101342-76-1 Purity
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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.
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.
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.
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.