SOD2 again

[lansbergen]

Anybody know which med the Julia Newton group used in the muscle cell studies?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3304004/#!po=13.1944

Manganese superoxide dismutase, MnSOD and its mimics

It is important in cancer too

an early report by Oberley and Buettner showed that many tumor types have low levels of
MnSOD [25, 26], and overexpression of MnSOD was shown to suppress the tumorigenicity
of human melanoma cells, breast cancer cells, and glioma cells, suggesting that MnSOD is a
tumor suppressor gene in a wide variety of cancer

Yet, Hempel et al. have presented data that show increased levels of MnSOD in different tumor types [19]. Additional increase of MnSOD level was found during progression of a tumor to the metastatic stage in head and neck, pancreatic, gastric, colorectal brain, and oral squamous cell carcinomas. Such apparently controversial data likely arise from the differences in the redox status of the tumors explored (Figure 1). Tumorigenesis and metastasis are strongly dependent on the intrinsic levels of reactive species, as well as external factors that would increase the production of reactive species

A “normal” cell which has low levels of MnSOD is susceptible to oxidative stress, which in turn may favor its progression to a tumor cell [19] (Figure 1). Further, studies with transgenic mice expressing a luciferase reporter gene under the control of human MnSOD promoter demonstrate that the levels of MnSOD in such already transformed cell were reduced prior to the formation of cancer [13, 27]. As transformed cell proliferates, it is possible that it fights oxidative stress by upregulating MnSOD, which might result in an imbalance between the superoxide and peroxide removing enzymes, resulting in turn in increased peroxide level

Peroxide would then perpetuate oxidative stress by affecting a broad array of signaling pathways that promote malignancy and metastasis