Colostrum supplementation with n-3 fatty acids and α-tocopherol alters plasma polyunsaturated fatty acid profile and decreases an indicator of oxidative stress in newborn calves

Opgenorth J, Sordillo LM, VandeHaar MJ

J Dairy Sci. 2020 Apr;103(4):3545-3553. doi: 10.3168/jds.2019-17380. Epub 2020 Jan 3

Abstract

Our objective was to characterize the effects of supplementing newborn calves with n-3 fatty acids (FA) and α-tocopherol on blood lipid profiles and oxidant status in early life. Sixteen calves received 0 or 60 mL of 1:1 fish and flaxseed oil with 200 mg of α-tocopherol in 2.8 L of colostrum within 6 h after birth. Colostrum was >22% on the Brix scale. Blood was sampled on d 1, 2, 4, 7, 14, and 21 after birth for assessment of plasma polyunsaturated FA, α-tocopherol, total serum protein, and oxidant status index, an indirect indicator of oxidative stress that examines the balance between the concentration of reactive oxygen and nitrogen species and antioxidant capacity in serum. Health was observed daily. Weight and hip height were recorded at birth, 3 wk, and 8 wk. Data were analyzed with a Mixed procedure of SAS 9.4 (SAS Institute Inc., Cary, NC). Treatment did not alter concentration of total protein in blood serum, prevalence of diarrhea or other signs of disease, or rate of growth. Feeding n-3 FA and α-tocopherol increased plasma concentrations of the n-3 FA, including α-linolenic, eicosapentaenoic, and docosahexaenoic acids, with a concomitant decrease in oxidant status index during the first week of life. Concentrations of α-tocopherol decreased with supplementation, but all calves maintained adequate concentrations. Oxidant status index of treated calves returned to the level of control calves by d 14. We conclude that a colostrum supplement of n-3 FA and α-tocopherol is safe to administer to newborn calves, reduces oxidant status in the first week of life, and may improve health and performance.

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Alpha-tocopherol exerts protective function against the mucotoxicity of particulate matter in amphibian and human goblet cells

Yang HS, Sim HJ, Cho H, Bang WY, Kim HE, Kwon TK, Kwon T, Park TJ

Sci Rep. 2020 Apr 10;10(1):6224. doi: 10.1038/s41598-020-63085-6.

Abstract

Exposure to particulate matter (PM) in ambient air is known to increase the risk of cardiovascular disorders and mortality. The cytotoxicity of PM is mainly due to the abnormal increase of reactive oxygen species (ROS), which damage cellular components such as DNA, RNA, and proteins. The correlation between PM exposure and human disorders, including mortality, is based on long-term exposure. In this study we have investigated acute responses of mucus-secreting goblet cells upon exposure to PM derived from a heavy diesel engine. To this end, we employed the mucociliary epithelium of amphibian embryos and human Calu-3 cells to examine PM mucotoxicity. Our data suggest that acute exposure to PM significantly impairs mucus secretion and results in the accumulation of mucus vesicles in the cytoplasm of goblet cells. RNA-seq analysis revealed that acute responses to PM exposure significantly altered gene expression patterns; however, known regulators of mucus production and the secretory pathway were not significantly altered. Interestingly, pretreatment with α-tocopherol nearly recovered the hyposecretion of mucus from both amphibian and human goblet cells. We believe this study demonstrates the mucotoxicity of PM and the protective function of α-tocopherol on mucotoxicity caused by acute PM exposure from heavy diesel engines.

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Effect of a short-term vitamin E supplementation on oxidative stress in infertile PCOS women under ovulation induction: a retrospective cohort study

Chen J, Guo Q, Pei YH, Ren QL, Chi L, Hu RK, Tan Y

BMC Womens Health. 2020 Apr 6;20(1):69. doi: 10.1186/s12905-020-00930-w.

Abstract

BACKGROUND:

Vitamin E, which is critically important in the whole process of reproduction, can antagonize the oxidative stress caused by the oxygen free radicals and antioxidant imbalance and regulate normal physiological function of the reproductive system. The effect of short-term supplementation of vitamin E on outcomes of infertile women with polycystic ovary syndrome (PCOS) when they underwent ovulation induction with clomiphene citrate (CC) and human menopausal gonadotropin (HMG) remains unknown.

METHODS:

This was a retrospective cohort clinical trial from October 2015 to April 2017. A total of 321 PCOS cases underwent ovulation induction with CC and HMG. Patients in group A (n = 110) did not receive vitamin E while patients in group B (n = 105) and group C (n = 106) received oral treatment of vitamin E at 100 mg/day during follicular phase and luteal phase, respectively.

RESULTS:

It was observed no significant differences of ovulation rate, clinical pregnancy rate, and ongoing pregnancy rate among the three groups. It was interesting that dosage of HMG were significant lower in group B compared with those in group A and group C (P<0.05).

CONCLUSIONS:

A short-term supplementation of vitamin E can improve oxidative stress, and reduce exogenous HMG dosage to lower the economic cost with a similar pregnancy rate in the ovulation induction cycle. However, the supplementation does not alter the pregnancy rate in the ovulation induction cycle.

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Plasma Non-Enzymatic Antioxidant Capacity (NEAC) in Relation to Dietary NEAC, Nutrient Antioxidants and Inflammation-Related Biomarkers

Carrión-García CJ, Guerra-Hernández EJ, García-Villanova B, Serafini M, Sánchez MJ, Amiano P, Molina-Montes E

Antioxidants (Basel). 2020 Apr 5;9(4). pii: E301. doi: 10.3390/antiox9040301.

Abstract

(1) Background: Little is known about the interlinkages between dietary and plasma non-enzymatic antioxidant capacity (D-NEAC and P-NEAC, respectively) and the body’s antioxidant and inflammation response. Our aim was to explore these associations in 210 participants from two Spanish European Prospective Investigation into Cancer and Nutrition (EPIC) centers. (2) Methods: D-NEAC was estimated using published NEAC values in food. P-NEAC and total polyphenols (TP) were quantified by FRAP (ferric-reducing antioxidant power), TRAP (total radical-trapping antioxidant parameter), TEAC-ABTS (trolox equivalent antioxidant capacity – Azino Bis Thiazoline Sulfonic), ORAC (oxygen radical absorbance capacity) and Folin-Ciocalteu assays. Nutrient antioxidants (carotenes, α-tocopherol, ascorbic acid, retinol, uric acid, Q9 and Q10 coenzymes) and inflammation markers (IL-6, IL-8, CRP, TNF-α, PAI-I, resistin and adiponectin) were also analyzed. Spearman correlation and linear regression analyses were performed in association analyses. Analyses were stratified by covariates and groups were defined using cluster analysis. (3) Results: P-FRAP was correlated with D-NEAC, and significantly associated with P-NEAC in multivariate adjusted models. P-FRAP levels were also significantly associated with plasma antioxidants (log2 scale: TP β = 0.26; ascorbic acid β = 0.03; retinol β = 0.08; α-tocopherol β = 0.05; carotenes β = 0.02; Q10 β = 0.06; uric acid β = 0.25), though not with inflammation-related biomarkers. Different profiles of individuals with varying levels of P-NEAC and biomarkers were found. (4) Conclusions: P-NEAC levels were to some extent associated with D-NEAC and plasma antioxidants, yet not associated with inflammation response.

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Protective Effect of Palm Oil-Derived Tocotrienol-Rich Fraction Against Retinal Neurodegenerative Changes in Rats with Streptozotocin-Induced Diabetic Retinopathy

Sadikan MZ, Nasir NAA, Agarwal R, Ismail NM

Biomolecules. 2020 Apr 5;10(4). pii: E556. doi: 10.3390/biom10040556.

Abstract

: Oxidative stress plays an important role in retinal neurodegeneration and angiogenesis associated with diabetes. In this study, we investigated the effect of the tocotrienol-rich fraction (TRF), a potent antioxidant, against diabetes-induced changes in retinal layer thickness (RLT), retinal cell count (RCC), retinal cell apoptosis, and retinal expression of vascular endothelial growth factor (VEGF) in rats. Additionally, the efficacy of TRF after administration by two different routes was compared. The diabetes was induced in Sprague-Dawley rats by intraperitoneal injection of streptozotocin. Subsequently, diabetic rats received either oral or topical treatment with vehicle or TRF. Additionally, a group of non-diabetic rats was included with either oral or topical treatment with a vehicle. After 12 weeks of the treatment period, rats were euthanized, and retinas were collected for measurement of RLT, RCC, retinal cell apoptosis, and VEGF expression. RLT and RCC in the ganglion cell layer were reduced in all diabetic groups compared to control groups (p < 0.01). However, at the end of the experimental period, oral TRF-treated rats showed a significantly greater RLT compared to topical TRF-treated rats. A similar observation was made for retinal cell apoptosis and VEGF expression. In conclusion, oral TRF supplementation protects against retinal degenerative changes and an increase in VEGF expression in rats with streptozotocin-induced diabetic retinopathy. Similar effects were not observed after topical administration of TRF.

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Nails: The Window to the Nose? Update on Yellow Nail Syndrome

Laura Vollono, Marco Adriano Chessa, Antonio Bruno, Michela Starace, Aurora Alessandrini, Bianca Maria Piraccini

Dermatol Pract Concept . 2020 Apr 3;10(2):e2020031. doi: 10.5826/dpc.1002a31.

Abstract

Background: Yellow nail syndrome is a rare condition characterized by typical nail alterations and variable presence of lymphedema and respiratory disease. The pathogenesis is still obscure, with most of the literature deriving from case reports and few investigations. The most reported respiratory conditions associated with yellow nail syndrome are pleural effusion and bronchiectasis, whereas association with rhinosinusitis is rarer.

Objectives: To describe a case of yellow nail syndrome and to provide a literature review regarding this disorder, discussing pathogenetic hypothesis, associated conditions, and therapeutic options.

Patients/methods: A 49-year-old man presented with arrested growth and alterations of his nails, without any history of previous trauma or inflammation but with a severe nasal septum deviation and a history of chronic rhinosinusitis. A diagnosis of yellow nail syndrome was made.

Results: Six months after undergoing rhinoseptoplasty and treatment with oral vitamin E, the patient’s nails were cured.

Conclusions: This case emphasizes the role of the dermatologist in detecting systemic conditions. The correct diagnosis led to complete resolution of both nail alterations and associated respiratory disorders.

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Vitamin E and selenium administration synergistically mitigates ivermectin and doramectin-induced testicular dysfunction in male Wistar albino rats

Ahmed AE, Alshehri A, Al-Kahtani MA, Elbehairi SEI, Alshehri MA, Shati AA, Alfaifi MY, Al-Doais AA, Taha R, Morsy K, El-Mansi AA

Biomed Pharmacother. 2020 Apr;124:109841. doi: 10.1016/j.biopha.2020.109841. Epub 2020 Jan 20.

Abstract

Avermectins are broad-spectrum antiparasitic drugs in veterinary and human medication. The current study aimed to examine the toxic effects of ivermectin (IVM) and doramectin (DRM), with or without co-treatment of vitamin E (Vit.E) and selenium (Se) on apoptosis, oxidative stress and male fertility in Wistar rats. Twenty five adult male animals were divided into five groups; G1; was control (CTL) received saline, G2; IVM (0.2 mg/kg b.w), G3; IVM plus Vit.E/Se (80/1.6 mg/kg b.w, respectively), G4; DRM (0.2 mg/kg b.w), and G5; DRM plus Vit.E/Se. Both IVM and DRM were given by subcutaneous (s.c) injections while Vit.E/Se was orally given. All treatments were administered once weekly for four consecutive weeks. By 24 h after the last treatment, the animals were sacrificed. Blood and tissue samples were collected for hematology, serobiochemistry, histopathology, and molecular assays for hepatic/ renal toxicities, oxidative stress, cell viability and fertility parameters. Apoptosis of the hepatic cells obtained from the treated rats was assayed by detection of annexin-V using the flow cytometric assay (FCA). The proliferating cellular nuclear antigen (PCNA) and DNA fragmentation in the treated rats’ testicular tissues were also assayed. Moreover, the direct effects of IVM or DRM with or without concomitant administration of Vit.E/Se on testicular cells isolated from adult rat were also performed in vitro. Apoptosis of those cultured testicular cells in response to the different treatments was assayed by detection of the inhibition-concentration fifty (IC50) using the SRB method, and evaluating the viable versus apoptotic cells microscopically after staining with acridine orange-ethidium bromide (AO/EB). In conclusion, both avermectins induced apoptosis in the living and cultured cells, while those antioxidants; Vit.E and Se, reduced the oxidative stress and cytotoxicity both in vivo and in vitro, either. Furthermore, the reprotoxicity and reduced male fertility were seriously evoked by IVM, but not DRM with dramatic ameliorative effect of Vit.E/Se if concomitantly administered. Avermectins, especially ivermectin, should be given according to the dose recommended by the manufacturer company and repeated dosages should be given with Vit.E/Se.

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E-cigarette or Vaping Product Use-Associated Lung Injury

Philip W Ind

Br J Hosp Med (Lond) . 2020 Apr 2;81(4):1-9. doi: 10.12968/hmed.2019.0371.

Abstract

E-cigarette or vaping product use-associated lung injury is a recently recognised, acute pulmonary syndrome which has been reported (particularly from June to October 2019) throughout the USA, but not in Europe (although one probable case, in the UK, has been reported; Medicines and Healthcare products Regulatory Agency, 2020). It presents acutely, most often in young men, as severe pulmonary consolidation, usually with respiratory failure. The mortality is around 2%. The cause(s) are unknown, but it is associated with vaping, particularly using unlicensed cannabis-containing products with tetrahydrocannabinol. Vitamin E acetate, often present in tetrahydrocannabinol-containing vape products as a solvent, has been implicated, as it has been identified in the bronchoalveolar lavage fluid of patients with e-cigarette or vaping product use-associated lung injury. This article reviews the recent literature, including clinical features, presentation and investigations, and possible mechanisms, in the context of vaping practices in the USA and the UK.

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Dietary antioxidants, non-enzymatic antioxidant capacity and the risk of osteoarthritis in the Swedish National March Cohort

Veen L, Hantikainen E, Bellocco R, Ye W, Serafini M, Ponzano M, Grotta A, Trolle Lagerros Y

Eur J Nutr. 2020 Apr 2. doi: 10.1007/s00394-020-02239-8. [Epub ahead of print]

Abstract

PURPOSE:

Oxidative stress might play an important role in the development of osteoarthritis, but not much is known about the effect of antioxidants on osteoarthritis risk. We, therefore, aimed to investigate the effect of dietary vitamin C, E, beta-carotene, and non-enzymatic antioxidant capacity (NEAC), which measures overall antioxidant activity from the diet, on the risk of osteoarthritis.

METHODS:

For this study 43,865 men and women from the Swedish National March Cohort (SNMC) were followed for up to 19 years. We computed dietary intake of vitamin C, E and beta-carotene using information from a Food Frequency Questionnaire (FFQ). To estimate dietary NEAC we combined the information from the FFQ with food item-specific antioxidant capacity values from an antioxidant food database. Cases of osteoarthritis were identified through the Swedish National Patient Registers. We categorized all exposure variables into sex-specific quartiles and used multivariable-adjusted Cox proportional hazards regression models to estimate hazard ratios (HRs) with 95% confidence intervals (95% CIs).

RESULTS:

In total, we observed 5976 cases of OA during 469,148 person-years of follow-up. After adjusting for potential confounders, we did not find any association between vitamin C, beta-carotene and NEAC (p-values for trend > 0.5), but a positive association was found with higher dietary vitamin E intake (HR Q4 vs Q1: 1.11; 95% CI 1.02-1.21; p for trend = 0.01) and the risk of OA.

CONCLUSION:

Our findings do not provide evidence for dietary antioxidants to protect from the development of OA, and a higher dietary vitamin E intake might even increase the risk.

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Injectable Enzyme-Based Hydrogel Matrix with Precisely Oxidative Stress Defense for Promoting Dermal Repair of Burn Wound

Zhang D, Wang B, Sun Y, Wang C, Mukherjee S, Yang C, Chen Y

Macromol Biosci. 2020 Apr 2:e2000036. doi: 10.1002/mabi.202000036. [Epub ahead of print]

Abstract

Burn wound healing remains a challenging health problem worldwide due to the lack of efficient and precise therapy. Inherent oxidative stress following burn injury is importantly responsible for prolonged inflammation, fibrotic scar, and multiple organ failure. Herein, a bioinspired antioxidative defense system coupling with in situ forming hydrogel, namely, multiresponsive injectable catechol-Fe3+ coordination hydrogel (MICH) matrix, is engineered to promote burn-wound dermal repair by inhibiting tissue oxidative stress. This MICH matrix serves as the special traits of “Fe-superoxide dismutases,” small molecular antioxidant (vitamin E), and extracellular matrix (ECM) in alleviating cellular oxidative damage, which demonstrates precise scavenging on reactive oxygen species (ROS) of different cellular locations, blocking lipid peroxidation and cell apoptosis. In in vivo burn-wound treatment, this MICH promptly integrates with injured surrounding tissue to provide hydration microenvironment and physicochemical ECM for burn wounds. Importantly, the MICH matrix suppresses tissue ROS production, reducing the inflammatory response, prompting re-epithelization and neoangiogenesis during wound healing. Meanwhile, the remodeling skin treated with MICH matrix demonstrates low collagen deposition and normal dermal collagen architecture. Overall, the MICH prevents burn wound progression and enhances skin regeneration, which might be a promising biomaterial for burn-wound care and other disease therapy induced by oxidative stress.

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