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KMID : 0848119970220020097
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International Journal of Oral Biology
1997 Volume.22 No. 2 p.97 ~ p.105
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Reactive Oxygen Species Modulate Nitric Oxide-mediated Cytotoxicity in Osteoblasts
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Petros D. Damoulis
Peter V. Hauschka
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Abstract
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Nitric oxide (NO), a free radical produced enzymatically through the L-arginine/NO synthase (NOS) pathway, has been shown to cause apoptotic cell death in osteoblasts when present at high concentrations Loss of osteoblast viability could be a potentially important factor during inflammatory bone loss. Post-connuent MC3T3-E1 mouse clonal osteogenic cells were cultured under high NO conditions in the presence of reactive oxygen species (ROS) scavengers. The superoxide scavengers, superoxide dismutase (SOD) and TEMPOL, increased cytokine-mediated cytotoxicity in osteoblasts, and they dramatically enhanced SNAP-mediated cell death. On the other hand, catalase, a hydrogen peroxide scavenger.
protected the cells from cytokine whereas it showed no effect on osteoblast survival after SNAP treatment. Interestingy, catalase also abolished cytokine-induced nitrite production, possibly by inhibiting the inducible NOS. Simultaneous inhibition of NO and in cytokine-stimulated MC3T3-E1 inhibited Iytic cell death when compared to NO inhibition alone, but such treatment also increased loss of viable cells, possibly by increasing the available free NO which induced apoptosis. These results indicate that osteoblasts produce ROS which can react with nitric and implicate NO as the primary mediator
of cytokine It is suggested that the mechanism of these interactions should be further clarified so that the potential of free radical-targeted treatment of inflammatory bone diseases could be subsequently explored.
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KEYWORD
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nitric oxide, superoxide, hydrogen peroxide, osteoblasts, cell death
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