Bi-layered α-tocopherol acetate loaded membranes for potential wound healing and skin regeneration

Zahid S, Khalid H, Ikram F, Iqbal H, Samie M, Shahzadi L, Shah AT, Yar M, Chaudhry AA, Awan SJ, Khan AF, Rehman IU

Mater Sci Eng C Mater Biol Appl. 2019 Aug;101:438-447. doi: 10.1016/j.msec.2019.03.080. Epub 2019 Mar 23.

Abstract

With an increase in the demand for skin regeneration products, there is a noticeable increase in developing materials that encourage, wound healing and skin regeneration. It has been reported that antioxidants play an important role in anti-inflammatory reactions, cellular proliferation and remodeling phase of wound healing. While consideration all these factors, a novel α-tocopherol acetate (vitamin E) (VE) loaded bi-layered electrospun membrane, based on lower polycaprolactone (PCL) layer and upper polylactic acid (PLA) layer, was fabricated through electrospinning. Fourier-transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM), in-vitro degradation studies, swelling studies and VE release studies were performed to evaluate structural, physical and in-vitro behavior of membranes. Biological properties of membranes were evaluated through cell proliferation assay, cell adhesion studies, live/dead cell assay and CAM assay. SEM images showed that the average diameter of nanofibers ranged from 1 to 6 μm, while addition of VE changed the diameter and morphology of fibers. Bi-layered membranes showed significant swelling behavior through water uptake, membranes loaded with 30% VE showed 8.7% and 6.8% degradation in lysozyme and H2O2 respectively. 20% and 30% VE loaded membranes followed Korsmeyer-Peppas and first order drug release kinetics followed by non-fickian drug release kinetics. Membranes showed non-toxic behavior and supported cell proliferation via alamar blue assay, cell adhesion via SEM, cell viability via live/dead assay and wound healing by scratch assay. CAM assay showed that membranes having VE supported angiogenesis and showed significant formation of blood vessels making it suitable for skin regeneration and wound healing. Results showed that large surface area of nanofibers, porous structure and biocompatible nature are suitable for targeted clinical applications.

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Effect of dietary vitamin E on oxidative stress-related gene-mediated differences in anxiety-like behavior in inbred strains of mice

Matsuo K, Watanabe T, Takenaka A

Physiol Behav. 2019 Aug 1;207:64-72. doi: 10.1016/j.physbeh.2019.04.026. Epub 2019 May 4.

Abstract

It has been reported that the degree of anxiety-like behavior differs between inbred strains of mice, and that this phenomenon was linked to the expression levels of the oxidative stress-related genes glyoxalase 1 (Glo1) and glutathione reductase 1 (Gsr) in the brain. Therefore, we investigated whether antioxidative activity in the brain affects the Glo1 and Gsr mRNA expressions and strain-dependent anxiety-like behavior using mice fed different amounts of vitamin E. First, we measured brain Glo1 and Gsr mRNA levels and evaluated the anxiety-like behaviors presented by C57BL/6J (B6) and DBA/2C (D2) mice. We demonstrated that D2 mice presented both significantly elevated Glo1 and Gsr mRNA levels as well as more prominent anxiety-like behavior in elevated plus-maze and open field tests. Next, we fed mice from these two strains either a control, vitamin E-free, or vitamin E-supplemented diet for four weeks. Plasma, liver, and brain α-tocopherolconcentrations changed in a dose-dependent manner. However, neither brain Glo1 and Gsr mRNA levels nor anxiety-like behavior were affected by dietary vitamin E intake. These results demonstrated that while strain-dependent anxiety-like behavior in mice was related to oxidative stress-related gene expression, the regulatory mechanisms for these genes and anxiety-like behaviors were independent of antioxidative activity in the brain. Strain-dependent differences of the anxiety in mice are probably related to the anxiolytic effects of methylglyoxal, a substrate for Glo1 and Gsr.

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A five-year follow-up study of antioxidants, oxidative stress and polyunsaturated fatty acids in schizophrenia

Solberg DK, Refsum H, Andreassen OA, Bentsen H

Acta Neuropsychiatr. 2019 Aug;31(4):202-212. doi: 10.1017/neu.2019.14. Epub 2019 Jun 10.

Abstract

OBJECTIVE:

Oxidative stress and dysregulated antioxidant defence may be involved in the pathophysiology of schizophrenia. In the present study, we investigated changes in antioxidants and oxidative stress from an acute to a later stable phase. We hypothesised that the levels of oxidative markers are increased in schizophrenia compared with healthy controls; change from the acute to the stable phase; and are associated with the levels of membrane polyunsaturated fatty acids (PUFAs) and symptom severity.

METHODS:

Fifty-five patients with schizophrenia spectrum disorders, assessed during an acute phase and 5 years later during a stable phase, and 51 healthy controls were included. We measured antioxidants (α-tocopherol, uric acid, albumin and bilirubin), markers of oxidative stress (F2-isoprostane and reactive oxygen metabolites) and membrane fatty acids. Antioxidants and oxidative stress markers were compared in schizophrenia versus healthy controls, adjusting for differences in sex, age and smoking, and changes over time. Associations between symptoms and PUFA were also investigated.

RESULTS:

In the acute phase, α-tocopherol was significantly higher (p < 0.001), while albumin was lower (p < 0.001) compared with the stable phase. Changes in α-tocopherol were associated with PUFA levels in the acute phase. In the stable phase, schizophrenia patients had higher uric acid (p = 0.009) and lower bilirubin (p = 0.046) than healthy controls. CRP was higher in patients in the stable phase (p < 0.001), and there was no significant change from the acute phase.

CONCLUSION:

The present findings of change in antioxidant levels in the acute versus stable phase of schizophrenia the present findings suggest that redox regulation is dynamic and changes during different phases of the disorder.

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Preventative Effects of Vitamin E on Testicular Damage and Sperm Parameters in the First-Generation Mice Pups due to Pre- and Postnatal Mancozeb Exposure

Saddein E, Haghpanah T, Nematollahi-Mahani SN, Seyedi F, Ezzatabadipour M

J Toxicol. 2019 Aug 1;2019:4763684. doi: 10.1155/2019/4763684. eCollection 2019.

Abstract

The present study aimed to evaluate the effects of vitamin E on mancozeb-induced testis damage of the first-generation pups during intrauterine and lactating periods. Two groups of pregnant NMRI mice received 500 mg/kg mancozeb (MNZ) as MNZ group and 200 mg/kg vitamin E as MNZ+vit.E group before receiving MNZ. In addition, a vehicle and a control group were designed every other day in gestation and lactation periods. The male pups from each group were maintained until adulthood (8-10 W). The left testes and epididymides were removed following the sacrifice of the pups. Then, they were weighed, and sperm parameters including number, viability, motility, and morphology and testis structure were evaluated. A significant decrease occurred in sperm parameters of the mancozeb-treated pups compared to the control and vehicle groups. Treatment with vitamin E reversed the deleterious effects of MNZ to a nearly normal condition. Testis parameters including the weight, gonadosomatic index, seminiferous tubule diameters, and Johnsen’s score, as well as the number of germ cells such as spermatogonia, spermatocyte, spermatid, and Sertoli, decreased significantly in the MNZ group, compared to the amount in the control and vehicle groups. Interestingly, the treatment with vitamin E was reversed in most of these parameters. Based on the results, the exposure of pups to mancozeb during pregnancy and lactating periods negatively affects the reproductive system of male pups. However, the coadministration of vitamin E could prevent the deleterious effects of mancozeb on sperm and testis parameters.

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The Effect of Diazinon on Cell Proliferation and Apoptosis in Testicular Tissue of Rats and The Protective Effect of Vitamin E

Rahimi Anbarkeh F, Nikravesh MR, Jalali M, Sadeghnia HR, Sargazi Z

Int J Fertil Steril. 2019 Jul;13(2):154-160. doi: 10.22074/ijfs.2019.5612. Epub 2019 Apr 27.

Abstract

BACKGROUND:

Diazinon (DZN) is an organophosphate pesticide, and nowadays this pesticide is mostly used in agriculture. In this study, we analyzed the effects of DZN and vitamin E (Vit E) on apoptosis and the proliferation of germ cells in rat testis.

MATERIALS AND METHODS:

In this experimental study, 30 male Wistar rats were divided into five groups (n=6 per group) consisting of control, sham (received olive oil), experimental group i (60 mg/kg DZN), experimental group ii (60 mg/kg DZN and 200 mg/kg Vit E), and experimental group iii (200 mg/kg Vit E). After six weeks, left testis of rats was removed for the detection of proliferative cell nuclear antigen (PCNA) and terminal deoxynucleotidyl transferase end-labeling (TUNEL).

RESULTS:

Compared with the control group, DZN in the experimental group i decreased the number of PCNA-positive cells and increased the number of TUNEL-positive cells (P<0.001). Vit E improved detrimental changes by the decrease in the rate of apoptosis and the increase in the proliferation of testicular germ cells (P<0.001).

CONCLUSION:

Vit E can decrease the number of TUNEL-positive cells and increase the number of PCNA-positive cells by the neutralization of the toxicity caused by DZN in the testicular tissue.

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Antioxidant supplementation during illness in dogs: effect on oxidative stress and outcome, a pilot study

Hagen DM, Ekena JL, Geesaman BM, Viviano KR

J Small Anim Pract. 2019 Jul 10. doi: 10.1111/jsap.13050. [Epub ahead of print]

Abstract

OBJECTIVES:

To assess whether combination antioxidant supplementation for 30 days in systemically ill dogs alters antioxidant status, degree of lipid peroxidation, clinical score and survival.

MATERIALS AND METHODS:

Forty client-owned systemically-ill hospitalised dogs were eligible for inclusion. Dogs were randomised to no supplementation (NS; n=19) or supplementation with N-acetylcysteine/S-adenosylmethionine/silybin and vitamin E (AS; n=20) for 30 days. Clinical score and oxidative biomarkers including glutathione, cysteine, vitamin E, selenium and urine isoprostanes/creatinine (F2 -IsoPs/Cr) were determined on days 0 and 30. Glutathione, cysteine, vitamin E and urine F2 -IsoPs/Cr were quantified by high-performance liquid chromatography, and selenium concentrations determined using atomic absorption spectroscopy.

RESULTS:

Thirty-two dogs completed the study (NS, n=16; AS, n=16). Vitamin E concentrations were significantly greater in the supplemented compared to the non-supplemented group. No other markers of oxidative stress significantly changed with supplementation. There was no difference in Day 30 clinical scores or survival between the two groups.

CLINICAL SIGNIFICANCE:

In this population of systemically-ill hospitalised dogs, combination antioxidant supplementation did not alter redox state or clinical outcome.

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Familial vitamin E deficiency: Multiorgan complications support the adverse role of oxidative stress

Trotta E, Bortolotti S, Fugazzotto G, Gellera C, Montagnese S, Amodio P

Nutrition. 2019 Jul - Aug;63-64:57-60. doi: 10.1016/j.nut.2018.11.012. Epub 2018 Dec 1.

Abstract

Vitamin E is an essential micronutrient with relevant antioxidant and anti-inflammatory properties found in plant leaves, seeds, and products derived from their processing. Familial vitamin E deficiency is a rare inherited syndrome characterized by ataxia and peripheral neuropathy with a massive decrease in plasma vitamin E (<0.5 mg/dL). This report describes the history of two siblings suffering from ataxia with vitamin E deficiency who developed premature systemic disorders (atherosclerotic vascular disease, ischemic heart disease, and liver steatosis) in absence of relevant risk factors. The association of neuromuscular symptoms and multiorgan involvement in patients with ataxia with vitamin E deficiency has not been reported to our knowledge. The lack of an effective vitamin E activity seems to be implicated in the pathogenesis of cardiovascular, gastrointestinal, and other diseases in which oxidative stress is a risk factor.

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Beneficial effects of vitamin E on radioiodine induced gastrointestinal damage: an experimental and pathomorphological study.

Yumusak N, Sadic M, Akbulut A, Aydinbelge FN, Koca G, Korkmaz M

Bratisl Lek Listy. 2019;120(4):263-269. doi: 10.4149/BLL_2019_048.

Abstract

OBJECTIVES:

The aim of the present study was to investigate the radioprotective effect of vitamin E in the prevention of radioiodine (RAI) induced gastrointestinal damage.

METHOD:

Twenty-four rats were randomly divided into three groups as follows: Group-1 was untreated control group, Group-2 was orally administered single dose of 111 MBq RAI, and Group-3 was orally administered 111 MBq RAI and 1 mL of oral vitamin EVitamin E was started two days before RAI administration and was continued for five days once daily after RAI. Pathomorphological parameters of gastrointestinal tissues (stomach, small intestines and bowels) were measured using Hematoxylin-Eosin and Masson’s trichrome staining.

RESULTS:

Varying degrees of inflammation, edema, ulcer, mucosal degeneration, necrosis and fibrosis were seen in the stomach, small intestine and bowel tissues of the rats in both study groups and not in the control group. The differences were statistically significant between these groups for all parameters (p < 0.05). The histopathological damage in the vitamin E treated group was significantly less than the damage in the RAI only group (p < 0.05 for all pathomorphological parameters).

CONCLUSION:

The results of this study showed that vitamin E has a radioprotective property with antiinflammatory and antifibrotic effects protecting against gastrointestinal damage caused by radioiodine.

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Familial vitamin E deficiency: Multiorgan complications support the adverse role of oxidative stress

Trotta E, Bortolotti S, Fugazzotto G, Gellera C, Montagnese S, Amodio P

Nutrition. 2019 Jul - Aug;63-64:57-60. doi: 10.1016/j.nut.2018.11.012. Epub 2018 Dec 1.

Abstract

Vitamin E is an essential micronutrient with relevant antioxidant and anti-inflammatory properties found in plant leaves, seeds, and products derived from their processing. Familial vitamin E deficiency is a rare inherited syndrome characterized by ataxia and peripheral neuropathy with a massive decrease in plasma vitamin E (<0.5 mg/dL). This report describes the history of two siblings suffering from ataxia with vitamin E deficiency who developed premature systemic disorders (atherosclerotic vascular disease, ischemic heart disease, and liver steatosis) in absence of relevant risk factors. The association of neuromuscular symptoms and multiorgan involvement in patients with ataxia with vitamin E deficiency has not been reported to our knowledge. The lack of an effective vitamin E activity seems to be implicated in the pathogenesis of cardiovascular, gastrointestinal, and other diseases in which oxidative stress is a risk factor.

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Vitamin E δ-tocotrienol sensitizes human pancreatic cancer cells to TRAIL-induced apoptosis through proteasome-mediated down-regulation of c-FLIPs

Francois RA, Zhang A, Husain K, Wang C, Hutchinson S, Kongnyuy M, Batra SK, Coppola D, Sebti SM, Malafa MP

Cancer Cell Int. 2019 Jul 22;19:189. doi: 10.1186/s12935-019-0876-0. eCollection 2019.

Abstract

BACKGROUND:

Vitamin E δ-tocotrienol (VEDT), a vitamin E compound isolated from sources such as palm fruit and annatto beans, has been reported to have cancer chemopreventive and therapeutic effects.

METHODS:

We report a novel function of VEDT in augmenting tumor necrosis factor-related apoptosis-inducing ligand- (TRAIL-) induced apoptosis in pancreatic cancer cells. The effects of VEDT were shown by its ability to trigger caspase-8-dependent apoptosis in pancreatic cancer cells.

RESULTS:

When combined with TRAIL, VEDT significantly augmented TRAIL-induced apoptosis of pancreatic cancer cells. VEDT decreased cellular FLICE inhibitory protein (c-FLIP) levels without consistently modulating the expression of decoy death receptors 1, 2, 3 or death receptors 4 and 5. Enforced expression of c-FLIP substantially attenuated VEDT/TRAIL-induced apoptosis. Thus, c-FLIP reduction plays an important part in mediating VEDT/TRAIL-induced apoptosis. Moreover, VEDT increased c-FLIP ubiquitination and degradation but did not affect its transcription, suggesting that VEDT decreases c-FLIP levels through promoting its degradation. Of note, degradation of c-FLIP and enhanced TRAIL-induced apoptosis in pancreatic cancer cells were observed only with the anticancer bioactive vitamin E compounds δ-, γ-, and β-tocotrienol but not with the anticancer inactive vitamin E compounds α-tocotrienol and α-, β-, γ-, and δ-tocopherol.

CONCLUSIONS:

c-FLIP degradation is a key event for death receptor-induced apoptosis by anticancer bioactive vitamin E compounds in pancreatic cancer cells. Moreover, VEDT augmented TRAIL inhibition of pancreatic tumor growth and induction of apoptosis in vivo. Combination therapy with TRAIL agonists and bioactive vitamin E compounds may offer a novel strategy for pancreatic cancer intervention.

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