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American Journal of Physiology-Lung Cellular and Molecular Physiology , 290 , L790L796

Researchers should account for its short stability in solution and use freshly prepared aliquots [1][5]

Thus, as far as mitochondrial oxidative stress homeostasis is concerned, mGSH is a vital factor maintaining mitochondrial function, controlling cell survival/death, and its depletion causes cell damage and facilitates cell death [57, 59]

Upon activation, it inhibits the synthesis of methoxy-mycolic and keto-mycolic acids, leading to depletion of essential cell wall components and subsequent bacterial death (Lewis and Sloan, 2015