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 (O(2)(-)). 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; DeltaPsi(m)). While general ROS were decreased in PG-treated Calu-6 cells at 72h, intracellular O(2)(-) level including mitochondrial O(2)(-) 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 (DeltaPsi(m)) loss, ROS level and GSH deletion in PG-treated Calu-6 cells but p38 inhibitor mildly enhanced MMP (DeltaPsi(m)) loss, O(2)(-) 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 O(2)(-) level and GSH content changes. Copyright 2009 Elsevier Ltd. All rights reserved.