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However, their contribution is context-dependent, as genetic ablation of ABCC1 does not fully prevent apoptosis-associated GSH loss in certain models 43 , indicating the existence of compensatory or alternative efflux mechanisms

(n.d.-g)

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In our previous report (Ghergherehchi et al., 2019a), labeling of sensory terminals in the dorsal horn following intramuscular injection was found in only 4 of 26 cases after PEG-fusion repair

To make matters worse, chronic diseases (e.g., type 2 diabetes and heart disease ) can deplete GSH levels, making bodily cells more prone to oxidative stress, or cell damage ( 1 , 2 , 7 )

These results provide evidence that the reduction of peripheral GSH pools increases peripheral NGF circulation that orchestrates a neuroprotective response in the CNS, at least in the striatum, through the NGF/TrkA/Akt/Nrf2 pathway