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In particular, this latter product has been identified in cells treated with busulfan and is a chemically stable structural analogue of glutathione disulfide, of which it does not have the reducible disulfide bond but retains the structural motifs for recognition by the glutathione disulfide-binding site of the enzyme

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TNBC currently lacks effective targeted treatment, usually based on chemotherapy, with a poor prognosis

It has been shown that decreased levels of GSH will stimulate production of TGF F- and that when GSH is replenished, the production of TGF- will be decreased [56]

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