N-acetyl-cysteine
Phosgene is chemical warfare agent. It decreases Nrf2. Dysregulation of redox status could be the way that it causes harm. N-acetyl-cysteine elevates Nrf2 and restores the antioxidant defense system. (Could this be what's happening with mold? It decreases the Nrf2 system and causes harm that way, and various Nrf2 activators can restore Nrf2?)
N-acetylcysteine attenuates phosgene-induced acute lung injury via up-regulation of Nrf2 expression.
"However, both indicators could be reversed by NAC administration, indicating that dysregulation of redox status of glutathione might be the cause of phosgene-induced ALI. The nuclear factor (NF)-E2-related factor 2 (Nrf2), which has been proven to up-regulate the expression of glutathione reductase (GR), was obviously decreased by phosgene exposure. However, NAC administration elevated Nrf2 expression significantly. In conclusion, these data provided the first evidences showing that it was the transcriptional factor Nrf2 that connected phosgene-induced ALI with GSH metabolism. NAC protected against oxidative stress through acting on this newly disclosed Nrf2/GR/GSH pathway, by which NAC elevated the biosynthesis of protective GSH to repair and reconstitute the defense system destroyed by phosgene."
Phosgene is chemical warfare agent. It decreases Nrf2. Dysregulation of redox status could be the way that it causes harm. N-acetyl-cysteine elevates Nrf2 and restores the antioxidant defense system. (Could this be what's happening with mold? It decreases the Nrf2 system and causes harm that way, and various Nrf2 activators can restore Nrf2?)
N-acetylcysteine attenuates phosgene-induced acute lung injury via up-regulation of Nrf2 expression.
"However, both indicators could be reversed by NAC administration, indicating that dysregulation of redox status of glutathione might be the cause of phosgene-induced ALI. The nuclear factor (NF)-E2-related factor 2 (Nrf2), which has been proven to up-regulate the expression of glutathione reductase (GR), was obviously decreased by phosgene exposure. However, NAC administration elevated Nrf2 expression significantly. In conclusion, these data provided the first evidences showing that it was the transcriptional factor Nrf2 that connected phosgene-induced ALI with GSH metabolism. NAC protected against oxidative stress through acting on this newly disclosed Nrf2/GR/GSH pathway, by which NAC elevated the biosynthesis of protective GSH to repair and reconstitute the defense system destroyed by phosgene."
