Banner
Structure

Vitamin E (technical grade)

CAS
10191-41-0
Catalog Number
ACM10191410-6
Category
Promotional Products

If you have any other questions or need other size, please get a quote.

  • Product Description
  • Case Study
  • Custom Reviews
  • Custom Q&A
  • Synthetic Use
  • Related Resources

Specification

Synonyms
DL-α-Tocopherol

Vitamin E for the Amelioration of Intestinal Injury Under Ammonia-Nitrogen and Hypoxia Co-Exposure in Grass Carp

Vitamin E alleviates ammonia‑nitrogen and hypoxia co-exposure-induced intestinal damage in grass carp (Ctenopharyngodon idella) by modulating mitochondrial function, cellular autophagy and apoptosis Su R, et al. Aquaculture, 2025, 742868.

In a controlled 9-week feeding trial, the effects of DL-α-tocopherol acetate (Vitamin E) supplementation were evaluated on mitigating intestinal injury in Ctenopharyngodon idella subjected to environmental stressors. Grass carp were fed diets supplemented with graded levels of Vitamin E (5.44-230.12 mg/kg diet), followed by a 10-day co-exposure to ammonia-nitrogen and hypoxia. Each treatment group comprised nine fish. Histological analyses revealed that Vitamin E significantly preserved intestinal fold architecture and reduced mitochondrial damage. Western blotting and RT-qPCR demonstrated Vitamin E-induced upregulation of mitochondrial respiratory complex I-V subunits and mitochondrial biogenesis genes (e.g., ppargc1α, nrf1, tfam) as well as fusion markers (mfn1, opa1). Conversely, mitophagy and mitochondrial fission-related proteins (e.g., Pink1, Parkin, drp1) were downregulated. Vitamin E also attenuated autophagic activity by suppressing lc3, atg5, becn1, and increased anti-apoptotic bcl2 expression while lowering casp3, bax, and Lc3 protein levels. These findings confirm the role of DL-α-tocopherol acetate as a potent modulator of mitochondrial integrity and stress-induced autophagy/apoptosis in aquaculture species, showcasing its practical application in oxidative stress management under aquatic environmental challenges.

Enhancing Broiler Performance under Heat Stress: Experimental Application of Vitamin E with Hydroxy-Selenomethionine

The use of different selenium sources and vitamin e levels as a strategy to support the performance of broilers raised in a hot climate Lima M R, et al. Poultry Science, 2025, 104(9), 105350.

In a controlled factorial study assessing antioxidant strategies for poultry raised in tropical climates, Vitamin E was investigated alongside two selenium sources-sodium selenite (SS) and hydroxy-selenomethionine (OH-SeMet)-to evaluate their synergistic effect on broiler growth and oxidative resilience. A total of 800 male broiler chickens were allocated to four dietary treatments in a 2 × 2 factorial design, varying in selenium source (SS or OH-SeMet) and Vitamin E inclusion level (standard or reduced). Birds were monitored over a 44-day period, with feed conversion ratio (FCR), weight gain, and feed intake recorded.
Results demonstrated that OH-SeMet significantly enhanced growth performance and feed efficiency, outperforming SS across Vitamin E levels. While reduced Vitamin E compromised early-stage growth, it did not affect cumulative performance, suggesting partial compensatory effects. Notably, the optimal FCR was achieved in the group receiving OH-SeMet combined with standard Vitamin E, indicating a potent interaction between these antioxidants under heat-induced oxidative stress.

Vitamin E for Modulating Macrophage Polarization in LPS-Induced Acute Lung Injury: Experimental Application and Mechanistic Insights

Vitamin E exerts a mitigating effect on LPS-induced acute lung injury by regulating macrophage polarization through the AMPK/NRF2/NF-κB pathway Pan J, et al. International Immunopharmacology, 2025, 159, 114893.

Acute lung injury (ALI), triggered by lipopolysaccharide (LPS), involves excessive inflammatory responses mediated by macrophage polarization imbalance. This study employed Vitamin E as a therapeutic agent to evaluate its effect on ALI in a murine model. ALI was induced by intratracheal instillation of LPS, followed by Vitamin E administration. Lung injury was assessed by measuring lung wet/dry weight ratios and analyzing bronchoalveolar lavage fluid (BALF) for pro-inflammatory cytokines. Bone marrow-derived macrophages (BMDMs) were isolated for in vitro studies to elucidate macrophage polarization dynamics under Vitamin E treatment.
Vitamin E significantly decreased lung edema and inflammatory markers, indicating mitigation of ALI. Mechanistically, Vitamin E activated the AMP-activated protein kinase (AMPK) pathway and upregulated nuclear factor erythroid 2-related factor 2 (NRF2), enhancing reactive oxygen species (ROS) scavenging. This activation concurrently inhibited nuclear factor kappa B (NF-κB) signaling, shifting macrophage polarization from the pro-inflammatory M1 phenotype toward the anti-inflammatory M2 phenotype.

Vitamin E Supplementation for Enhancing Antioxidant Defense and Immune Response in Scylla paramamosain

Vitamin E inhibits inflammation and improves immune response of mud crabs (Scylla paramamosain) by activating an antioxidant enzyme system and apoptosis mechanism Li X, et al. Animal Nutrition, 2025.

A controlled 8-week feeding trial was conducted to investigate the experimental application of Vitamin E in modulating antioxidant and immune responses in Scylla paramamosain. Six diets containing increasing concentrations of dietary Vitamin E (9.65 to 199.00 mg/kg) were formulated and administered to 180 juvenile mud crabs (initial weight: 24.16 ± 1.08 g). Experimental endpoints included growth performance, antioxidant enzyme activity, immune gene expression, and apoptosis regulation. Crabs receiving 76.30 mg/kg Vitamin E exhibited superior growth parameters-final weight, percent weight gain, and specific growth rate (P < 0.01). Antioxidant biomarkers such as total antioxidant capacity and SOD in hemolymph peaked at this dosage. Additionally, POD and α-tocopherol transfer protein were significantly elevated at 102.00 mg/kg. Gene expression analysis revealed significant upregulation of cat, gpx, prx, and CytMn-sod, along with downregulation of pro-inflammatory (il-16, litaf, rab6a, relish) and pro-apoptotic (bax, bok) genes. Conversely, anti-inflammatory (tgf) and anti-apoptotic (pi3k, akt, bcl-2) genes were upregulated. The optimal Vitamin E requirement was estimated at 99.13 mg/kg via quadratic regression based on percent weight gain.

Alfa Chemistry

For product inquiries, please use our online system or send an email to .

Alfa Chemistry
Shopping basket
×
Download
Verification code
* I hereby give my consent that I may receive marketing e-mails with information on existing and new services from this company. I know that I can opt-out from receiving such e-mails at any time or by using the link which will be provided in each marketing e-mail.