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

Table 2 Comparison of the protective effect of Bo-SOD1 before and after intracellular delivery of the antioxidant enzyme to murine macrophages by Fc γ R-mediated endocytosis

Interferon-γ-Activated Cells	Superoxide Anion Production (nmol × 10⁶ cells)
Unloaded cells	0.7 ± 0.2
Unloaded cells + PMA	3.5 ± 0.5
Bo-SOD1-loaded cells	0.4 ± 0.1
Bo-SOD1-loaded cells + PMA	1.3 ± 0.2

IFN-γ-activated cells were treated or not with Bo-SOD1 IC (20 µg/ml of the anti-Bo-SOD1 Ab and 3,000 U/ml of Bo-SOD1) for 6 hr and then were washed and plated in 96-well culture plates (2 × 10⁵ cells per well) and were stimulated or not by 200 nM of PMA to trigger the production of superoxide anion that was measured, as described in Materials and Methods, by reduction of ferricytochrome c. Data represent of the mean ± SEM of three different experiments.

ISSN: 1528-3658