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Last Updated: 3 years ago

Possible Interaction: Acetylcysteine and Epigallocatechin Gallate

Research Papers that Mention the Interaction

Addition of 2 mM NAC increased the stability of EGCG in the presence of CL13 cells (t 1/2=8.5 h vs 22.7 h).
Intracellular levels of EGCG were increased 5.5-fold by the addition of 2 mM NAC.
The combination of NAC and EGCG caused an 8.8-fold increase in apoptosis in CL13 mouse lung cancer cells compared to treatment with either agent alone.
The present results show that under cell culture conditions, EGCG and NAC interact to form a previously unreported adduct, EGCG-2'-NAC, which may contribute to enhancement of EGCG-mediated cell killing.
We found that NAC (0-2 mM) dose dependently enhanced the growth inhibitory activity of EGCG against murine and human lung cancer cells.
Free radical biology & medicine  •  2008  |  View Paper
NAC could partially reverse the effects of EGCG in PEL cells.
Toxicology in vitro : an international journal published in association with BIBRA  •  2019  |  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.
Thus, these findings suggest that ascorbate and NAC interfere with the ability of EGCG , but not curcumin, to kill HCT116 cells.
Free radical research  •  2014  |  View Paper
The apoptotic effect of EGCG and the p38 activation were blocked by pretreatment of cells with the ROS scavenger N-acetylcysteine.
The Journal of nutritional biochemistry  •  2013  |  View Paper
Additionally, EGCG also inhibited TGF-β-stimulated gel contraction similar to other antioxidants DPI and NAC , but not SOD or catalase.
Rheumatology  •  2010  |  View Paper
EGCG induced an intracellular increase in reactive oxygen species and GSSG, both of which were also inhibited by NAC , and the decreased synthesis of glutathione rendered the cell susceptible to EGCG-induced apoptosis.
N -Acetyl-L-cysteine NAC ) almost completely abolished apoptosis induced by EGCG under conditions in which the apoptosis induced by VP16 or TNF was not affected.
The JNK/p38 activation by EGCG was also potently inhibited by NAC , whereas those by VP16 and TNF were either not or only minimally affected by NAC.
The Biochemical journal  •  2002  |  View Paper
Three anticancer drugs (tamoxifen, sulindac, doxorubicin), two metals (CuCl2, FeCl3) and two antioxidants (sodium ascorbate, tiopronin) did not significantly affect the cytotoxic activity of EGCG, Catalase and N-acetyl-L-cysteine only marginally reduced the cytotoxic activity of EGCG.
Anticancer research  •  1999  |  View Paper
The antioxidants N‐acetylcysteine and cell‐permeable catalase abolished this preventive effect of GTPP and EGCG , suggesting the involvement of sublethal levels of H2O2 in this process.
Journal of neurochemistry  •  2015  |  View Paper
Moreover, EGCG showed inhibition of ROS production in NB4 cells in the presence of N-acetyl-L-cysteine (NAC), as well as a partial blockage of neutrophil differentiation and apoptosis, indicating that EGCG-activities involve/or are in response of oxidative stress.
Scientific reports  •  2021  |  View Paper
The antioxidant N-acetyl-cysteine and alpha-lipoic acid also suppressed the effects of EGCG.
Cell Biology and Toxicology  •  2009  |  View Paper