It is established that thymoquinone (2-isopropyl-5-methyl-1,4-benzoquinone) and 1,4-benzoquinone regulate the intracellular reactive oxygen species (ROS) production and induce the death of tumor cells by different mechanisms. It is shown that the toxic action of 1,4-benzoquinone is associated with the inhibition of electron transfer in the mitochondrial respiratory chain and with the development of cellular oxidative stress. Thymoquinone initiating a lower level of ROS production in comparison with 1,4-benzoquinone is more toxic to tumor cells. It is established that thymoquinone-induced ROS are involved in the redox signaling processes that lead to the opening of mitochondrial transition pores of high permeability and the activation of the programmed death of cells.