Allen Institute for Artificial Intelligence
supp.ai logo
supp.ai

Discover Supplement-Drug Interactions

Disclaimer: The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The tool is not a substitute for the care provided… (more)
Last Updated: 2 years ago

Possible Interaction: Acetylcysteine and Ammonium Tetrathiomolybdate

Research Papers that Mention the Interaction

Notably, treatment with the antioxidant N-acetyl cysteine (NAC) significantly reduced upregulation of the DNA damage marker γH2AX, subsequent ATM activation, and cell death.
Cancer research  •  2016  |  View Paper
In addition, NAC suppresses carcinogenesis-associated biological markers in Atm deficient mice, such as DNA deletions and oxidative DNA damage (R. Reliene, E. Fischer, R.H. Schiestl, Effect of N-acetyl cysteine on oxidative DNA damage and the frequency of DNA deletions in atm-deficient mice, Cancer Res.
In this study, NAC significantly increased the lifespan and reduced both the incidence and multiplicity of lymphoma in Atm deficient mice.
DNA repair  •  2006  |  View Paper
Antioxidant NAC alleviated NaAsO2-induced ATM phosphorylation, cell cycle arrest, and subsequent stemness enhancement and chemoresistance in both DU145 and PC-3 cells.
Ecotoxicology and environmental safety  •  2020  |  View Paper
The antioxidant N-acetylcysteine reduced the expression of phosphorylated ATM and H2AX, and the ATM inhibitor, caffeine, inhibited p53 activation.
The Journal of toxicological sciences  •  2019  |  View Paper
Bortezomib caused an increase in intracellular reactive oxygen species (ROS) and treatment with the ROS scavenger NAC inhibited phosphorylation of ATM leading to a decrease in the number of cells in G2-M phase.
International journal of oncology  •  2012  |  View Paper
N-acetylcysteine (NAC), an antioxidant, suppressed the phosphorylation of ATM and p53 and, to a less extent, Chk2, but NAC increased the phosphorylation and nuclear foci formation of H2AX.
Biochimica et biophysica acta  •  2014  |  View Paper
Pre-treatment with ATM inhibitor (2-aminopurine) and antioxidant ( N-acetylcysteine ) significantly blocked the cellular senescence of BECs induced by oxidative stress or inflammatory cytokines.
Free radical research  •  2008  |  View Paper