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We expect in the near future growing recognition of GSH involvement, by S -glutathionylation and/or by the thiols redox state shift, not only in the induction of ATG and/or apoptosis, but also in the modulation of activities of molecular/transcription factors such as NEF2L2, PGC1, and p53 that by inducing the antioxidant defense and assuring mitochondrial homeostasis could block both processes
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Introduction Gliotoxin, which has a molecular mass of 326 Da and is an epipolythiodioxopiperazine (ETP), contains a disulphide bridge of unknown origin and has been shown to play a significant role in enabling the virulence of Aspergillus fumigatus [1][3]
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