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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Antioxidant defense and apoptotic effectors in ascorbic acid and beta-glycerophosphate-induced osteoblastic differentiation

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Author(s):
Chaves Neto, Antonio Hernandes [1] ; Machado, Daisy [1] ; Yano, Claudia Lumy [1] ; Ferreira, Carmen Verissima [1]
Total Authors: 4
Affiliation:
[1] State Univ Campinas UNICAMP, Inst Biol, Dept Biochem, Campinas, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: DEVELOPMENT GROWTH & DIFFERENTIATION; v. 53, n. 1, p. 88-96, JAN 2011.
Web of Science Citations: 3
Abstract

MC3T3-E1 cells grown in the presence of ascorbic acid and beta-glycerophosphate (AA/beta-GP) express alkaline phosphatase and produce an extensive collagenous extracellular matrix. Differentiated MC3T3-E1 cells are more sensitive to hydrogen peroxide-induced oxidative stress than undifferentiated cells. In this study, we compared the profile of antioxidant enzymes and molecular markers of apoptosis in undifferentiated and differentiated MC3T3-E1 cells (cell differentiation was induced by treatment with AA/beta-GP). Differentiated osteoblasts showed lower expression and activity of catalase, glutathione S-transferase and glutathione peroxidase. The total superoxide dismutase activity and the expression of Cu/Zn superoxide dismutase were also lower, while the expression of Mn superoxide dismutase was higher in differentiated osteoblasts. The level of malondialdehyde, a widely used marker for oxidative stress, was lower in the AA/beta-GP group compared with control cells, but this difference was not significant. Western blotting showed that treatment with AA/beta-GP increased the Bax/Bcl-2 ratio used as an index of cellular vulnerability to apoptosis. In addition, the activities of caspases 3, 8 and 9 and cleaved poly (ADP) ribose polymerase were significantly higher in differentiated cells. These findings provide new insights into how changes in the activities of major antioxidant enzymes and in the signaling pathways associated with apoptosis may influence the susceptibility of bone cells to oxidative stress. (AU)