The effects of MAPK inhibitors on pyrogallol-treated Calu-6 lung cancer cells in relation to cell growth, reactive oxygen species and glutathione

Pyrogallol (PG) as a polyphenol compound can generate superoxide anion (O₂^{{radical dot} -}). Here, we investigated the effects of PG and/or MAPK inhibitors on Calu-6 lung cells in relation to cell growth, cell death, reactive oxygen species (ROS) and GSH levels. PG inhibited the growth of Calu-6 cells and induced apoptosis, which was accompanied by the loss of mitochondrial membrane potential (MMP; ΔΨ_m). While general ROS were decreased in PG-treated Calu-6 cells at 72 h, intracellular O₂^{{radical dot} -} level including mitochondrial O₂^{{radical dot} -} was increased. PG also increased GSH depleted cell number in Calu-6 cells. MEK inhibitor slightly prevented cell growth inhibition, cell death and GSH depletion by PG. JNK inhibitor did not affect cell growth, cell death, MMP (ΔΨ_m) loss, ROS level and GSH deletion in PG-treated Calu-6 cells but p38 inhibitor mildly enhanced MMP (ΔΨ_m) loss, O₂^{{radical dot} -} level and GSH depletion in these cells. Conclusively, MEK inhibitor slightly prevented growth inhibition and death in PG-treated Calu-6 cells. Growth inhibition and death in Calu-6 cells by PG and/or MAPK inhibitors were partially related to O₂^{{radical dot} -} level and GSH content changes.