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In addition, the expression levels of antiapoptotic Bcl-2 and caspase-8 decreased, whereas expression levels of BAK, BAX, BID, and caspase-3 were significantly increased in both A549 and L132 cells, suggesting gliotxin induce the apoptosis of A459 and L132 cells via the activation of caspases and the Bax pathway, also implicating mitochondrial damage [47]

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Interestingly, there is also evidence that supports that Grx2 may also use TR as an electron donor to reduce the GSSG mitochondrial pool especially in times of GSH deficiency or mitochondrial dysfunction [26, 35]