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Aytekin, İsmail (Balikesir Author), The study aimed to investigate the effects of vitamin E injection for the prevention of transport stress on ewes. Kivircik ewes (2-3 years old, n = 24) were randomly separated into three groups; G1 (Control) and G2 treated with 14 ml. saline as the placebo, G3 treated with 2100 IU/ind. DL-alpha-tocopherol acetate prior to transport. G2 and G3 were transported at 80 km/h for 4 h on a truck. Serum samples were obtained before (T0) and after (T1) transport. Serum cortisol, catalase, IgG, ceruloplasmin, C-reactive protein, complement component 4, interleukin-1 beta, tumour necrosis factor-alpha, glutathione peroxidase (GPx), superoxide dismutase, malondialdehyde analyses performed by ELISA, and serum alpha-tocopherol concentrations were evaluated by HPLC-UV. Wilcoxon and Kruskal-Wallis tests were used for statistical assessments (p < 0.05). Alpha-tocopherol concentrations were founded 1.22 +/- 0.82, 0.27 +/- 0.14 and 0.14 +/- 0.07 mu mol/L, respectively, in G1, G2 and G3 at T1. Alpha-tocopherol concentration decreased significantly in G2 between T0 and T1. GPx concentrations were increased twofold in G2 and G3 between T0 and T1 (p < 0.01). As a result, G2 alpha-tocopherol concentrations decreased but, the stress and oxidative parameters tested in this study were not affected by treating 2100 IU/ind. DL-alpha-tocopherol acetate before transport., Istanbul University-Cerrahpasa TSA-2017-27532

The most important function of the placenta is the exchange of nutrients and oxygen between a mother and her fetus. To establish a healthy functioning placenta, placentation needs to occur with adequate remodelling of spiral arteries by extravillous trophoblasts. When this process is impaired, the resulting suboptimal and inadequate placenta function results in the manifestation of pregnancy complications. Impaired placenta function can cause preeclampsia and leads to fetal growth restriction due to hypoxia. Presence of hypoxia leads to oxidative stress due to an imbalance between reactive oxygen species and antioxidants, thereby causing damage to proteins, lipids and DNA. In the placenta, signs of morphological adaptation in response to hypoxia can be found. Different placental lesions like maternal or fetal vascular malperfusion or chronic villitis lead to a decreased exchange of oxygen between the mother and the fetus. Clinically, several biomarkers indicative for oxidative stress, e.g. malondialdehyde and reduced levels of free thiols are found. This review aims to give an overview of the causes and (potential) role of placental oxidative stress in the development of placental parenchymal pathology and its clinical consequences. Also, therapeutic options aiming at prevention or treatment of hypoxia of the placenta and fetus are described. (c) 2018 The Authors. Published by Elsevier Ltd.

Cardiovascular disease (CVD) is one of the major causes of morbidity and mortality, all around the world. Vitamin E is an important nutrient influencing key cellular and molecular mechanisms as well as gene expression regulation centrally involved in the prevention of CVD. Cell culture and animal studies have focused on the identification of vitamin E regulated signaling pathways and involvement on inflammation, lipid homeostasis, and atherosclerotic plaque stability. While some of these vitamin E functions were verified in clinical trials, some of the positive effects were not translated into beneficial outcomes in epidemiological studies. In recent years, the physiological metabolites of vitamin E, including the liver derived (long- and short-chain) metabolites and phosphorylated (-, -tocopheryl phosphate) forms, have also provided novel mechanistic insight into CVD regulation that expands beyond the vitamin E precursor. It is certain that this emerging insight into the molecular and cellular action of vitamin E will help to design further studies, either in animal models or clinical trials, on the reduction of risk for CVDs. This review focuses on vitamin E-mediated preventive cardiovascular effects and discusses novel insights into the biology and mechanism of action of vitamin E metabolites in CVD. (c) 2019 IUBMB Life, 71(4):507-515, 2019

Harri Hemilä Department of Public Health, University of Helsinki, Helsinki, Finland Background: Vitamin E has influenced the immune system in laboratory studies. Dozens of animal experiments have found that vitamin E offered protection against infections caused by viruses and bacteria. Previously, significant heterogeneity was found in the effect of vitaminE supplementation on pneumonia in humans. The aim of this study was to examine how the effect of vitamin E on pneumonia risk depends on age. Methods: Secondary analysis of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention study in Finland, 1985–1993, was performed. Participants were male smokers aged 50–69 years at the baseline who started to smoke at ≥21 years (N=7,469). Intervention was 50 mg/d of vitamin E for 5–8 years. The outcome was the incidence of hospital-treated, community-acquired pneumonia by the age at the follow-up. Results: Among 2,216 participants who smoked 5–19 cigarettes per day at baseline and exercised at leisure time, vitamin E supplementation reduced the incidence of pneumonia by 69% (95% confidence interval [CI]: 43%–83%; 57 pneumonia cases). In this subgroup, vitamin E prevented pneumonia in 12.9% of participants by the age of 74 years. Among 5,253 participants who smoked ≥20 cigarettes per day at baseline or did not exercise, the incidence of pneumonia was 14% lower in the vitamin E participants (95% CI: -38% to +21%; 139 cases). One-third of the participants quit smoking for a period, of whom 27 got pneumonia. The incidence of pneumonia was 72% (95% CI: 31%–89%) lower in the vitamin E group, and this benefit was also seen among those males who smoked ≥20 cigarettes per day at baseline or did not exercise. Conclusion: Although the evidence of benefit from vitamin E against pneumonia in elderly males is strong in this analysis, the overall findings about vitamin E have been complex. Further research on vitamin E in nonsmoking elderly males is warranted. Trial registration: NCT00342992. Keywords: antioxidants, exercise, randomized controlled trial, respiratory tract infections, smoking

Berry et al. studied the between-trial variation in the effect of vitamin E on mortality in 22 trials, concluding in the abstract that “vitamin E intake is unlikely to affect mortality regardless of dose.” However, their discussion of the vitamin E literature is biased to such an extent that it does not provide a proper context for their paper. Non

We have previously found a 28% reduction in common cold incidence with 50 mg/day vitamin E supplementation in a subgroup of the Alpha-Tocopherol Beta-Carotene Cancer Prevention (ATBC) Study cohort: older city-dwelling men (or =65 years) who smoked only 5-14 cigarettes/day.To carry out more detailed analyses to explore the modification of vitamin E effect by age, smoking, and residential neighborhood.We examined the effect of vitamin E on common cold risk in subjects consisting of the placebo and vitamin E arms (n = 14,573) of the ATBC Study, which recruited males aged 50-69 years who smokedor =5 cigarettes/day at the baseline. The ATBC Study was conducted in southwestern Finland in 1985-1993; the active follow-up lasted for 4.7 years (mean). We modeled common cold risk as a function of age-at-follow-up in the vitamin E arm compared with the placebo arm using linear splines in Poisson regression.In participants of 72 years or older at follow-up, the effect of vitamin E diverged. Among those smoking 5-14 cigarettes per day at baseline and living in cities, vitamin E reduced common cold risk (RR = 0.54; 95% CI 0.37-0.80), whereas among those smoking more and living away from cities, vitamin E increased common cold risk (RR = 1.58; 1.23-2.01).Vitamin E may cause beneficial or harmful effects on health depending on various modifying factors. Accordingly, caution should be maintained in public health recommendations on vitamin E supplementation until its effects are better understood.