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FK506 affects mitochondrial protein synthesis and oxygen consumption in human cells |
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| Authors: | María Palacín Eliecer Coto Laura Llobet David Pacheu-Grau Julio Montoya Eduardo Ruiz-Pesini |
| Affiliation: | 1. Genética Molecular, Hospital Universitario Central de Asturias (HUCA), Oviedo, Spain 4. Departamento de Bioquímica Biología Molecular y Celular and Centro de Investigaciones Biomédicas En Red de Enfermedades Raras (CIBERER), Zaragoza, Spain 2. Departamento de Medicina, Universidad de Oviedo, Oviedo, Spain 3. Fundación Renal I. Alvarez de Toledo, Madrid, Spain 5. Fundación ARAID, Universidad de Zaragoza, Zaragoza, Spain 6. Departamento de Bioquímica, Biología Molecular y Celular, Universidad de Zaragoza, C/Miguel Servet, 177, 50013, Zaragoza, Spain |
| Abstract: | FK506 is an important immunosuppressive medication. However, it can provoke neurotoxicity, nephrotoxicity, and diabetes as adverse side effects. The decrease in oxygen consumption of rat cells treated with pharmacologically relevant concentrations of FK506, along with other evidences, has insinuated that some of the toxic effects are probably caused by drug-induced mitochondrial dysfunction at the level of gene expression. To confirm this suggestion, we have analyzed cell respiration and mitochondrial protein synthesis in human cell lines treated with FK506. This drug provokes an important decrease in oxygen consumption, accompanied by a slight reduction in the synthesis of mitochondria DNA-encoded proteins. These results are similar to those triggered by rapamycin, another macrolide with immunosuppressive properties, therefore insinuating a common toxic pathway. |
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