L-arginine administration exacerbates myocardial injury in diabetics via prooxidant and proinflammatory mechanisms along with myocardial structural disruption

Figure 4 Effect of L-arginine on the activities of serum tumor necrosis factor-alpha, interleukin-1 beta, superoxide dismutase and glutathione peroxidase, malondialdehyde, nitric oxide, in the normal and treated rat groups. A: Tumor necrosis factor-alpha; B: Interleukin-1 beta; C: Superoxide dismutase; D: Glutathione peroxidase; E: Malondialdehyde; F: Nitric oxide. G1 = Control group, G2 = Normal rats received 0.5 g/kg/day of L-arginine (L-Arg), G3 = Normal rats received 1 g/kg/day of L-Arg, G4 = Normal rats received 1.5 g/kg/day of L-Arg, G5 = Diabetic group, G6 = Diabetic rats received 0.5 g/kg/day of L-Arg, G7 = Diabetic rats received 1 g/kg/day of L-Arg, G8 = Diabetic rats received 1.5 g/kg/day of L-Arg. The data presented as means ± SE (n = 12). ^aP < 0.05 vs the control group. ^bP < 0.05 vs the diabetic group. ^cP < 0.05 vs to the diabetic + L-Arg 05 g/kg group. ^dP < 0.05 vs the diabetic + L-arg 1 g/kg group. TNF-α: Tumor necrosis factor-alpha; IL-1β: interleukin-1 beta; SOD: superoxide dismutase; GSH-Px: Glutathione peroxidase; MDA: Malondialdehyde.