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Reactive oxygen species induce apoptosis of synoviocytes in vitro. Alpha-tocopherol provides no protection.
Galleron, S; Borderie, D; Ponteziere, C; Lemarechal, H; Jambou, M; Roch-Arveiller, M; Ekindjian, O G; Cals, M J.
Afiliación
  • Galleron S; Laboratoire de Biochimie, Hôpital Cochin, Paris, France.
Cell Biol Int ; 23(9): 637-42, 1999.
Article en En | MEDLINE | ID: mdl-10728575
Reactive oxygen species (ROS) are released during the inflammation of the synovial membrane associated with cartilage degradation in osteoarthritis. In this work, we exposed synoviocytes to superoxide anions at concentrations that may cause either apoptosis or necrosis. We studied membrane organization, dehydrogenase mitochondrial activity and nuclear morphology and integrity, to determine the nature of the death process initiated by superoxide anions and tried to counteract ROS effects with alpha-tocopherol. We found that oxidative stress caused synoviocytes to undergo a process of cell death of an apoptotic nature rather than necrotic. Mitochondrial injury occurred at an early stage, and the FITC-annexin-V-positive/propidium iodide-positive cells occurred later than the metabolic changes. DNA strand breaks were evident at 8 h and nuclear condensation at 24 h. No LDH activity was detected in culture supernatants. In our experimental conditions, alpha-tocopherol had little effect on stress damage; the antioxidant properties of this molecule did not affect the apoptosis caused by superoxide anions.
Asunto(s)
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Membrana Sinovial / Vitamina E / Especies Reactivas de Oxígeno / Apoptosis / Superóxidos Límite: Humans Idioma: En Revista: Cell Biol Int Año: 1999 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Reino Unido
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Membrana Sinovial / Vitamina E / Especies Reactivas de Oxígeno / Apoptosis / Superóxidos Límite: Humans Idioma: En Revista: Cell Biol Int Año: 1999 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Reino Unido