event for the development of bowel stenosis in Crohn's disease patients. Transforming growth factor-β plays a key role in this process. We aimed at characterizing the effects of tocotrienol rich fraction on ECM proteins production and molecules that regulate the synthesis and degradation of extracellular matrix, matrix metalloproteinase-3 and tissue inhibitor of metalloproteinases-1, in human intestinal fibroblasts, and at elucidating whether the effects of tocotrienol rich fraction (TRF) are mediated through inhibition of TGF-β1. HIF were isolated from colonic or ileal tissue from Crohn's disease patients and control subjects, and were treated with TRF from palm oil either alone or in combination with TGF-β1. Procollagen 1, procollagen 3, TIMP-1 and MMP-3 production, and Smad3 phosphorylation were analyzed by Western-blotting. TRF significantly diminished procollagen 1 and 3 synthesis in HIF. Treatment of HIF with TRF increased MMP-3 production but did not modify TIMP-1. TGF-β1 induced Smad3 phosphorylation and enhanced procollagen 1 and 3 and TIMP-1 production. Pre-treatment of HIF with TRF prevented Smad3 phosphorylation and minimized the increase in collagen 1 and 3 production caused by TGF-β1. TRF has anti-fibrogenic effects on HIF, decreasing ECM production and increasing its degradation. This effect is mediated, at least in part, by inhibition of TGF-β1.

Tocotrienol rich fraction supplementation improved lipid profile and oxidative status in healthy older adults: A randomized controlled study

BackgroundVitamin E supplements containing tocotrienols are now being recommended for optimum health but its effects are scarcely known. The objective was to determine the effects of Tocotrienol Rich Fraction (TRF) supplementation on lipid profile and oxidative status in healthy older individuals at a dose of 160 mg/day for 6 months.MethodsSixty-two subjects were recruited from two age groups: 35-49 years (n = 31) and above 50 years (n = 31), and randomly assigned to receive either TRF or placebo capsules for six months. Blood samples were obtained at 0, 3rd and 6th months.ResultsHDL-cholesterol in the TRF-supplemented group was elevated after 6 months (p < 0.01). Protein carbonyl contents were markedly decreased (p < 0.001), whereas AGE levels were lowered in the > 50 year-old group (p < 0.05). Plasma levels of total vitamin E particularly tocopherols were significantly increased in the TRF-supplemented group after 3 months (p < 0.01). Plasma total tocotrienols were only increased in the > 50 year-old group after receiving 6 months of TRF supplementation. Changes in enzyme activities were only observed in the > 50 year-old group. SOD activity was decreased after 3 (p < 0.05) and 6 (p < 0.05) months of TRF supplementation whereas CAT activity was decreased after 3 (p < 0.01) and 6 (p < 0.05) months in the placebo group. GPx activity was increased at 6 months for both treatment and placebo groups (p < 0.05).ConclusionThe observed improvement of plasma cholesterol, AGE and antioxidant vitamin levels as well as the reduced protein damage may indicate a restoration of redox balance after TRF supplementation, particularly in individuals over 50 years of age.