Abstract
Glutathione disulfide efflux from perfused rat liver, initially observed during metabolism of externally added hydroperoxides, was studied more recently in different conditions possibly associated with changes in endogenous hydroperoxide metabolism, including drug oxidations, phenobarbital pretreatment, and selenium deficiency. While GSSG efflux was increased during oxidative transitions like drug oxidations or hydroperoxide reduction, GSH efflux remained unchanged. Further, it was found that there are distinct pathways for GSSG and GSH efflux: GSSG is released into bile, whereas GSH is released into the caval perfusate. Thus, GSSG appears to be acted upon by the biliary excretory system as the “glutathione-S-conjugate of glutathione”.
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