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Fig. 8 | Molecular Medicine

Fig. 8

From: Fc-Receptor-Mediated Intracellular Delivery of Cu/Zn-superoxide Dismutase (SOD1) Protects Against Redox-Induced Apoptosis Through a Nitric Oxide Dependent Mechanism

Fig. 8

Schematic representation of the putative mechanism of action of heterologous Cu/Zn-SOD on Fc receptor-bearing cells. Macrophages expression Fcγ receptors can trigger immune complexes to generate the concomitant production of superoxide anion (high oxygen toxicity) and of nitric oxide, which then are chemically combined to generate peroxynitrites that are principally responsible in cell degenerescence notably by affecting cell respiration and inducing cell death by apoptosis. In the present work, we demonstrate that when the triggering antigen is Bo-SOD1, the production of superoxide anion, after intracellular antigen translocation, is inhibited (low oxygen toxicity) whereas NO◦ production was maintained and in that case is protective notably by inducing the expression of protective antioxidant enzymes.

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