Figure 3
From: Hyperglycemia-induced diaphragm weakness is mediated by oxidative stress
Polyethylene glycol superoxide dismutase (PEG-SOD) restores hyperglycemia-induced reductions in the diaphragm force-frequency response. Data are shown for intact diaphragm strips from control (black), hyperglycemia (red), hyperglycemia + PEG-SOD (blue) and hyperglycemia + denatured (heat inactivated) PEG-SOD groups (green) obtained at two weeks after administration of citrate buffer (controls) or streptozotocin (hyperglycemia) (n = 6 animals/group). PEG-SOD and denatured PEG-SOD were administered intraperitoneally at Day 7 after the initial injection for a total duration of seven days. Administration of PEG-SOD largely restored diaphragm force generation in hyperglycemic animals to that of controls, whereas denatured PEG-SOD had no effect; recovery of diaphragm specific force with PEG-SOD was not due to normalization of glucose levels. (P ≤0.001, *control and hyperglycemic + PEG-SOD groups significantly different compared to hyperglycemia and hyperglycemia + denatured PEG-SOD groups).