Reduction of DNA damage in older healthy adults by Tri E® Tocotrienol supplementation

Chin, Siok‐Fong; Hamid, Noor Aini Abdul; Latiff, Azian Abd; Zakaria, Zaiton; Mazlan, Musalmah; Yusof, Yasmin Anum Mohd; Karim, Aminuddin Abdul Hamid; Ibahim, Mohammad Johari; Hamid, Zalina; Ngah, Wan Zurinah Wan

doi:10.1016/j.nut.2007.08.006

Cited by 67 publications

(47 citation statements)

References 43 publications

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“…Some evidence has suggested that T3s have greater potential physiologic functions than TPs (7,8). T3 has been shown to mediate its activity against a variety of chronic diseases, including cardiovascular diseases, neurologic diseases, diabetes, and cancer (9)(10)(11)(12)(13)(14). T3s have shown anticancer activity against cancers such as colon, breast, liver, lung, kidney, prostate, skin, and other cancers both in vitro (15)(16)(17)(18)(19)(20) and in vivo (21)(22)(23)(24)(25).…”

Section: Introductionmentioning

confidence: 99%

γ-Tocotrienol Promotes TRAIL-Induced Apoptosis through Reactive Oxygen Species/Extracellular Signal-Regulated Kinase/p53–Mediated Upregulation of Death Receptors

Kannappan

Ravindran

Prasad

et al. 2010

Molecular Cancer Therapeutics

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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a member of the tumor necrosis factor superfamily, is in clinical trials for cancer therapy, but its anticancer potential is limited by the development of resistance. We investigated the ability of tocotrienol (T3), an unsaturated vitamin E present in palm oil, rice bran, barley, oats, and wheat germ, to sensitize tumor cells to TRAIL. Results from esterase staining, colony formation, caspase activation, and sub-G 1 cell cycle arrest revealed that γ-T3 can sensitize human colon cancer cells to TRAIL. When examined for the mechanism, we found that γ-T3 significantly downregulated the expression of antiapoptotic proteins (c-IAP2 and Bcl-xL). We also found that γ-T3, but not tocopherol, induced the expression of the TRAIL receptors death receptor (DR)-4 and DR5. This induction was not cell type specific, as upregulation was also found in pancreatic, kidney, and leukemic cells. Upregulation of DRs by γ-T3 required the production of reactive oxygen species (ROS), and sequestering of ROS abolished both upregulation of the receptors and potentiation of TRAIL-induced apoptosis. Induction of DRs by γ-T3 also required activation of extracellular signal-regulated kinase 1 (ERK1), as silencing of ERK1 by specific siRNA abrogated the upregulation of TRAIL receptors. Further, induction of DRs by γ-T3 required the expression of p53 and Bax, as no induction of the receptors was found in colon cancer cells with deletion of these genes. Overall, our results show that γ-T3 sensitizes tumor cells to TRAIL by upregulating DRs through the ROS/ ERK/p53 pathway and by downregulating cell survival proteins. Mol Cancer Ther; 9(8); 2196-207. ©2010 AACR.

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Section: Introductionmentioning

confidence: 99%

γ-Tocotrienol Promotes TRAIL-Induced Apoptosis through Reactive Oxygen Species/Extracellular Signal-Regulated Kinase/p53–Mediated Upregulation of Death Receptors

Kannappan

Ravindran

Prasad

et al. 2010

Molecular Cancer Therapeutics

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“…Hence, it is a better preventive agent of chronic inflammatory diseaserelated such as cardiovascular disease. In addition, a study on healthy elderly found that supplementation of tocotrienol-rich fraction (TRF) decreased deoxyribonucleic acid (DNA) damage [24]. The same improvement trend was observed in lipoprotein-lipid profile, with a reduction in markers of protein and lipid damage in the same study [25].…”

Section: Introductionmentioning

confidence: 70%

Tri-E® Prevents Cognitive Impairment and Deoxyribonucleic Acid Damage in Diabetes Mellitus

Asmara

Latif

Faisal

et al. 2017

Asian J Pharm Clin Res

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Objective: The aim of the current study is to compare the difference of Tri-E ® and ATF potentials in reducing diabetic adverse event due to hyperglycemia that might cause the DNA damage and cognitive impairment indirectly. Methods: Diabetic model sample from Sprague Dawley was developed by combination of twice low-dose streptozotocin injection and high fat diet. The diabetic rat model was treated with Tri-E ® and ATF in different groups, control group were provided. The DNA was collected from the whole blood and DNA damage was measured using the comet assay method. While cognitive status was measured using Morris water-maze method. Result: Reduction of the DNA damage and improvement of cognitive function were observed in both ATF and Tri-E ® supplementations that elevated in diabetic. However, the DNA damage reduction by Tri-E ® was onefold higher compared to ATF supplementation. Conclusion: This study provided data that Tri-E ® has superior potential than ATF as a preventative agent to DNA damage and cognitive impairment in diabetes indirectly.

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“…Some researchers reported collaborative and/or synergistic outcomes of the combined supplementation on lipids. Tri-E supplement was found to maintain a reduction in DNA damage in healthy subjects at 3 months up until 6 months (p<0.01) with lower levels of urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) compared to control subjects [20]. Roza et al showed that three months combined supplementation of citrus flavonoids and tocotrienols compared to the placebo group significantly reduced TC (20-30%), LDL-c (19-27%) and triglycerides (24-34%) [21].…”

Section: Discussionmentioning

confidence: 99%

A Randomized Pilot Study on the Effects of Combined Tocotrienol-Tocopherol Mixed Fraction and Vitamin C on Inflammatory Status and Lipid Profile in Statin-Treated High Risk Patients

Muid

et al. 2016

Int Arch Med

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Previous studies have suggested that combination of Tocotrienoltocopherol mixed fraction (TTMF) vitamin E and vitamin C supplementation act synergistically in vivo to enhance their anti-oxidant properties. However, additional effects beyond that of anti-oxidation of combined vitamin E and vitamin C in statin-treated high coronary risk patients remains unclear. The aim of this study was to investigate pleiotropic effects of TTMF and vitamin C on inflammatory biomarkers and lipid profile in statin-treated high coronary risk patients.This was a pilot, randomized, double-blind, placebo controlled clinical trial. Twenty nine high coronary risk hypercholesterolaemic subjects were randomized into TTMF+C (160mg TTMF, 75% tocotrienol: 25% alpha-tocopherol plus 500mg vitamin C) intervention or placebo groups for 12 months. Blood samples were collected at entry, baseline, 2 weeks, 3, 6 and 12 months post-randomization for analysis of inflammatory biomarkers [(high sensitive C-reactive protein (hsCRP), interleukin-6 (IL-6), tumour necrosis factor alpha (TNFα)] and serum lipid profile [Total cholesterol (TC), low density lipoprotein cholesterol (LDL-c), high density lipoprotein cholesterol (HDL-c) and triglycerides (TG)]. There was no significant difference observed between TTMF+C and placebo groups with regards to percent change of hsCRP, IL-6 and TNF-α concentrations (p>0.05) and TC, at baseline, 2 weeks, 3, 6 and 12 months of intervention. There was also no significant change seen in the mean concentration of all inflammatory biomarkers and serum lipid profile between TTMF+C and placebo groups at all timelines. TTMF and vitamin C supplementation did not significantly improve the inflammatory status and lipid profile. This could in part be con-

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Reduction of DNA damage in older healthy adults by Tri E® Tocotrienol supplementation

Cited by 67 publications

References 43 publications

γ-Tocotrienol Promotes TRAIL-Induced Apoptosis through Reactive Oxygen Species/Extracellular Signal-Regulated Kinase/p53–Mediated Upregulation of Death Receptors

γ-Tocotrienol Promotes TRAIL-Induced Apoptosis through Reactive Oxygen Species/Extracellular Signal-Regulated Kinase/p53–Mediated Upregulation of Death Receptors

Tri-E® Prevents Cognitive Impairment and Deoxyribonucleic Acid Damage in Diabetes Mellitus

A Randomized Pilot Study on the Effects of Combined Tocotrienol-Tocopherol Mixed Fraction and Vitamin C on Inflammatory Status and Lipid Profile in Statin-Treated High Risk Patients

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