The microbiome hypothesis: Lipkin's collaborative, part 1 (Simon McGrath blog)

[percyval577]

Your article, @Learner1, Ribas et al 2014 says on p.13:

• "Unlike these permeable GSH prodrugs that directly boost mGSH, strategies that aim to increase cytosol GSH (e.g. NAC) may not be an optimal approach for boosting mGSH ... as it would result in mainly increasing cytosol GSH without replenshing mGSH levels."

Clearly, the article does not provide your opininion. It doesn´t mention any glutathione supplement, intead is already sceptical enough about NAC.
(It seems to me that @Hip indeed referred to a common knowledge, and glutathione would not easily pass through the cellmembrane, as your article @Learner1 preferres to speak about NAC as an example for boosting cytosolic GSH and not about the first one that would have come to mind, GSH itself.)
Ive read now that the production of GSH (which occurs in the cytosol) is not coupled to the downstream actions (into the mt). This indicates once more that a depletion of GSH in the mitochondria will not be helped by boosting cytosolic levels, if there wouldn´t be any huge enough cytosolic GSH depletion.

The article then @mariovitali put, Shelly Lu 2013, mentions - only - in the context of sepsis a GSH "supplementation", p11:

• "Exogenous GSH treatment suppressed LPS-induced systemic inflammatory response and reduced mortality. ... This may be related to GSH´s ability to influence toll like receptor 4 (TLR4) signaling."

Summarized, the success you say to experience does not point to a depletion in the mitochondria under halfway known circumstances. Your success might indicate something (very) special:

• You would suffer from very low cytosolic GSH, and then GSH supplemtation would pass better through the cell membrane (due to moelcule gradient) (???).
• Or you are able to make choline ester of Glutathione, which would pass completly into the mitochondria (cf Angajala, Lim et al. 2018) (???).

A third (more reasonable) explanation might be that your success would have to do with toll like receptor4, which should be also and already under physiological circumstances of interest.