Table 5.
Tocotrienols are more potent than tocopherols
In-vitro studies | References |
---|---|
• T3 is more potent than TP in reducing gamma-glutamyl transpeptidase and glutathione S-transferase | [212] |
• T3 is more potent than TP in inducing apoptosis of tumor cells | [94] |
• T3s are more potent than TP in inhibiting growth & inducing apoptosis of mouse mammary epithelial cells |
[70] |
• T3s preferentially accumulate than TP in mouse mammary epithelial cells | [70] |
• T3s are more effective than TP in preventing glutamate-induced neuronal cell death | [61] |
• T3s, but not TP, inhibited both the proliferation & tube formation of bovine aortic endothelial cells | [188] |
• T3s are more readily transferred and incorporated into the membranes than TP | [183] |
• T3 had greater peroxy radical scavenging activity than TP in liposomal membrane | [182] |
• T3, not TP inhibited human endothelial cell proliferation & suppressed tumor-induced angiogenesis | [189, 195] |
• T3, not TP reduced VEGF-stimulated tube formation in HUVEC | [49] |
• T3 protects astrocytes better than TP from H202 induced-cell loss and apoptosis | [191] |
• T3 is more effective than TP in protecting against glutamate-induced cell death in HT4 neuron cell | [61] |
• T3s are more potent than TP in protecting cerebellar granule cells against methyl mercury toxicity | [192] |
• Accumulation and secretion rate of T3 isomers in Caco2 cells is faster than TP isomers; oral administration caused faster appearance and disappearance of T3 than TP |
[154] |
• T3 is more effective than TP in suppressing LPS-induced IL-6, PGE2 production from macrophages | [193] |
In-vivo Studies | |
• T3 were more effective in inhibiting the growth of sarcoma 180, Ehrlich carcinoma, & IMC carcinoma than TP |
[100] |
• T3 showed significant increase in DMB A-induced tumor latency than TP | [105] |
• T3 showed 40–60 times higher antioxidant activity against induced lipid peroxidation and 6.5 times better protection of cytochrome P-450 against oxidative damage than TP. |
[181] |
• Reduction of linoleic acid desaturation was more clear with T3 than with TP | [111] |
• No T3 in plasma but platelet concentration of 8-T3 doubled; TP was found in LDL and HDL in human; T3 deposited in adipose tissue while TP was detected in all tissue except adipose in hamster |
[159] |
• Lymphatic transport & recovery of T3 was twice higher than that of TP in thoracis duct-cannulated rats | [146] |
• T3 feeding (0.2% in diet) gave higher CD4+/CD8+ ratio than T in mesenteric lymphnode lymphocytes | [140] |
• T3 exerted stronger antioxidant activity than TP in vivo | [140] |
• T3 (60 mg/kg bw/day) was more effective than TP in reducing body fat mass and preventing steroid-induced osteoporosis |
[139] |
• Concentration of T3 increased markedly in eye tissue than TP | [152] |
• T3 but not a-TP reduced the serum levels of IL-1 and IL-6 in rats | [55] |
• T3 (60 mg/kg bw) was better than TP in protecting bone resorption caused by free-radicals | [55] |
• T3 has the ability to block the stress-induced changes in the gastric acidity and gastrin level than TP | [141] |
• T3 are detected in postprandial (fasted) human plasma earlier than TP but at significantly lower level than TP |
[240] |
• T3 is a better antioxidant than TP in a deep fat frying system | [198] |
• Total cholesterol and LDL-C levels declined in T3 group but not in those on TP | [163] |
• T3 is superior than TP in suppressing nicotine-induced loss of calcium from bone | [54] |
• T3 but not TP reduced the levels of lipid peroxidation and increased GPO activity in the femur of rats | [137] |
• T3, but not TP can maintain the noradrenalin level and prevent gastric lesions in rats exposed to stress | [245] |
• T3 is more extensively than TP metabolized to sulfated CEHC form. | [143] |
• T3 was superior than TP, in reversing nicotine induced bone loss in rats | [134] |
• T3 was better effects than TP on static and dynamic bone histomorphometric parameters | [135] |
• T3 is better than TP as an anabolic agent for bone in normal male rats | [136] |
CEHC, 2-(beta-carboxyethyl)-6hydroxychromon; DMBA, 7, 12-dimethylbenz(a)anthracene. GPO, glutathione peroxidase; HDL, high-density lipoprotein; HUVEC-human umbilical vein endothelial cells; IL, interleukins; LDL, low-density lipoprotein; LPS, lipopolysaccharide; PGE2, prostaglandin-2; PKC, protein kinase-C; T3, tocotrienols; TP, tocopherols; VEGF-vascular endothelial growth factor;