Monthly Archives: June 2020

Feasibility of Using Vitamin E-Loaded Poly(ε-caprolactone)/Gelatin Nanofibrous Mat to Prevent Oxidative Stress in Skin

Kalantary S, Golbabaei F, Latifi M, Shokrgozar MA, Yaseri M

J Nanosci Nanotechnol. 2020 Jun 1;20(6):3554-3562. doi: 10.1166/jnn.2020.17486.

Abstract

Some occupational skin exposures lead to the formation of reactive oxygen species (ROS). The occupational exposure of workers to ROS has been found to be associated with an increased risk of developing skin injuries; therefore, it is essential to protect skin against ROS formation. Recently, some studies have been conducted on introducing better alternatives for skin protection. Nanofibers are good candidates for this purpose. The current study was carried out to assess vitamin E-loaded hybrid Poly(ε-caprolactone) (PCL)/gelatin (Gt) nanofibres mats as protective layers of skin exposed to occupational exposures. Vitamin E (VE) was successfully incorporated into PCL/Gt nanofibers while they were formed by electrospinning method. Nanofibers mats were characterized using scanning electron microscopy (SEM) and fourier transform infrared spectroscopy (FTIR). Their degradation behavior, in vitro release, biocompatibility, and antioxidant activity were studied. The diameters of the PCL/Gt/VE nanofibers decreased with the addition of vitamin E. The degradation rate of nanofibers was equal to 42.98 and 50.69% during 7 and 14 days, respectively. Nanofibers containing vitamin E showed an initial burst followed by a sustained release. The PCL/Gt/VE nanofibers exhibited good free radical scavenging activities despite being exposed to a high electrical potential during electrospinning. PCL/Gt/VE nanofibers supported a higher level of viability compared to PCL/Gt ones and significantly assisted human skin cells against tert-Butyl hydroperoxide (t-BHP) induced oxidative stress. Overall, PCL/Gt/VE nanofibers can potentially be used to protect skin against oxidative stress as a novel approach for worker’s healthcare.

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Reduction of Senescence-Associated Beta-Galactosidase Activity by Vitamin E in Human Fibroblasts Depends on Subjects’ Age and Cell Passage Number

Roberta Ricciarelli, Angelo Azzi, Jean-Marc Zingg

Biofactors . 2020 Jun 1. doi: 10.1002/biof.1636. Online ahead of print.

Abstract

Cell senescence is due to the permanent cell cycle arrest that occurs as a result of the inherent limited replicative capacity toward the Hayflick limit (replicative senescence), or in response to various stressors (stress-induced premature senescence, SIPS). With the acquisition of the senescence-associated secretory phenotype (SASP), cells release several molecules (cytokines, proteases, lipids), and express the senescence-associated beta-galactosidase (SA-β-Gal). Here we tested whether vitamin E affects SA-β-Gal in an in vitro model of cell ageing. Skin fibroblasts from human subjects of different age (1, 13, 29, 59, and 88 years old) were cultured until they reached replicative senescence. At different passages (Passages 2, 9, 13, and 16), these cells were treated with vitamin E for 24 hr. Vitamin E reduced SA-β-Gal in all cells at passage 16, but at earlier passage numbers it reduced SA-β-Gal only in cells isolated from the oldest subjects. Therefore, short time treatment with vitamin E decreases SA-β-Gal in cells both from young and old subjects when reaching replicative senescence; but in cells isolated from older subjects, a decrease in SA-β-Gal by vitamin E occurs also at earlier passage numbers. The possible role of downregulation of CD36 by vitamin E, a scavenger receptor essential for initiation of senescence and SASP, is discussed.

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Increased Anxiety-Like Behavior Is an Early Symptom of Vitamin E Deficiency That Is Suppressed by Adrenalectomy in Rats

Yuki Terada, Hiroya Ohashi, Yuki Otani, Kanako Tokunaga, Asako Takenaka

Br J Nutr . 2020 Jun 1;1-27. doi: 10.1017/S0007114520001889. Online ahead of print

Abstract

We previously reported that dietary vitamin E deficiency increased anxiety-like behavior in rats exposed to social isolation. Here, we performed a detailed investigation of this phenomenon and its underlying mechanism. First, we fed Wistar rats with vitamin E-free diet for 3 days, 1 week, or 2 weeks and found an increase in anxiety-like behavior after 1 and 2 weeks of vitamin E deficiency based on behavioral indicators. Next, we examined the effect of a control diet (150 mg all-racemic α-tocopherol acetate/kg) on anxiety-like behaviors in rats that received a 4- week vitamin E-free diet. We found that increased anxiety-like behavior was reversed to control levels after refeeding vitamin E for 7 days but not for 1 or 3 days. Further, anxiety-like behavior increased or decreased gradually based on the amount of vitamin E intake; however, it had a quicker progression than physical symptoms of vitamin E deficiency. Moreover, rats fed with excess vitamin E (500 mg all-racemic α-tocopherol/kg diet) showed less anxiety-like behavior than control rats, indicating that vitamin E supplementation is effective for preventing anxiety increase under social isolation stress. Since plasma corticosterone levels were higher in vitamin E deficient rats, we investigated the effect of adrenalectomy on anxiety-like behavior and found that adrenal hormones played an essential role in the increased anxiety-like behavior induced by vitamin E deficiency. In conclusion, increased anxiety-like behavior is a symptom that emerges earlier than physical vitamin E deficiency and is caused by adrenal hormone-dependent mechanisms.

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Effects of Acrylamide in the Presence of Vitamin E on Sperm Parameters, Chromatin Quality, and Testosterone Levels in Mice

Morteza Anvari, Ali Reza Talebi, Esmat Mangoli, Abbas Shahedi, Mohammad Rasool Ghasemi, Majid Pourentezari

Clin Exp Reprod Med . 2020 Jun;47(2):101-107. doi: 10.5653/cerm.2019.03230. Epub 2020 Jun 1.

Abstract

Objective: The present study investigated sperm chromatin quality and testosterone levels in acrylamide-treated mice and the possible protective effects of vitamin E on the fertility potential of spermatozoa.

Methods: Thirty-two adult male mice were divided equally into four groups. Group 1 was the control, group 2 received acrylamide (10 mg/kg, water solution), group 3 received vitamin E (100 mg/kg, intraperitoneal), and group 4 received both acrylamide and vitamin E. After 35 days, spermatozoa from the right cauda epididymis were analyzed in terms of count, motility, morphology, and viability. Sperm DNA integrity and chromatin condensation were assessed by acridine orange (AO), aniline blue (AB), toluidine blue (TB), and chromomycin A3 (CMA3) staining.

Results: In acrylamide-treated mice, significantly lower sperm concentration, viability, motility, and testosterone levels were found in comparison with the control and acrylamide+vitamin E groups (p<0.05). In the vitamin E group, significantly more favorable sperm parameters and testosterone levels were found than in the other groups (p<0.05). There were also significantly more spermatozoa with less condensed chromatin in the acrylamide-treated mice than in the other groups. Moreover, significantly more spermatozoa with mature nuclei (assessed by AB, CMA3, AO, and TB staining) were present in the vitamin E group than in the control and acrylamide+vitamin E groups.

Conclusion: This study revealed the deleterious effects of acrylamide on sperm parameters and sperm chromatin quality. Vitamin E can not only compensate for the toxic effects of acrylamide, but also improve sperm chromatin quality in mice.

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Effects of Royal Jelly and Tocotrienol Rich Fraction in Obesity Treatment of Calorie-Restricted Obese Rats: A Focus on White Fat Browning Properties and Thermogenic Capacity

Naimeh Mesri Alamdari, Pardis Irandoost, Neda Roshanravan, Mohammadreza Vafa, Mohammad Asghari Jafarabadi, Shahriar Alipour, Leila Roshangar, Mohammadreza Alivand, Farnaz Farsi, Farzad Shidfar

Nutr Metab (Lond) . 2020 Jun 1;17:42. doi: 10.1186/s12986-020-00458-8. eCollection 2020.

Abstract

Background: Obesity has reached an alarming rate worldwide. Promoting thermogenesis via increasing the function of brown adipose tissue (BAT) or white adipose tissue (WAT) browning has been proposed as a new protective approach against obesity. The goal of this study was to evaluate the effects of Royal Jelly (RJ) and tocotrienol rich fraction (TRF) on BAT activation and WAT browning during calorie restriction diet (CRD) in obesity model.

Methods: In this experimental study, 50 obese Wistar rats were randomly divided into 5 groups and then received one of the following treatments for a period of 8-week: High-fat diet (HFD), CRD, RJ + CRD, TRF + CRD, and RJ + TRF + CRD. Effects of RJ and TRF, individually and in combination on body weight and the expression of key thermoregulatory genes in WAT and BAT were examined by quantitative real-time (qRT-PCR). Also, morphological alterations were assessed by hematoxylin and eosin staining.

Results: RJ (- 67.21 g ±4.84 g) and RJ + TRF (- 73.29 g ±4.51 g) significantly reduced weight gain relative to the CRD group (- 40.70 g ±6.50 g, P < 0.001). In comparison with the CRD group, RJ and RJ + TRF remarkably enhanced the uncoupling protein1 (UCP1) expression in WAT (5.81, 4.72 fold, P < 0.001) and BAT (4.99, 4.75 fold, P < 0.001). The expression of PR domain containing 16(PRDM 16), cAMP response element-binding protein1 (CREB1), P38 mitogen-activated protein kinases (P38MAPK), and Bone morphogenetic protein8B (BMP8B) have significantly increased following RJ and RJ + TRF treatments (P < 0.001). However, the expression levels of CCAAT/enhancer-binding protein beta (CEBPβ) and Bone morphogenetic protein7 ( BMP7) did not remarkably change. Multilocular beige cells in WAT and compacted dense adipocytes were also observed in BAT of RJ and RJ + TRF received groups. TRF showed no substantial effects on the expression of the mentioned thermoregulatory genes and brown fat-like phenotype.

Conclusion: Our results suggest that, Royal Jelly promotes thermogenesis and browning of WAT, contributing to an increase in energy expenditure. Thus, Royal Jelly may give rise to a novel dietary choice to attenuate obesity.

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