Ga(III) compounds are highly promising candidates for antitumor therapy. The level of intracellular reactive oxygen species (ROS) is significantly increased after Ga(III) complex treatment, but these complexes are redox-inactive. To investigate the effects of Ga(III) complexes on ROS levels, we synthesized three bis-ligated gallium(III)–2-benzoylpyridine-thiosemicarbazone complexes and studied their antitumor mechanisms. The structures of the Ga(III) complexes were identified by X-ray single-crystal diffraction. Cytotoxicity analysis demonstrated that the ligands and gallium complexes exerted a higher antitumor activity and a lower cytotoxicity than those of normal cells. The most active complex was C3, which exhibited a better antitumor viability than its related ligands and the anticancer agent 3-AP. Thus, the Ga(III) complexes not only transmitted the iron ions but also induced intracellular Ca²⁺ release. As a result, the ROS standards in redox-active iron complexes were increased. The mechanism involved the release of Cyt C from the mitochondria which lack membrane potential, and then the activation of the caspase family proteins stimulated cell apoptosis.