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This underscores the critical role of SLC25A39-mediated mitochondrial GSH import in maintaining cellular redox balance and overall mitochondrial function

Abstract Background: Iron overload cardiomyopathy (IOC) is a major co-morbidity of genetic hemochromatosis and secondary iron overload with limited therapeutic options

It has been shown that pharmacological inhibition or knockdown of a single mGSH transporter significantly sensitized neurons to oxidative and nitrosative stress (Wilkins et al., 2013)

The same reconstitution approach applies for either route, but users often dose lower or less often than the unmodified forms

Sep 2018;25(9):1046-1055