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As a control, normal RBCs (nRBC) were vehicle-treated and incubated under identical conditions

In addition, GSSG retained in mitochondria during oxidative stress can lead to the S-gluthionylation of target proteins with mitochondrial dysfunction (20, 21)

One possible explanation for such a response is that inhibition of mTORC1 and activation of GCN2 collectively suppresses global translation to conserve nutrients, while selective translation of mRNA such as ATF4 (mediated by increased p-eIF2) activates the expression of AARE genes to mitigate cellular stress