Possible Interaction: Acetylcysteine and Curcumin

“Curcumin modified the cytotoxic action of etoposide in HL-60 cells through intensification of free radical production because preincubation with N-acetyl-l-cysteine (NAC) significantly reduced the cytotoxic effect of curcumin itself and a combination of two compounds.”

“In addition, curcumin induced ER stress by triggering ROS generation, which was supported by the finding that treating cells with the antioxidant NAC alleviated curcumin-mediated ER stress and vacuolation-mediated death.”

“Additionally, GSH and NAC decreased the intracellular content of curcumin.”

“Conversely, curcumin decreased intracellular glutathione and also increased the formation of reactive oxygen species (ROS) in cells, but either GSH or NAC prevented both of these effects of curcumin.”

“ Curcumin increased the expression of the phosphorylated forms of PTK, PDK1, and PKC‐δ, which was attenuated by either GSH or NAC and potentiated by BSO.”

“ROS generation by curcumin was suppressed by antioxidants such as N-acetyl-L-cysteine (NAC) and glutathione (GSH) and by scavengers of hydroxy radicals such as mannitol, but, conversely, was promoted by prooxidants such as the transition metal ions Cu(II) and Zn(II).”

“Moreover, inhibition of the production of intracellular ROS with n-acetylcysteine (NAC) improved the degree of apoptosis and pyrolysis induced by curcumin.”

“Intervention: the patient was prescribed curcumin 90 mg/day (as phospholipid complex) and dose of N-AC was increased from 600 to 1800 mg per day.”

“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).”

“Furthermore, the viability of cells treated with PPHC nanoparticles was significantly increased in the presence of N-acetyl-cysteine (NAC), which blocks Cur release through ROS inhibition.”

“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.”

“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).”