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

Table 3 Effect of a cell-permeable SOD mimetic on IgG ₁ IC-induced superoxide anion, nitric oxide, and peroxynitrite production by interferon- γ -activated macrophages

Stimulation of IFN-γ-Activated Cells	Superoxide Anion (nmol × 10⁶ cells)	Nitrites (µM)	Peroxynitrite Rhodamine (nM)
Control	0.9 ± 0.2	2.4 ± 0.5	98 ± 2.5
MnTBAP	0.3 ± 0.1	0.9 ± 0.2	45 ± 1.2
IgG₁ IC	3.1 ± 0.3	10.5 ± 1.0	208 ± 8.5
IgG₁ IC + MnTBAP	1.2 ± 0.4	18.0 ± 1.2	108 ± 2.4

Resting or interferon-γ-treated cells were challenged overnight by Bo-SOD1 IC (20 µg of anti-Bo-SOD1 and 10 µg of Bo-SOD1) IgG₁IC (20 µg/20 µg) and/or free Bo-SOD1 (10 µg/ml). After extraction of total intracellular proteins, as described in Materials and Methods, the presence of Bo-SOD1 was evaluated by specific ELISA. Data are the mean ± SD (triplicate samples) of one representative experiment out of four.

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