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 Arsenic Trioxide

Research Papers that Mention the Interaction

Furthermore, NAC , an ROS scavenger, abrogated the effects of ATO on TFEB-dependent autophagic cell death.
Biochemical and biophysical research communications  •  2018  |  View Paper
NAC reversed cell death and molecular changes induced by ATO via restoring GSH and reducing ROS content.
International journal of oncology  •  2015  |  View Paper
The antioxidant N-acetylcysteine decreased GSK3β phosphorylation and poly(ADP-ribose) polymerase cleavage induced by 4HPR, As2O3 , and PEITC, implicating oxidative stress in these effects.
Neoplasia  •  2014  |  View Paper
Pretreatment of lung cancer cells with the antioxidant N-acetyl-cysteine markedly suppressed the cell death induced by combined treatment with TWIST1 siRNA and ATO or IR.
Biochemical and biophysical research communications  •  2014  |  View Paper
Furthermore, As2O3 (10 μM) effectively decreased the phosphorylation of Akt, which could be reversed by NAC.
Pretreatment with antioxidant N-acetylcysteine (NAC, 0.5 mM) dramatically suppressed the increases in reactive oxygen species (ROS), lipid peroxidation, ER stress, caspase cascade activity, and apoptosis in As2O3 (10 μM)-treated myoblasts.
Archives of Toxicology  •  2012  |  View Paper
NAC attenuated HPF cell death by ATO whereas vitamin C and BSO enhanced the death.
Oncology reports  •  2012  |  View Paper
Enhanced superoxide production and autophagy by ATO in siXPC cells were suppressed by co-incubation with N-acetylcysteine ( NAC).
Toxicological sciences : an official journal of the Society of Toxicology  •  2010  |  View Paper
Darinaparsin induced apoptosis in multiple myeloma cell lines in a dose-dependent manner, and the addition of N-acetylcysteine , which increases intracellular glutathione (GSH), blocked cytotoxicity of both darinaparsin and arsenic trioxide.
Molecular Cancer Therapeutics  •  2009  |  View Paper
In addition, we demonstrate that As2O3 markedly alters nuclear levels of Nrf2 and Bach1, two redox‐sensitive regulators of stress genes, and represses expression of the transcription factor EGR2 which is involved in mouse macrophage differentiation; such effects are reduced by N‐acetylcysteine.
Notably, As2O3 alters neither activity of the redox‐sensitive transcription factor Sp1 nor that of AP‐1 or NF‐κB. In contrast, N‐acetylcysteine , a potent cysteine reductive compound, significantly prevents up‐regulation of HMOX1, GCLM, and CXCL2 genes, and repression of MMP9 and CCL22 genes induced by As2O3.
Journal of cellular biochemistry  •  2009  |  View Paper
In contrast, we found that N-acetyl-cysteine , an antioxidant and glutathione precursor, completely and partially eliminated the anti-HCV activity of ATO after 24 h and 72 h of treatment, respectively.
Journal of Virology  •  2008  |  View Paper
Show More