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Decreased GSH content in the apical fluid in cystic fibrosis could be the result of abnormal GSH transport associated with a defective cystic fibrosis transmembrane conductance regulator as mentioned previously (126)

[1] It is a process through which, after prolonged agonist exposure, the receptor is uncoupled from its signaling cascade and thus the cellular effect of receptor activation is attenuated

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They are associated with oxidative stress, even though the causes differ

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