Monthly Archives: June 2021

Implications of advanced oxidation protein products and vitamin E in atherosclerosis progression

Leila Azouaou Toualbi, Adnane Mounir, Ballouti Wafa, Arab Medina, Khelfi Abderrezak, Toualbi Chahine, Chader Henni, Bennoui Abdelghani, Seba Atmane

Arch Med Sci Atheroscler Dis . 2021 Jun 30;6:e135-e144. doi: 10.5114/amsad.2021.107823. eCollection 2021.

Abstract

Introduction: Advanced oxidation protein products (AOPP) are considered as markers of oxidative stress and inflammation, and highly predictive of atherosclerosis. Vitamin E (Vit-E) is a powerful antioxidant, but no consensus on its effectiveness at the level of AOPP or the process of atherosclerosis has been made. Hence this was the aim of the present study.

Material and methods: A longitudinal study was conducted on 205 patients with chronic kidney disease (CKD) and 40 controls. The correlations between AOPP and glomerular filtration rate (GFR) and different biological markers were analyzed. Supra-aortic trunk echo-Doppler was conducted to assess the correlation of AOPP with intima-media thickness. The effects of Vit-E treatment on AOPP levels and atherosclerosis progression were also investigated.

Results: AOPP levels increased in parallel to the alteration of renal functions in CKD patients, compared to the control group (p < 0.05). The mean value of AOPP increased concomitantly with the intima-media thickness (p < 0.05). Furthermore, AOPP mean value was higher in patients with atherosclerotic plaques (p < 0.05) compared to those without plaques. Vit-E treatment stabilized the levels of AOPP but had no effect on the atherosclerotic progression.

Conclusions: AOPP were proved to be effective markers of oxidative stress and their high levels help to predict the progression of atherosclerosis. As a powerful antioxidant, Vit-E stabilized the AOPP levels.

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Activated Nrf-2 Pathway by Vitamin E to Attenuate Testicular Injuries of Rats with Sub-chronic Cadmium Exposure

Zhuo Chen, Zhicai Zuo, Kejie Chen, Zhuangzhi Yang, Fengyuan Wang, Jing Fang, Hengmin Cui, Hongrui Guo, Ping Ouyang, Zhengli Chen, Chao Huang, Yi Geng, Wentao Liu, Huidan Deng

Biol Trace Elem Res . 2021 Jun 25. doi: 10.1007/s12011-021-02784-1. Online ahead of print.

Abstract

Cadmium (Cd), a heavy metal element, cumulates in the testis and can cause male reproductive toxicity. Although vitamin E (VE) as one of potential antioxidants protects the testis against toxicity of Cd, the underlying mechanism remained uncompleted clear. The aim of this study was to investigate whether the Nrf-2 pathway is involved with the protective effect of VE on testicular damages caused by sub-chronic Cd exposure. Thirty-two SD rats were divided into four groups and orally administrated with VE and/or Cd for 28 consecutive days: control group, VE group (100 mg VE/kg), Cd group (5 mg CdCl2/kg), and VE + Cd group (100 mg VE/kg + 5 mg CdCl2/kg). The results showed that 28-day exposure of Cd caused accumulation of Cd, histopathological lesions, and alternations of sperm parameters (elevated rate of abnormal sperm, decreased count of sperm, declined motility, and viability of sperm). Moreover, the rats exposed to Cd showed significant oxidative stress (increased contents of MDA and decreased levels or activities of T-AOC, GSH, CAT, SOD and GSH-Px) and inhibition of Nrf-2 signaling pathway (downregulation of Nrf-2, HO-1, NQO-1, GCLC, GCLM and GST) of the testes. In contrast, VE treatment significantly reduced the Cd accumulation, alleviated histopathological lesions and dysfunctions, activated Nrf-2 pathway, and attenuated the oxidative stress caused by Cd in the testes of rats. In conclusion, VE, through upregulating Nrf-2 pathway, could protect testis against oxidative damages induced by sub-chronic Cd exposure.

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Effects of vitamin E on neurodegenerative diseases: an update

Mehmet Arif Icer, Neslihan Arslan, Makbule Gezmen-Karadag

Acta Neurobiol Exp (Wars) . 2021;81(1):21-33. doi: 10.21307/ane-2021-003.

Abstract

Vitamin E deficiency is associated with many neurological problems. Although the mechanisms of vitamin E action in neurodegenerative diseases are not clear, there are many possible mechanisms. Examples of such mechanisms are the protective effects of vitamin E against oxidative stress damage and its suppressive role in the expression of many genes involved in the development of neurodegeneration. Many studies have evaluated the relationship between vitamin E intake or vitamin E levels in body fluids and neurodegenerative diseases. Some studies concluded that vitamin E can play a protective role in neurodegeneration with respect to diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke and amyotrophic lateral sclerosis (ALS). Vitamin E supplementation was also associated with risk factors for some neurodegenerative diseases. In this review, we discuss the possible effects of vitamin E on the development and course of AD, PD, stroke and ALS, and the potential mechanisms involved.

Vitamin E deficiency is associated with many neurological problems. Although the mechanisms of vitamin E action in neurodegenerative diseases are not clear, there are many possible mechanisms. Examples of such mechanisms are the protective effects of vitamin E against oxidative stress damage and its suppressive role in the expression of many genes involved in the development of neurodegeneration. Many studies have evaluated the relationship between vitamin E intake or vitamin E levels in body fluids and neurodegenerative diseases. Some studies concluded that vitamin E can play a protective role in neurodegeneration with respect to diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke and amyotrophic lateral sclerosis (ALS). Vitamin E supplementation was also associated with risk factors for some neurodegenerative diseases. In this review, we discuss the possible effects of vitamin E on the development and course of AD, PD, stroke and ALS, and the potential mechanisms involved.

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Vitamin A and E Homologues Impacting the Fate of Acrylamide in Equimolar Asparagine-Glucose Model System

Su Lee Kuek, Azmil Haizam Ahmad Tarmizi, Raznim Arni Abd Razak, Selamat Jinap, Maimunah Sanny

Antioxidants (Basel) . 2021 Jun 22;10(7):993. doi: 10.3390/antiox10070993.

Abstract

This study aims to evaluate the influence of Vitamin A and E homologues toward acrylamide in equimolar asparagine-glucose model system. Vitamin A homologue as β-carotene (BC) and five Vitamin E homologues, i.e., α-tocopherol (AT), δ-tocopherol (DT), α-tocotrienol (ATT), γ-tocotrienol (GTT), and δ-tocotrienol (DTT), were tested at different concentrations (1 and 10 µmol) and subjected to heating at 160 °C for 20 min before acrylamide quantification. At lower concentrations (1 µmol; 431, 403, 411 ppm, respectively), AT, DT, and GTT significantly increase acrylamide. Except for DT, enhancing concentration to 10 µmol (5370, 4310, 4250, 3970, and 4110 ppm, respectively) caused significant acrylamide formation. From linear regression model, acrylamide concentration demonstrated significant depreciation over concentration increase in AT (Beta = -83.0, R2 = 0.652, p ≤ 0.05) and DT (Beta = -71.6, R2 = 0.930, p ≤ 0.05). This study indicates that different Vitamin A and E homologue concentrations could determine their functionality either as antioxidants or pro-oxidants.

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Tocotrienols Activate Nrf2 Nuclear Translocation and Increase the Antioxidant- Related Hepatoprotective Mechanism in Mice Liver

Ahmed Atia, Nadia S Alrawaiq, Azman Abdullah

Curr Pharm Biotechnol . 2021;22(8):1085-1098. doi: 10.2174/1389201021666200928095950.

Abstract

Background: The most common preparation of tocotrienols is the Tocotrienol-Rich Fraction (TRF). This study aimed to investigate whether TRF induced liver Nrf2 nuclear translocation and influenced the expression of Nrf2-regulated genes.

Methods: In the Nrf2 induction study, mice were divided into control, 2000 mg/kg TRF and diethyl maleate treated groups. After acute treatment, mice were sacrificed at specific time points. Liver nuclear extracts were prepared and Nrf2 nuclear translocation was detected through Western blotting. To determine the effect of increasing doses of TRF on the extent of liver nuclear Nrf2 translocation and its implication on the expression levels of several Nrf2-regulated genes, mice were divided into 5 groups (control, 200, 500 and 1000 mg/kg TRF, and butylated hydroxyanisole-treated groups). After 14 days, mice were sacrificed and liver RNA was extracted for qPCR assay.

Results: 2000 mg/kg TRF administration initiated Nrf2 nuclear translocation within 30 min, reached a maximum level of around 1 h and dropped to half-maximal levels by 24 h. Incremental doses of TRF resulted in dose-dependent increases in liver Nrf2 nuclear levels, along with concomitant dosedependent increases in the expressions of Nrf2-regulated genes.

Conclusion: TRF activated the liver Nrf2 pathway resulting in increased expression of Nrf2-regulated cytoprotective genes.

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Effect of vitamin E on periodontitis: Evidence and proposed mechanisms of action

Saminathan Shadisvaaran, Kok-Yong Chin, Mohd-Said Shahida, Soelaiman Ima-Nirwana, Xin-Fang Leong

J Oral Biosci . 2021 Jun;63(2):97-103. doi: 10.1016/j.job.2021.04.001. Epub 2021 Apr 20.

Abstract

Background: Periodontitis is a noncommunicable inflammatory disease of the soft tissue and bone surrounding the teeth in the jaw, which affects susceptible individuals with poor oral hygiene. A growing interest has been seen in the use of dietary supplements and natural products for the treatment and prevention of periodontitis. Vitamin E consists of two major groups, namely tocopherols and tocotrienols, which are botanical lipophilic compounds with excellent anti-inflammatory and antioxidant properties.

Highlight: This review aimed to summarize the preclinical and clinical findings on the effects of vitamin E on periodontitis. The current literature suggests that vitamin E could improve the periodontal status by correcting redox status imbalance, reducing inflammatory responses, and promoting wound healing, thus highlighting the potential of vitamin E in the management of periodontitis.

Conclusion: Direct evidence for the use of vitamin E supplementation or treatment of periodontitis in humans is still limited. More well-designed and controlled studies are required to ascertain its effectiveness.

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Protective role of vitamin E in testicular development of mice exposed to valproic acid

Daniel Conei, Mariana Rojas, Luis Santamaría, Jennie Risopatrón

Andrologia . 2021 Jun 21;e14140. doi: 10.1111/and.14140. Online ahead of print.

Abstract

Valproic acid (VPA) is a teratogenic antiepileptic, causing alterations in oxidative stress in prenatal development, being altered the development of the male reproductive system. The purpose of this study was to determine the protective effect of vitamin E (VE) on the testicular development in embryos, foetuses and pubertal mice exposed to VPA, VPA+VE and only VE. Sixty pregnant adult female mice were used, to which they were administered 600 mg/kg of VPA (VPA groups), 600 mg/kg of VPA and 200 IU of VE (VPA+VE groups), 200 IU VE (VE groups) and 0.3 ml of 0.9% physiological solution (control groups), showing at 12.5 days post-coital (dpc), 17.5 dpc and 6 weeks postnatal testicular development, and proliferative and apoptotic indices. The groups treated with VPA presented a smaller testicular volume, with greater interstitial space and a delay in the conformation of the testicular cords, shorter lengths and diameters of the germinal epithelium, a smaller number of germline and somatic cells, an increase in cells apoptotic and less proliferation, with significant differences. VE-treated groups behaved similarly to controls. In conclusion, VE reduces the effects caused by VPA throughout testicular development, from embryonic stages, continuing until pubertal stages.

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Associations between vitamin E, oxidative stress markers, total homocysteine levels, and physical activity or cognitive capacity in older adults

Ahmad H Alghadir, Sami A Gabr, Shahnawaz Anwer, Heng Li

Sci Rep . 2021 Jun 18;11(1):12867. doi: 10.1038/s41598-021-92076-4.

Abstract

This study examined the associations between vitamin E, oxidative stress markers, total homocysteine levels, and physical activity or cognitive capacity in older adults. One hundred and six older adults (62 men, 44 women) within the age range of 56-81 years participated. The Global Physical Activity Questionnaire and the Loewenstein Occupational Therapy Cognitive Assessment were used to assess physical activity and cognitive function, respectively. Vitamin E (e.g., α-tocopherol and γ-tocopherol), oxidative stress markers (e.g., total antioxidant capacity and nitric oxide), and total homocysteine were estimated. There were significant associations between physical activity (high versus moderate versus poor) and all biomarkers (all p = 0.000, and p = 0.010 for γ-tocopherol). While total homocysteine and total antioxidant capacity were significantly associated with cognitive capacity (p = 0.000), vitamin E levels (e.g., α-tocopherol and γ-tocopherol) and nitric oxide (p = 0.354, 0.103 and 0.060, respectively) were not related to cognitive capacity in older adults. This study concludes that physical activity was associated with Vitamin E, oxidative stress markers, total homocysteine, and cognitive capacity in older adults. Although cognitive capacity was associated with total homocysteine and total antioxidant capacity, it was unrelated to vitamin E levels and nitric oxide in older adults.

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Protective Effects of Vitamin E on Chemotherapy-Induced Peripheral Neuropathy: A Meta-Analysis of Randomized Controlled Trials

Huikai Miao, Rongzhen Li, Dongni Chen, Jia Hu, Youfang Chen, Chunmei Xu, Zhesheng Wen

Ann Nutr Metab . 2021 Jun 18;1-11. doi: 10.1159/000515620. Online ahead of print.

Abstract

Introduction: Chemotherapy-induced peripheral neuropathy (CIPN) is a common symptom, but prophylactic measures cannot still be carried out effectively. In addition, the efficacy of vitamin E in preventing peripheral neurotoxicity caused by chemotherapy is inconclusive. Therefore, we collected the relevant randomized controlled trials (RCTs) and performed a meta-analysis to examine whether the vitamin E has a positive effect in CIPN.

Methods: We searched PubMed, EMBASE, Cochrane, and other databases in December 2019 for eligible trials. Two reviewers conducted the analysis independently when studies were homogeneous enough.

Results: Eight RCTs, involving 488 patients, were identified. Upon pooling these RCTs, patients who received vitamin E supplementation of 600 mg/day had a lower incidence of CIPN (risk ratio [RR] 0.31; 95% confidence interval [CI] 0.14-0.65; p = 0.002) than the placebo group. Vitamin E played a key role in decreasing the incidence of peripheral neuropathy in the cisplatin chemotherapy group (RR 0.28; 95% CI 0.14-0.54; p = 0.0001). Moreover, vitamin E supplementation significantly decreased patients’ sural amplitude after 3 rounds of chemotherapy (RR -2.66; 95% CI -5.09 to -0.24; p = 0.03) in contrast with that of placebo supplementation, while no significant difference was observed when patients were treated with vitamin E after 6 rounds of chemotherapy. In addition, the vitamin E-supplemented group had better improvement in the neurotoxicity score and lower incidence of reflexes and distal paraesthesias than the control group.

Conclusion: Available data in this meta-analysis showed that vitamin E supplementation can confer modest improvement in the prevention of CIPN.

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