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. 2010 Mar 19;298(5):H1600–H1607. doi: 10.1152/ajpheart.01108.2009

Fig. 1.

Fig. 1.

Expression of antioxidant genes (A–F), prooxidant genes (G–I), and nitric oxide synthase (NOS) isoforms (J–L) in wild-type (WT) and manganese superoxide dismutase (MnSOD)-deficient mice with or without heart failure (HF). Note that the compensatory increases in antioxidant enzymes (A–F) that occur in WT mice with HF are abolished in MnSOD-deficient mice with HF. Also, only endothelial nitric oxide synthase (eNOS) was significantly increased in WT mice with HF. Values are means ± SE; n = 7–15 mice/group. *P < 0.05. HET, MnSOD-deficient (+/−) mice; CuZnSOD, copper-zinc superoxide dismutase; ecSOD, extracellular SOD; GPx, glutathione peroxidase; Nox, NAD(P)H oxidase; iNOS, inducible NOS; nNOS, neuronal NOS; CHF, chronic HF.