Docetaxel (DOCX) kills tumor cells through the formation of microtubules, calcium ion influx, apoptosis, and inflammation. However, DOCX has adverse effect on normal tissues through the production of reactive oxygen species (ROS), despite the adverse effect was inhibited by antioxidants. We investigated the protective role of selenium against DOCX-induced apoptosis and mitochondrial oxidative injury in laryngotracheal epithelial (LARYN) cells of mice. Thirty-two mice were divided into four groups (n = 8). The first group was used as a control. The second and third groups were treated with sodium selenite (Na-Sel) and DOCX, respectively. The fourth group was the combined group of Na-Sel and DOCX. At the end of the experiment, LARYN mucosa and cells were obtained from the mice. In the LARYN cells, the cell viability level was low in DOCX group, although glutathione peroxidase activity and cell viability level were increased by the treatment of Na-Sel. Increased lipid peroxidation, intracellular ROS, mitochondrial membrane depolarization, cell death levels, TNF-alpha, IL-1 beta, IL-6, caspase -3, and -9 activities in the DOCX group of LARYN cells were diminished by the treatment of Na-Sel. In conclusion, DOCX increased mitochondrial ROS, cell death, and inflammation in the LARYN cells, although the increase was reduced in the cells by Na-Sel treatment. DOCX-induced adverse oxidant, inflammatory, and apoptotic effects in the tissue might be reduced by the Na-Sel treatment.