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A number of clinically and experimentally utilized chemotherapeutic drugs, including the cytostatic agent BCNU, gold and platinum complexes, and compounds acting at the dimer-interface have already been shown to inhibit TrxR1 effectively 2,3,7

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In addition, the cycle can produce NADPH through the activity of isozymes that reside either in the mitochondria (isocitrate dehydrogenase [IDH] 2) or in the cytosol (IDH1 and malic enzyme/ME1) (Rydstrom, 2006)