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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

Established fine lines show measurable reduction

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BSO treatment was not included, because this already induced a significant oxidative stress response (data no shown)

This interaction could hypothetically result in lower expression of genes that promote inflammation, controlled by NF-B