Background:: Vitamin E has antioxidant properties, which help in scavenging free radicals, thereby reducing oxidation of lipids and proteins. This study aims to evaluate the efficacy of oral vitamin E supplementation in preventing retinopathy of prematurity (ROP) in very low birth weight (VLBW) infants with respiratory distress syndrome (RDS) and decreasing oxidative stress 15 and 28 days post-intervention.

Methods:: Ninety VLBW infants were randomly assigned to two groups:

1. 1.Treatment (treatment group (T), n = 48) or
2. 2.Placebo (control group (C), n = 42).

Each group received 25 IU of vitamin E (T) or placebo (C).

Results:: The incidence of ROP in groups T and C was 12.5% (n=6) and 31% (n = 13), respectively (RR: 0.40; 95% CI: 0.10–0.96). There were no differences in mortality between groups. As expected, the vitamin E concentration was significantly increased 28 days post-intervention in group T.

Conclusion:: Oral supplementation with vitamin E may effectively prevent ROP development in VLBW infants with RDS. Oxidative damage markers were significantly lower, whereas total antioxidant capacity was increased in group T. However, levels of other antioxidants as vitamin A and C were not measured in two groups.

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Vitamin E is a major lipid-soluble antioxidant obtained exclusively from the diet. It was discovered in the 1920s as an essential dietary element required by rats for reproduction. There are approximately eight different vitamin E-related molecules, but the dominant molecule in humans is alpha-tocopherol. Tocotrienols are the other molecules that are widely studied for vitamin E supplementation. These two molecules have been studied in various dosages and for many different health purposes. Vitamin E has peroxyl radical scavenger properties. While vitamin E toxicity is associated with an increased risk of bleeding, its deficiency has been associated with neurologic diseases and anemia.

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(1) Background: the current research was conducted to investigate the potential non-antioxidant roles of vitamin E in the protection of hepatocysts from oxidative damage. (2) Methods: primary sheep hepatocytes were cultured and exposed to 200, 400, 600, or 800 μmol/L hydrogen peroxide, while their viability was assessed using a CCK-8 kit. Then, cells were treated with 400 μmol/L hydrogen peroxide following a pretreatment with 50, 100, 200, 400, and 800 μmol/L vitamin E and their intracellular ROS levels were determined by means of the DCF-DA assay. RNA-seq, verified by qRT-PCR, was conducted thereafter: non-treated control (C1); cells treated with 400 μmol/L hydrogen peroxide (C2); and C2 plus a pretreatment with 100 μmol/L vitamin E (T1). (3) Results: the 200-800 μmol/L hydrogen peroxide caused significant cell death, while 50, 100, and 200 μmol/L vitamin E pretreatment significantly improved the survival rate of hepatocytes. ROS content in the cells pretreated with vitamin E was significantly lower than that in the control group and hydrogen-peroxide-treated group, especially in those pretreated with 100 μmol/L vitamin E. The differentially expressed genes (DEGs) concerning cell death involved in apoptosis (RIPK1, TLR7, CASP8, and CASP8AP2), pyroptosis (NLRP3, IL-1β, and IRAK2), and ferroptosis (TFRC and PTGS2). The abundances of IL-1β, IRAK2, NLRP3, CASP8, CASP8AP2, RIPK1, and TLR7 were significantly increased in the C1 group and decreased in T1 group, while TFRC and PTGS2 were increased in T1 group. (4) Conclusions: oxidative stress induced by hydrogen peroxide caused cellular damage and death in sheep hepatocytes. Pretreatment with vitamin E effectively reduced intracellular ROS levels and protected the hepatocytes from cell death by regulating gene expression associated with apoptosis (RIPK1, TLR7, CASP8, and CASP8AP2) and pyroptosis (NLRP3, IL-1β, and IRAK2), but not ferroptosis (TFRC and PTGS2).

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Congenital malformations are a common adverse outcome in pregnancies complicated by pregestational obesity, although the underlying mechanisms are still unrevealed. Our aim was to study the effect of oxidative stress in obesity-induced teratogenesis. Wistar rats were fed a high-fat diet for 13 weeks, with (OE group) or without (O group) vitamin E supplementation. Then, rats were mated and sacrificed at day 11.5 of gestation. Embryos from O dams presented a 25.9 ± 3.5% rate of malformations (vs. 8.7 ± 3.4% in C rats), which was reduced in the OE group (11.5 ± 2.3%). Pregestational obesity induced hepatic protein and DNA oxidation and a decline in antioxidant enzymes. Importantly, glutathione content was also decreased, limiting the availability of this antioxidant in the embryos. Vitamin E supplementation efficiently maintained glutathione levels in the obese mothers, which could be used in their embryos to prevent oxidation-induced malformations. To test the effect of decreasing glutathione levels alone in a cell culture model of neuroepithelium, murine embryonic stem cells (ESC) were induced to form neuronal precursors and glutathione synthesis was inhibited with the gamma-glutamylcysteine synthesis inhibitor, buthionine sulfoximine (BSO). BSO inhibited the expression of Pax3, a gene required for neural tube closure that is also inhibited by oxidative stress. Taken together, our data indicate that obesity causes malformations through the depletion of maternal glutathione, thereby decreasing glutathione-dependent free radical scavenging in embryos, which can be prevented by vitamin E supplementation.

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Ferroptosis, a newly defined mode of regulated cell death caused by unbalanced lipid redox metabolism, is implicated in various tissue injuries and tumorigenesis. However, the role of ferroptosis in stem cells has not yet been investigated. Glutathione peroxidase 4 (GPX4) is a critical suppressor of lipid peroxidation and ferroptosis. Here, we study the function of GPX4 and ferroptosis in hematopoietic stem and progenitor cells (HSPCs) in mice with Gpx4 deficiency in the hematopoietic system. We find that Gpx4 deletion solely in the hematopoietic system has no significant effect on the number and function of HSPCs in mice. Notably, hematopoietic stem cells (HSCs) and hematopoietic progenitor cells lacking Gpx4 accumulated lipid peroxidation and underwent ferroptosis in vitro. α-Tocopherol, the main component of vitamin E, was shown to rescue the Gpx4-deficient HSPCs from ferroptosis in vitro. When Gpx4 knockout mice were fed a vitamin E-depleted diet, a reduced number of HSPCs and impaired function of HSCs were found. Furthermore, increased levels of lipid peroxidation and cell death indicated that HSPCs undergo ferroptosis. Collectively, we demonstrate that GPX4 and vitamin E cooperatively maintain lipid redox balance and prevent ferroptosis in HSPCs.

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Achiote (Bixa orellana) is highly appreciated as a condiment and as the main source of bixin and tocotrienols, both having antioxidant properties. To explore the possibility of maximizing the antioxidant activity of achiote seed extracts using clean methodologies, the use of sonication and green solvents were tested. Ethyl lactate, isopropyl acetate, and ethanol combined with probe sonication produced the best results, obtaining similar bixin contents but higher δ-tocotrienol contents, as well as significantly higher in vitro and in vivo antioxidant activity compared with the maceration method extract, requiring low energy and saving time and solvents. The probe-sonicated achiote extract with the highest δ-tocotrienol content was better at increasing the Caenorhabditis elegans resistance to oxidative stress than the extract obtained through maceration. This is the first report about the effect of sonication combined with green solvents on the bixin and δ-tocotrienol content in achiote seed extracts and its relevance on the in vitro and in vivo antioxidant activity.

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