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The effects of selenium deficiency on differentiation, degradation, and cell lysis of L8 rat skeletal muscle cells.
Ueda, Y; Whanger, P D; Forsberg, N E.
Afiliación
  • Ueda Y; Department of Animal Sciences, Oregon State University, Corvallis 97331, USA.
Biol Trace Elem Res ; 69(1): 1-13, 1999 Jul.
Article en En | MEDLINE | ID: mdl-10383095
We investigated the effects of selenium (Se) deficiency on differentiation, protein degradation, and cell lysis in cultured skeletal muscle cells, using L8 rat skeletal muscle cells cultured in serum-free (SF) medium to induce differentiation and to maintain myotubes. Creatine kinase activity was reduced (p < 0.05) by approximately 15% without Se supplementation for 96 h. Confluent myoblasts were treated with SF media with four different levels of vitamin E (0, 10, 35, and 100 microM) in the absence and presence of Se (0 and 0.25 microM, respectively). After 96 h, vitamin E at a high dose (100 microM) was effective in the prevention of the decrease of differentiation caused by Se deficiency (p < 0.05). Following differentiation, the effects of three Se concentrations (0, 0.25, and 2.5 microM) on degradation of proteins as assessed by release of 3H-labeled free amino acids secreted into the media were studied. Selenium supplementation did not affect (p > 0.05) total protein degradation. However, Se deficiency increased (p < 0.05) lactate dehydrogenase released from lyzed dead cells. The results indicate that Se is required to maintain an optimal rate of muscle cell differentiation and health of myotube cultures.
Asunto(s)
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Selenio / Diferenciación Celular / Muerte Celular / Músculo Esquelético Límite: Animals Idioma: En Revista: Biol Trace Elem Res Año: 1999 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Selenio / Diferenciación Celular / Muerte Celular / Músculo Esquelético Límite: Animals Idioma: En Revista: Biol Trace Elem Res Año: 1999 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos