Conditions associated with selenium (Se) and/or vitamin E (VitE) deficiency are still being reported in high-yielding pigs fed the recommended amounts. Here, the dietary effects of Se source (sodium selenite, NaSe, 0.40 or 0.65 mg Se/kg; L-selenomethionine, SeMet, 0.19 or 0.44 mg Se/kg; a NaSe-SeMet mixture, SeMix, 0.44-0.46 mg Se/kg) and VitE concentration (27, 50-53 or 101 mg/kg) on the antioxidant status of finisher pigs were compared with those in pigs fed non-Se-supplemented diets (0.08-0.09 mg Se/kg). Compared to NaSe-enriched diets, SeMet-supplemented diets resulted in significantly (p < 0.0018) higher plasma concentrations of total Se (14-27%) and selenospecies (GPx3, SelP, SeAlb; 7-83%), significantly increased the total Se accumulation in skeletal muscles, myocardium, liver and brain (10-650%), and enhanced the VitE levels in plasma (15-74%) and tissues (8-33%) by the end of the 80-day trial, proving better Se distribution and retention in pigs fed organic Se. Injecting lipopolysaccharide (LPS) intravenously half-way into the trial provoked a pyrogenic response in the pigs followed by a rapid increase of inorganic Se after 5-12 h, a drastic drop of SeMet levels between 12 and 24 h that recovered by 48 h, and a small increase of SeCys by 24-48 h, together with a gradual rise of GPx3, SelP and SeAlb in plasma up to 48 h. These changes in Se speciation in plasma were particularly significant (0.0024 > p > 0.00007) in pigs receiving SeMet- (0.44 mg Se/kg, above EU-legislated limits) or SeMix-supplemented (SeMet and NaSe both at 0.2 mg Se/kg, within EU-legislated limits) diets, which demonstrates Se metabolism upregulation to counteract the LPS-induced oxidative stress and a strengthened antioxidant capacity in these pigs. Overall, a Se source combination (without exceeding EU-legislated limits) and sufficient VitE supplementation (≥ 50 mg/kg) improved the pigs' antioxidant status, while doubling the allowed dietary organic Se increased the Se in tissues up to sixfold without compromising the animal's health due to toxicity. This study renders valuable results for revising the current dietary SeMet limits in swine rations.
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http://dx.doi.org/10.1007/s12011-022-03516-9 | DOI Listing |
Tissue Cell
January 2025
Department of Biology, Universidade Estadual Paulista (UNESP), São Paulo, Brazil; Campus de Três Lagoas, Universidade Federal de Mato Grosso do Sul (CPTL/UFMS), Mato Grosso do Sul, Brazil. Electronic address:
Sickle cell disease (SCD) is a hereditary hemolytic anemia associated with the alteration of the membrane composition of the sickle erythrocytes, the loss of glycolysis, dysregulation of the pyruvate phosphatase pathway, and changes in nucleotide metabolism of the sickle red blood cell (RBC). This review provides a comprehensive overview of the impact of the presence of Hb S, which leads to the disruption of the normal RBC metabolism. The intricate interplay between the redox and energetic balance in erythrocytic cells, where the glycolysis, pentose phosphate pathway, and methemoglobin reductase pathways are all altered in sickle RBC, is a key focus.
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Department of Biomedical sciences, Oklahoma State University Centre for Health and Science, Oklahoma, USA.
The effect of the aqueous extract of (AAI) on gentamicin (GEN)-induced kidney injury was investigated. The study involves 20 adult male Wistar rats (housed in four separate plastic cages) such that graded dosages of AAI were administered to the experimental group for 14 days per oral (PO) before exposure to GEN toxicity (100 mg/kg) for 1 week. At the end of the study, comparisons of some markers of renal functions, antioxidant status, and inflammatory and apoptotic markers were made between the control, GEN, and AAI-pretreated groups at < .
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Department of Zoology, Faculty of Science, Menoufia University, Shebin El-Kom, Egypt.
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Department of Evaluation of Natural Resources, Environmental Studies and Research Institute, University of Sadat City, Egypt.
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Department of Nutrition and Dietetics, University of Thessaly, Trikala, Argonafton 1, 42132 Trikala, Greece. Electronic address:
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