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Table 5 Role of nitric oxide in the control of the anti-oxidant armature in interferon- γ -treated macrophages stimulated by SOD1 IC

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

Interferon-γ-Treated Cells+

Mn-SOD

Glutathion Peroxidase (U/mg/protein)

Catalase

Glutathion nmoles/106 Cells

None

75 ± 2

9.3 ± 1

870 ± 31

22 ± 3

L-NAME

7 ± 1

9.1 ± 2

520 ± 15

15 ± 2

SOD1

12 ± 2

8.4 ± 1

695 ± 25

19 ± 1

SOD1 IC

212 ± 1

15.5 ± 2

920 ± 15

30 ± 3

SOD1 IC + L-NAME

85 ± 2

29.0 ± 2

1025 ± 30

55 ± 4

  1. Interferon-γ-treated cells (2 X 106 cells/ml) were challenged overnight by Bo-SOD1 IC (20 µg of anti-Bo-SOD1 and 10 µg of Bo-SOD1) and/or of 1 mM L-NAME. After extraction of total intracellular proteins, antioxidant enzymes activities and glutathion measurements were done as described in Materials and Methods. Data are the mean ± SD (triplicate samples) of one representative experiment out of four.