Comparison of the Effects of Omega 3 and Vitamin E on Palcitaxel-Induced Peripheral Neuropathy

Anoushirvani AA, Poorsaadat L, Aghabozorgi R, Kasravi M

Open Access Maced J Med Sci. 2018 Oct 21;6(10):1857-1861. doi: 10.3889/oamjms.2018.333. eCollection 2018 Oct 25.

Abstract

BACKGROUND:

Paclitaxel-induced peripheral neuropathy is the most important side effect limiting the use of this medication.

AIM:

This study aimed to compare the effects of omega-3 and vitamin E on the incidence of peripheral neuropathy in patients receiving Taxol.

METHODS:

In this clinical trial, 63 patients who were a candidate for receiving taxol, were enrolled based on inclusion and exclusion criteria. In group O, patients received 640 mg omega-3 three times a day, and group E, received 300 mg vitamin E two times a day. Patients took the supplements up to three months after the onset of Taxol. Group P received placebo for a similar period. All patients referred to a neurologist for electrophysiological evaluation before the onset of chemotherapy and at months 1 and 3. The presence of neuropathy and its progression was recorded by the neurologist.

RESULTS:

Neurological examination in this study indicated that 6 patients (28.6%) in Group O, 7 patients (33.3%) in group E, and 15 patients (71.4%) in placebo group started peripheral neuropathy. There was a significant difference between intervention groups and the placebo group (p = 0.0001) and no significant difference between intervention groups (p = 0.751).

CONCLUSION:

Our data suggested that vitamin E and omega-3 may significantly reduce the incidence of Paclitaxel-induced peripheral neuropathy. Routine administration of such supplements that have no special side effect for patients under chemotherapy may greatly enhance their quality of life.

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Hepatoprotective effects of vitamin E against hexachlorobenzene-induced hepatotoxicity and oxidative stress in rats: histological, biochimical and antioxidant status changes

Chalouati H, Ben Sâad MM, Payrastre L

Toxicol Mech Methods. 2018 Oct 3:1-8. doi: 10.1080/15376516.2018.1506847. [Epub ahead of print]

Abstract

The protective effects of α-Tocopherol (vitamin E) on liver injury induced by hexachlorobenzene (HCB) were investigated in adult male rats of Wistar strain. Animals were randomly divided into six groups of eight rats each. Group 1 and 2 have received HCB, dissolved in olive oil, at a dose of 4 mg or 16 mg/kg b.w., respectively. Group 3 and 4 were treated by the same doses of HCB (4 mg and 16 mg/kg b.w.) after 1 h of pretreatment with α-tocopherol at a dose of 100 mg kg-1 b.w. The other two groups served as controls; which received either olive oil only, a solvent of HCB, or α-tocopherol. A significant increase in hepatic lipid peroxidation (LPO) and GSH activity were observed following HCB administration. The activities of antioxidant enzymes like superoxide dismutase and catalase were significantly decreased while glutathione peroxidase was significantly increased following HCB administration. Similarly, a significant increase in plasma levels of various marker enzymes [aminotransferase (aspartate aminotransférase (AST) and alanine aminotransferase (ALT)), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH)] and a decrease of total protein level were observed. Pretreatment with vitamin E of HCB treated rats ameliorated all biochemical parameters to near normal values. Liver histological study confirmed biochemical parameters and the beneficial role of vitamin E.

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An evaluation of crude palm oil (CPO) and tocotrienol rich fraction (TRF) of palm oil as percutaneous permeation enhancers using full-thickness human skin

Singh I, Nair RS, Gan S, Cheong V, Morris A

Pharm Dev Technol. 2018 Oct 3:1-7. doi: 10.1080/10837450.2018.1509347. [Epub ahead of print]

Abstract

The drawbacks associated with chemical skin permeation enhancers such as skin irritation and toxicity necessitated the research to focus on potential permeation enhancers with a perceived lower toxicity. Crude palm oil (CPO) is obtained by direct compression of the mesocarp of the fruit of the oil palm belonging to the genus Elaeis. In this research, CPO and tocotrienol-rich fraction (TRF) of palm oil were evaluated for the first time as skin permeation enhancers using full-thickness human skin. The in vitro permeation experiments were conducted using excised human skin mounted in static upright ‘Franz-type’ diffusion cells. The drugs selected to evaluate the enhancing effects of these palm oil derivatives were 5-fluorouracil, lidocaine and ibuprofen: compounds covering a wide range of Log p values. It was demonstrated that CPO and TRF were capable of enhancing the percutaneous permeation of drugs across full-thickness human skin in vitro. Both TRF and CPO were shown to significantly enhance the permeation of ibuprofen with flux values of 30.6 µg/cm2 h and 23.0 µg/cm2 h respectively, compared to the control with a flux of 16.2 µg/cm2 h. The outcome of this research opens further scope for investigation on the transdermal penetration enhancement activity of pure compounds derived from palm oil.

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Tocopherol suppresses 24(S)-hydroxycholesterol-induced cell death via inhibition of CaMKII phosphorylation

Kimura Y, Asa M, Urano Y, Saito Y, Nishikawa K, Noguchi N

Biochimie. 2018 Oct;153:203-209. doi: 10.1016/j.biochi.2018.07.004. Epub 2018 Jul 7.

Abstract

Although 24(S)-hydroxycholesterol (24S-OHC) plays an important role to maintain homeostasis of cholesterol in the brain, it induces neuronal cell death at high concentrations. 24S-OHC-induced cell death was suppressed by γ-tocopherol (γ-Toc) but not by γ-tocotrienol (γ-Toc3) in a similar way to α-tocopherol (α-Toc) and α-tocotrienol (α-Toc3) in human neuroblastoma SH-SY5Y cells. Both γ-Toc and γ-Toc3 significantly inhibited cumene hydroperoxide-induced cell death, as previously shown in the case of α-Toc and α-Toc3. Lipid droplet-like structure formation induced by 24S-OHC was suppressed by neither γ-Toc nor γ-Toc3. The phosphorylation of calcium/calmodulin-dependent protein kinase II (CaMKII) was induced by 24S-OHC, which was suppressed by CaMKII phosphorylation-site inhibitor mM3 but not by calmodulin-binding-site inhibitor KN62. A calcium chelator, BAPTA-AM, inhibited calcium ionophore A23187-induced CaMKII phosphorylation but not 24S-OHC-induced CaMKII phosphorylation. Receptor-interacting protein kinase 1 (RIPK1) phosphorylation induced by 24S-OHC was not inhibited by either mM3 or KN62, suggesting that CaMKII activation does not affect RIPK1 phosphorylation. Knockdown of RIPK1 using siRNA induced not only inhibition of CaMKII phosphorylation but also reduction of total CaMKII protein levels, suggesting that RIPK1 may regulate CaMKII signalling. 24S-OHC-induced RIPK1 phosphorylation was inhibited by neither α-Toc nor α-Toc3. In contrast, CaMKII phosphorylation induced by 24S-OHC was significantly suppressed by α-Toc but not by α-Toc3. These results suggest that CaMKII activation is involved in the mechanism of 24S-OHC-induced cell death and that Toc inhibits the cell death via inhibition of CaMKII activation through a RIPK1 phosphorylation-independent pathway.

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Vitamin E Analogue Protects Red Blood Cells against Storage-Induced Oxidative Damage

Antosik A, Czubak K, Cichon N, Nowak P, Zbikowska H

Transfus Med Hemother. 2018 Oct;45(5):347-354. doi: 10.1159/000486605. Epub 2018 Mar 9

Abstract

BACKGROUND:

To investigate i) the effects of Trolox® or mannitol, which represent two different classes of antioxidants, on oxidative changes generated in manually isolated red blood cells (RBCs) from citrate-phosphate-dextrose (CPD) preserved whole blood, followed by up to 20 days refrigerated storage, and ii) whether Trolox supplemented to the blood bank-manufactured saline-adenine-glucose-mannitol (SAGM) preserved RBC units would offer better storage conditions compared with SAGM alone.

METHODS:

The percentage of hemolysis and extracellular activity of lactate dehydrogenase (LDH) was measured to assess RBC membrane integrity. Lipid peroxidation, reduced glutathione (GSH) levels and total antioxidant capacity (TAC) were quantified by thiobarbituric acid-reactive substances (TBARS), Ellman’s reagent and 2, 2′-azinobis-(3-ethylbenzothiazoline-6-sulfonate) (ABTS.+) based assay, respectively.

RESULTS:

Trolox was little more effective than mannitol in protecting against progressive RBC hemolysis. Trolox (0.125-3.125 mmol/l) inhibited storage-induced leakage of LDH, lipid peroxidation, and to a lesser extent GSH depletion. Mannitol at these concentrations neither inhibited TBARS formation nor prevented GSH depletion. RBC units stored in SAGM-Trolox had significantly lower hemolysis, LDH leakage, and lipid peroxidation level compared to RBCs stored in SAGM.

CONCLUSION:

There is evidence of the beneficial effects of supplementing RBC-additive solutions with membrane-interacting antioxidants such as vitamin E analogues.

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Induction of peroxisomal changes in oligodendrocytes treated with 7-ketocholesterol: Attenuation by α-tocopherol

Nury T, Sghaier R, Zarrouk A, Ménétrier F, Uzun T, Leoni V, Caccia C, Meddeb W, Namsi A, Sassi K, Mihoubi W, Riedinger JM, Cherkaoui-Malki M, Moreau T, Vejux A, Lizard G

Biochimie. 2018 Oct;153:181-202. doi: 10.1016/j.biochi.2018.07.009. Epub 2018 Jul 19.

Abstract

The involvement of organelles in cell death is well established especially for endoplasmic reticulum, lysosomes and mitochondria. However, the role of the peroxisome is not well known, though peroxisomal dysfunction favors a rupture of redox equilibrium. To study the role of peroxisomes in cell death, 158 N murine oligodendrocytes were treated with 7-ketocholesterol (7 KC: 25-50 μM, 24 h). The highest concentration is known to induce oxiapoptophagy (OXIdative stress + APOPTOsis + autoPHAGY), whereas the lowest concentration does not induce cell death. In those conditions (with 7 KC: 50 μM) morphological, topographical and functional peroxisome alterations associated with modifications of the cytoplasmic distribution of mitochondria, with mitochondrial dysfunction (loss of transmembrane mitochondrial potential, decreased level of cardiolipins) and oxidative stress were observed: presence of peroxisomes with abnormal sizes and shapes similar to those observed in Zellweger fibroblasts, lower cellular level of ABCD3, used as a marker of peroxisomal mass, measured by flow cytometry, lower mRNA and protein levels (measured by RT-qPCR and western blotting) of ABCD1 and ABCD3 (two ATP-dependent peroxisomal transporters), and of ACOX1 and MFP2 enzymes, and lower mRNA level of DHAPAT, involved in peroxisomal β-oxidation and plasmalogen synthesis, respectively, and increased levels of very long chain fatty acids (VLCFA: C24:0, C24:1, C26:0 and C26:1, quantified by gas chromatography coupled with mass spectrometry) metabolized by peroxisomal β-oxidation. In the presence of 7 KC (25 μM), slight mitochondrial dysfunction and oxidative stress were found, and no induction of apoptosis was detected; however, modifications of the cytoplasmic distribution of mitochondria and clusters of mitochondria were detected. The peroxisomal alterations observed with 7 KC (25 μM) were similar to those with 7 KC (50 μM). In addition, data obtained by transmission electron microcopy and immunofluorescence microscopy by dual staining with antibodies raised against p62, involved in autophagy, and ABCD3, support that 7 KC (25-50 μM) induces pexophagy. 7 KC (25-50 μM)-induced side effects were attenuated by α-tocopherol but not by α-tocotrienol, whereas the anti-oxidant properties of these molecules determined with the FRAP assay were in the same range. These data provide evidences that 7 KC, at concentrations inducing or not cell death, triggers morphological, topographical and functional peroxisomal alterations associated with minor or major mitochondrial changes.

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δ-Tocotrienol, Isolated from Rice Bran, Exerts an Anti-Inflammatory Effect via MAPKs and PPARs Signaling Pathways in Lipopolysaccharide-Stimulated Macrophages

Shen J, Yang T, Xu Y, Luo Y, Zhong X, Shi L, Hu T, Guo T, Nie Y, Luo F, Lin Q

Int J Mol Sci. 2018 Oct 4;19(10). pii: E3022. doi: 10.3390/ijms19103022.

Abstract

δ-Tocotrienol, an important component of vitamin E, has been reported to possess some physiological functions, such as anticancer and anti-inflammation, however their molecular mechanisms are not clear. In this study, δ-tocotrienol was isolated and purified from rice bran. The anti-inflammatory effect and mechanism of δ-tocotrienol against lipopolysaccharides (LPS) activated pro-inflammatory mediator expressions in RAW264.7 cells were investigated. Results showed that δ-tocotrienol significantly inhibited LPS-stimulated nitric oxide (NO) and proinflammatory cytokine (TNF-α, IFN-γ, IL-1β and IL-6) production and blocked the phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular regulated protein kinases 1/2 (ERK1/2). δ-Tocotrienol repressed the transcriptional activations and translocations of nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1), which were closely related with downregulated cytokine expressions. Meanwhile, δ-tocotrienol also affected the PPAR signal pathway and exerted an anti-inflammatory effect. Taken together, our data showed that δ-tocotrienolinhibited inflammation via mitogen-activated protein kinase (MAPK) and peroxisome proliferator-activated receptor (PPAR) signalings in LPS-stimulated macrophages.

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The Effect of Magnesium and Vitamin E Co-Supplementation on Glycemic Control and Markers of Cardio-Metabolic Risk in Women with Polycystic Ovary Syndrome: A Randomized, Double-Blind, Placebo-Controlled Trial

Jamilian M, Sabzevar NK, Asemi Z

Horm Metab Res. 2018 Oct 4. doi: 10.1055/a-0749-6431. [Epub ahead of print]

Abstract

Data on the effects of magnesium and vitamin E co-supplementation on glycemic control and markers of cardio-metabolic risk of patients with polycystic ovary syndrome (PCOS) were collected. This investigation was conducted to evaluate the effects of magnesium and vitamin E co-supplementation on glycemic control and markers of cardio-metabolic risk in women with PCOS. This randomized, double-blind, placebo-controlled trial was carried out on 60 women with PCOS, aged 18-40 years old. Participants were randomly divided into two groups to receive 250 mg/day magnesium plus 400 mg/day vitamin E supplements or placebo (n=30 each group) for 12 weeks. Fasting blood samples were taken at baseline and after the 12-week intervention to quantify related variables. After the 12-week intervention, compared with the placebo, magnesium and vitamin E co-supplementation led to a significant reduction in serum insulin levels (-1.1±3.0 vs. +1.6±3.7 μIU/ml, p=0.003) and homeostatic model of assessment for insulin resistance (-0.2±0.7 vs. +0.4±0.9, p=0.002), and a significant increase in the quantitative insulin sensitivity check index (+0.01±0.01 vs. -0.009±0.02, p=0.003). Furthermore, magnesium plus vitamin E supplementation significantly decreased serum triglycerides (-15.0±24.4 vs. +6.7±22.2 mg/dl, p=0.001) and VLDL-cholesterol concentrations (-3.0±4.9 vs. +0.6±2.4 mg/dl, P=0.01) compared with the placebo. A trend toward a greater decrease in total cholesterol levels was observed in magnesium plus vitamin Egroup compared to placebo group (-7.0±32.6 vs. +8.1±26.6 mg/dl, p=0.05). In conclusion, magnesium and vitamin E co-supplementation for 12 weeks to PCOS women had beneficial effects on parameters of insulin metabolism and few markers of cardio-metabolic risk.

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Nonalcoholic steatohepatitis, obesity, and cardiac dysfunction

Mathews SE, Kumar RB, Shukla AP

Curr Opin Endocrinol Diabetes Obes. 2018 Oct;25(5):315-320. doi: 10.1097/MED.0000000000000432.

Abstract

PURPOSE OF REVIEW:

Obesity and nonalcoholic steatohepatitis (NASH) are epidemiologically and pathophysiologically linked disorders. Here, we summarize the effect of obesity on NASH and how it has a cascading effect on cardiovascular dysfunction. We also review the current and emerging treatment options for NASH.

RECENT FINDINGS:

The link between NASH and cardiac dysfunction has been further delineated in recent studies demonstrating endothelial dysfunction, diastolic dysfunction, and increased coronary artery calcification in patients with known NASH. Standard treatment of obesity with lifestyle interventions including diet, exercise, and behavioral modification has been shown to improve NASH as well as reduce cardiovascular dysfunction. In addition to FDA-approved drugs like vitamin E and pioglitazone, several agents including NGM282, obeticholic acid, elafibranor, and liraglutide are currently being investigated for their therapeutic potential in NASH. Recent studies show that bariatric surgery results in significant improvement or resolution of NASH.

SUMMARY:

Obesity is a major factor in the development of nonalcoholic fatty liver disease (NAFLD) and its progression to steatohepatitis. Patients with NAFLD have a significant increase in cardiovascular disease risk. For biopsy-proven NASH, vitamin E and pioglitazone are the recommended medical treatments in addition to lifestyle modification.

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Safety Assessment of Tocopherols and Tocotrienols as Used in Cosmetics

Fiume MM, Bergfeld WF, Belsito DV, Hill RA, Klaassen CD, Liebler DC, Marks JG Jr, Shank RC, Slaga TJ, Snyder PW, Andersen FA, Heldreth B

Send to Int J Toxicol. 2018 Sep/Oct;37(2_suppl):61S-94S. doi: 10.1177/1091581818794455.

Abstract

The Cosmetic Ingredient Review (CIR) Expert Panel (Panel) assessed the safety of 14 tocopherols and tocotrienols and concluded these ingredients are safe as used in cosmetics. The tocopherols are reported to function in cosmetics as antioxidants or skin-conditioning agents; in contrast, tocotrienols are not reported to function as an antioxidants in cosmetics but as a light stabilizer, oral care agent, or skin-conditioning agent. The Panel reviewed the new and existing animal and clinical data to determine the safety of these ingredients and found it appropriate to extrapolate the existing information to conclude on the safety of all the tocopherols and tocotrienols.

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