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Therefore, it would be valuable to develop therapeutic strategies to break the redox homeostasis in cancer cells and activate cell death pathways to limit cancer progression

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To investigate the importance of correct GSH homeostasis for the neurotrophic capacity of NO, 2 -Tyr) protein accumulation ( Figure 1 )

This conversion process is remarkably efficient when selenium status is optimal, with approximately 80% of circulating T3 produced through peripheral deiodination rather than direct thyroid secretion