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Last Updated: 3 months ago

Possible Interaction: Acetylcysteine and Curcumin

supplement:

Acetylcysteine

Research Papers that Mention the Interaction

In addition, Curcumin caused oxidative stress through inducing further ROS burst, decreasing GSH, and wrecking mitochondria membrane potential (MMP), which were reversed by ROS inhibitor N-acetylcysteine (NAC).
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie  •  2017  |  View Paper
Inhibition of NFκB activity as well as suppression of ROS generation with NAC resulted in the partial relief of cells from G2/M checkpoint after curcumin treatment in wt MCF-7 cells.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie  •  2016  |  View Paper
In addition, curcumin induced ER stress by triggering ROS generation, which was supported by the finding that treating cells with the antioxidant N-acetylcystein alleviated curcumin-mediated ER stress and vacuolation-mediated death.
In addition, curcumin induced ER stress by triggering ROS generation, which was supported by the finding that treating cells with the antioxidant N-acetylcystein alleviated curcumin-mediated ER stress and vacuolation-mediated death.
We also found that the production of ROS and formation of autophagic vacuoles following curcumin treatment was almost completely blocked by each of N-acetylcystein , the mitochondrial-targeted antioxidants, MitoQ or SKQ1, the calcium chelator, BAPTA-AM, and the mitochondrial calcium uniport inhibitor, ruthenium red (Figure 1).
We also found that the production of ROS and formation of autophagic vacuoles following curcumin treatment was almost completely blocked by each of N-acetylcystein , the mitochondrial-targeted antioxidants, MitoQ or SKQ1, the calcium chelator, BAPTA-AM, and the mitochondrial calcium uniport inhibitor, ruthenium red (Figure 1).
Cell Death and Disease  •  2015  |  View Paper
However, curcumin induced ASK1-MKK4-JNK signaling was attenuated by NAC.
International journal of molecular sciences  •  2014  |  View Paper
The DNA-damaging ability of EGCG, but not curcumin , was hindered by either ascorbate or NAC , which was also shown in HT29 and SW480 colon cancer cells.
Free radical research  •  2014  |  View Paper
We have also observed that curcumin induced reactive oxygen species (ROS) production and autophagic vacuoles formation by curcumin was almost completely blocked in the presence of N-acetylcystein (NAC), an antioxidant.
Archives of oral biology  •  2012  |  View Paper
The use of the antioxidant N-acetyl cysteine prevented the induction of HO-1 by curcumin.
Molecular nutrition & food research  •  2011  |  View Paper
Coadministration of the antioxidants N-acetylcysteine and curcumin attenuated phosphamidon-induced apoptosis.
Journal of biochemical and molecular toxicology  •  2010  |  View Paper
Exogenous GSH and its precursor N-acetyl-cysteine , but not ascorbic acid (AA) or ebselen, decreased curcumin accumulation in PC3 cells and also prevented curcumin-induced DNA fragmentation.
Nutrition and cancer  •  2010  |  View Paper
The effects of curcuminoids on keratinocytes mirrored some aspects of UVB and could be inhibited by N-acetylcysteine , suggesting that these compounds activate p38 through a mechanism that involves glutathione depletion.
Experimental dermatology  •  2010  |  View Paper
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