1. george george New Zealand says:

    http://www.ncbi.nlm.nih.gov/pubmed/12555134
    Wang et al. are able to explain the b-crystallin effect in cardiomyopathy satisfactorily without involving reduced glutathione. Elevated GSH may just be a side effect of excessive desmin; the cell's effort to compensate, perhaps, or a harmless side effect. The fact that Benjamin et al. found that enzymes (including GPx) were elevated suggests the former. I don't understand why Benjamin ignores desmin. If you factor it in, it can explain everything. The cell makes more GSH because it is already struggling; and the upregulation of GPx and glutathione reductase means that there is lots of oxidised GSSG there as well - which makes nonsense of the reductive stress claim if you think about it. In any case, any role of GSH in heart disease is irrelevant to people lacking the b-crystallin, desmin mutation. To me Benjamin's experiment (as reported here and in the abstract) does not prove his thesis, even on its own terms.

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