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The Effect of Alpha-Tocopherol on Morphine Tolerance-induced Expression of c-fos Proto-oncogene from a Biotechnological Perspective

Mehrabi S, Nasirinezhad F, Barati M, Abutaleb N, Barati S, Dereshky BT, Amini N, Milan PB, Jahanmahin A, Sarveazad A, Samadikuchaksaraei A, Mozafari M

Recent Pat Biotechnol. 2019;13(2):137-148. doi: 10.2174/1872208312666181120105333.

Abstract

BACKGROUND:

The increase of oxidant compounds is the most well-known reasons for the tolerance to the analgesic properties of Morphine. Additionally, the production of proxy-nitrite impairs receptors, proteins and enzymes involved in the signaling pathways of analgesia, apoptosis and necrosis. Also, we revised all patents relating to opioid tolerance control methods.

OBJECTIVE:

The aim of this study was to assess the effects of Alpha-tocopherol as an anti-oxidant agent to reduce Morphine tolerance.

METHOD:

Forty male rats randomly divided into four groups. 10 mg/kg of morphine was injected subcutaneously to create the desired level of tolerance. After modeling, 70 mg/kg Alpha- Tocopherol was injected intraperitoneal. Also, the hot plate recorded pain threshold alterations was used to evaluate the behavioral test. All tissue samples were extracted from the spinal cord, thalamus and frontal cortex for molecular and gene expression evaluations. Also, the effect of Alpha- Tocopherol on the apoptosis and necrosis parameters was analyzed using nissl staining and tunel test.

RESULTS:

The time latency results showed that there were no significant differences in the different days in groups treated with Morphine plus Alpha-Tocopherol. However, our data highlighted that the pain threshold and their time latency in respond to it had substantially increased in comparison with the control group. Furthermore, we found that the Alpha-Tocopherol obviously decreased c-fos gene expression, especially in the spinal cord.

CONCLUSION:

Thus, co-administration of Alpha-Tocopherol with Morphine can decrease the adverse effects of nitrite proxy, which is released due to repeated injections of Morphine.

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Alpha-tocopherol in intravenous lipid emulsions imparts hepatic protection in a murine model of hepatosteatosis induced by the enteral administration of a parenteral nutrition solution

Fell GL, Anez-Bustillos L, Dao DT, Baker MA, Nandivada P, Cho BS, Pan A, O'Loughlin AA, Nose V, Gura KM, Puder M

PLoS One. 2019 Jul 11;14(7):e0217155. doi: 10.1371/journal.pone.0217155. eCollection 2019.

Abstract

Intestinal failure-associated liver disease (IFALD) is a risk of parenteral nutrition (PN)-dependence. Intravenous soybean oil-based parenteral fat can exacerbate the risk of IFALD while intravenous fish oil can minimize its progression, yet the mechanisms by which soybean oil harms and fish oil protects the liver are uncertain. Properties that differentiate soybean and fish oils include α-tocopherol and phytosterol content. Soybean oil is rich in phytosterols and contains little α-tocopherol. Fish oil contains abundant α-tocopherol and little phytosterols. This study tested whether α-tocopherol confers hepatoprotective properties while phytosterols confer hepatotoxicity to intravenous fat emulsions. Utilizing emulsions formulated in the laboratory, a soybean oil emulsion (SO) failed to protect from hepatosteatosis in mice administered a PN solution enterally. An emulsion of soybean oil containing α-tocopherol (SO+AT) preserved normal hepatic architecture. A fish oil emulsion (FO) and an emulsion of fish oil containing phytosterols (FO+P) protected from steatosis in this model. Expression of hepatic acetyl CoA carboxylase (ACC) and peroxisome proliferator-activated receptor gamma (PPARγ), was increased in animals administered SO. ACC and PPARγ levels were comparable to chow-fed controls in animals receiving SO+AT, FO, and FO+P. This study suggests a hepatoprotective role for α-tocopherol in liver injury induced by the enteral administration of a parenteral nutrition solution. Phytosterols do not appear to compromise the hepatoprotective effects of fish oil.

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Combination Effect of Bowman-Birk Inhibitor and α-Tocopheryl Succinate on Prostate Cancer Stem-Like Cells

Kaneko S, Yamazaki T, Kohno K, Sato A, Kato K, Yano T

J Nutr Sci Vitaminol (Tokyo). 2019;65(3):272-277. doi: 10.3177/jnsv.65.272.

Abstract

The reoccurrence of androgen-dependent prostate cancer after anti-androgen therapy mainly depends on prostate cancer stem-like cells. To reduce the risk, it is important to delete the cancer stem-like cells. Furthermore, to induce differentiation of cancer stem-like cells is critical to abrogate stemness of the cells. Therefore, we tried to investigate a possibility on the establishment of a new effective therapy to eradicate the cancer stem-like cells via the induction of differentiation in this study. Prostate cancer stem-like cells from an androgen-dependent prostate cancer cell line (LNCaP cell) had severe resistance against an anti-androgen therapeutic agent. We selected Bowman-Birk inhibitor (BBI) from soybeans reported as a chemopreventive agent in prostate cancer to differentiate the caner stem-like cells and α-tocopheryl succinate (TOS) known as a mitocan to induce effectively cytotoxic effect against the cancer stem-like cells. In fact, only TOS treatment had cytotoxic effect against the cancer stem-like cells, but the addition of BBI treatment to the cells treated with TOS reinforced TOS-mediated cytotoxicity in the cancer stem-like cells. This reinforcement coincided with the combination-enhanced apoptosis in the stem-like cells. Also, we confirmed caspase9-caspase3 cascade mainly contributed to the enhancement of the cytotoxicity in the stem-like cells caused by the combination, indicating that the reinforcement of BBI on TOS-mediated apoptosis via mitochondria related to the enhancing cytotoxic effect of the combination on the prostate cancer stem-like cells. Overall, it seems that the combination is an effective new approach to reduce the reoccurrence of prostate cancer targeting prostate cancer stem cells.

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Vitamin E and Alzheimer’s disease: what do we know so far?

Browne D, McGuinness B, Woodside JV, McKay GJ

Clin Interv Aging. 2019 Jul 18;14:1303-1317. doi: 10.2147/CIA.S186760. eCollection 2019.

Abstract

Vitamin E has been proposed as a potential clinical intervention for Alzheimer’s disease (AD) given the plausibility of its various biological functions in influencing the neurodegenerative processes associated with the condition. The tocopherol and tocotrienol isoforms of vitamin Ehave multiple properties including potent antioxidant and anti-inflammatory characteristics, in addition to influences on immune function, cellular signalling and lowering cholesterol. Several of these roles offer a theoretical rationale for providing benefit for the treatment of AD-associated pathology. Diminished circulating concentrations of vitamin E have been demonstrated in individuals with AD. Reduced plasma levels have furthermore been associated with an increased risk of AD development while intake, particularly from dietary sources, may limit or reduce the rate of disease progression. This benefit may be linked to synergistic actions between vitamin E isoforms and other micronutrients. Nevertheless, randomised trials have found limited and inconsistent evidence of vitamin E supplementation as an effective clinical intervention. Thus, despite a strong rationale in support of a beneficial role for vitamin E for the treatment of AD, the evidence remains inconclusive. Several factors may partly explain this discrepancy and represent the difficulties of translating complex laboratory evidence and dietary interactions into clinical interventions. Methodological design limitations of existing randomised trials and restrictions to supplementation with a single vitamin E isoform may also limit the influence of effect. Moreover, several factors influence individual responsiveness to vitamin E intake and recent findings suggest variation in the underlying genetic architecture attenuates vitamin E biological availability and activity which likely contributes to the variation in clinical responsiveness and the failure of randomised trials to date. Importantly, the clinical safety of vitamin E remains controversial and warrants further investigation.

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Antioxidant vitamin supplementation prevents oxidative stress but does not enhance performance in young football athletes

de Oliveira DCX, Rosa FT, Simões-Ambrósio L, Jordao AA, Deminice R

Nutrition. 2019 Jul - Aug;63-64:29-35. doi: 10.1016/j.nut.2019.01.007. Epub 2019 Jan 24.

Abstract

OBJECTIVES:

The aim of this study was to verify the effects of supplementation with antioxidants (vitamins C and E) on oxidative stress, delayed-onset muscle soreness (DOMS), and performance in football players during a recovery period after an exercise-induced oxidative stress protocol.

METHODS:

Twenty-one football athletes were randomly assigned to two groups: placebo and antioxidant-supplemented. Supplementation was performed in a double-blind, controlled manner using vitamin C (500 mg/d) and E (400 UI/d) for 15 d. After 7 d of supplementation, athletes were submitted to an exercise-induced oxidative stress protocol consisting of plyometric jumping and strength resistance sets to exhaustion. Blood samples, performance tests, and DOMS were determined before and 24, 48, and 72 h after exercise.

RESULTS:

Antioxidant supplementation was continued during the recuperation week and for a total of 15 d. Antioxidant supplementation caused a significant increase in plasma vitamins C and E. The antioxidant supplementation could inhibit oxidative stress characterized by elevated lipid peroxidation markers malondialdehyde and total lipid peroxidation as well as reduced ratio of glutathione to oxidized glutathione promoted by exercise. Antioxidant supplementation, however, did not significantly reduce the plasma creatine kinesis concentration or DOMS during the recovery days. Likewise, supplementation with vitamin C and E did not improve lower body power, agility, or anaerobic power, nor did it provide any indication of faster muscle recovery.

CONCLUSION:

Antioxidant supplementation does not attenuate elevated markers of muscle damage or muscle soreness promoted by acute exercise and do not exert any ergogenic effect on football performance of young athletes, although it reduced oxidative stress.

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THE SKIN BENEFITS OF VITAMIN E

If you could, you might hire an army to defend your skin against all the assaults it has to deal with day in and day out: pollution, stress, smoke and less-than-healthy foods, to name just a few. Luckily, you can think of antioxidants like vitamin E as your skin’s own battalion.

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7 Natural Ways to Combat Chapped Skin on Little Faces

Are there any ways to treat or even prevent chapped skin naturally? Of course! Over the years I’ve learned what works—and what doesn’t—for protecting little chins, cheeks, and noses from the dry winter air. Here are the best ways to prevent, and in some cases treat, irritated facial skin in winter.

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Shaping the future of palm oil

Looking into the future we know that palm oil is here to stay. Palm oil is a superior vegetable oil when done right. It brings functional benefits to markets and economic progress to producing countries, so it has the capacity to bring benefits to many.  But it is up to all of us to decide what the future for palm oil will look like. We can create a bright tomorrow when we make the right choices.

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Take palm Vitamin E tocotrienols to protect your heart

It seems that humankind has been in search of cures for heart diseases for as long as medical science existed. The phenomenon was said to have first reared its ugly head in the 1920s and 1930s, when physicians across Britain and the United States were alerted that an uncommon disease was quickly becoming a leading cause of death.

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Effect of atherosclerosis and the protective effect of the antioxidant vitamin E on the rabbit cerebellum

Elbeltagy MAF, Elkholy WB, Salman AS

Microscopy (Oxf). 2019 Jul 15. pii: dfz023. doi: 10.1093/jmicro/dfz023. [Epub ahead of print]

Abstract

BACKGROUND:

Atherosclerosis is a major cardiovascular disease and one of the commonest causes of mortality in the world. Speech, balance, fine motor control and cognition are affected by atherosclerosis of cerebellar arteries. This study investigated the protective role of vitamin E against induced atherosclerosis in the rabbit cerebellum.

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