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Hydrogen peroxide (H2O2) is frequently applied to cultured cells to induce oxidative stress. The present study investigated the molecular and cellular effects of exogenous H2O2 on Calu‑6 and A549 lung cancer cells. Based on MTT assays, H2O2 inhibited the growth of Calu‑6 and A549 cells with IC50 values of ~50 and 100 µM at 24 h, respectively. Cells treated with H2O2 demonstrated a considerable G1‑phase arrest of the cell cycle. H2O2 dose‑dependently augmented the numbers of dead (trypan blue‑positive) and Annexin V‑FITC‑stained cells in these cells, which was accompanied by the reduction of Bcl‑2 and pro‑caspase‑3 levels, as well as the upregulation of caspase‑3 and ‑8 activities. In addition, H2O2 triggered the failure of mitochondrial membrane potential (MMP; ΔΨm). However, relatively higher doses of H2O2 did not raise the percentages of sub‑G1 cells in these cell lines. All the tested caspase inhibitors (Z‑VAD for pan‑caspases, Z‑DEVD for caspase‑3, Z‑IETD for caspase‑8 and Z‑LEHD for caspase‑9) decreased the percentages of sub‑G1 and Annexin V‑FITC‑stained cells in the H2O2‑treated Calu‑6 and A549 cells. However, caspase inhibitors did not significantly prevent the loss of MMP (ΔΨm) in H2O2‑treated lung cancer cells. In conclusion, H2O2 inhibited the growth of Calu‑6 and A549 lung cancer cells through cell death and G1‑phase arrest. H2O2‑induced cell death resulted from necrosis, as well as caspase‑dependent apoptosis.

Hydrogen peroxide inhibits the growth of lung cancer cells via the induction of cell death and G1‑phase arrest