The Journal of nutrition, 2013-05, Vol.143 (5), p.613-619
2013
Details
- Autor(en) / Beteiligte
- Titel
- Gene Expression of Endoplasmic Reticulum Resident Selenoproteins Correlates with Apoptosis in Various Muscles of Se-Deficient Chicks
- Ist Teil von
- The Journal of nutrition, 2013-05, Vol.143 (5), p.613-619
- Ort / Verlag
- Bethesda, MD: Elsevier Inc
- Erscheinungsjahr
- 2013
- Link zum Volltext
- Quelle
- Oxford Journals 2020 Medicine
- Beschreibungen/Notizen
- Dietary selenium (Se) deficiency causes muscular dystrophy in various species, but the molecular mechanism remains unclear. Our objectives were to investigate: 1) if dietary Se deficiency induced different amounts of oxidative stress, lipid peroxidation, and cell apoptosis in 3 skeletal muscles; and 2) if the distribution and expression of 4 endoplasmic reticulum (ER) resident selenoprotein genes (Sepn1, Selk, Sels, and Selt) were related to oxidative damages in these muscles. Two groups of day-old layer chicks (n = 60/group) were fed a corn-soy basal diet (33 μg Se/kg; produced in the Se-deficient area of Heilongjiang, China) or the diet supplemented with Se (as sodium selenite) at 0.15 mg/kg for 55 d. Dietary Se deficiency resulted in accelerated (P < 0.05) cell apoptosis that was associated with decreased glutathione peroxidase activity and elevated lipid peroxidation in these muscles. All these responses were stronger in the pectoral muscle than in the thigh and wing muscles (P < 0.05). Relative distribution of the 4 ER resident selenoprotein gene mRNA amounts and their responses to dietary Se deficiency were consistent with the resultant oxidative stress and cell apoptosis in the 3 muscles. Expression of Sepn1,Sels, and Selt in these muscles was correlated with (r > 0.72; P < 0.05) that of Sepsecs encoding a key enzyme for biosynthesis of selenocysteine (selenocysteinyl-tRNA synthase). In conclusion, the pectoral muscle demonstrated unique expression patterns of the ER resident selenoprotein genes and GPx activity, along with elevated susceptibility to oxidative cell death, compared with the other skeletal muscles. These features might help explain why it is a primary target of Se deficiency diseases in chicks.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0022-3166, 1541-6100eISSN: 1541-6100DOI: 10.3945/jn.112.172395Titel-ID: cdi_swepub_primary_oai_prod_swepub_kib_ki_se_126654074
- Format
- –
- Schlagworte
- Amino Acyl-tRNA Synthetases - metabolism, Animals, Apoptosis, B-cell lymphoma 2, Bax, Bcl2, Bcl2-associated X protein, Biological and medical sciences, Chickens, Deficiency Diseases - metabolism, Dietary Supplements, Disease Models, Animal, endoplasmic reticulum, Endoplasmic Reticulum - genetics, Endoplasmic Reticulum - metabolism, exudative diathesis, Feeding. Feeding behavior, Fundamental and applied biological sciences. Psychology, Gene Expression, glutathione peroxidase, Glutathione Peroxidase - metabolism, GPx, Lipid Peroxidation, malondialdehyde, MDA, Medicin och hälsovetenskap, Muscle Proteins - genetics, Muscle Proteins - metabolism, Muscle, Skeletal - metabolism, Oxidative Stress, p53, RNA, Messenger - metabolism, RNA, Transfer, Amino Acyl - metabolism, Se, Se-adequate, Se-deficient, Selenium - deficiency, Selenium - metabolism, Selenium - pharmacology, Selenocysteine - biosynthesis, Selenoproteins - genetics, Selenoproteins - metabolism, TdT-mediated dUTP nick end labeling, Trace Elements - deficiency, Trace Elements - metabolism, Trace Elements - pharmacology, tumor protein 53, TUNEL, Vertebrates: anatomy and physiology, studies on body, several organs or systems