Vitamin E, particularly in the form of alpha-tocopheryl succinate, has been investigated for its potential effects on mitochondrial health. As a lipid-soluble antioxidant, Vitamin E protects cell membranes, including those of mitochondria, from oxidative damage due to reactive oxygen species (ROS). Scientific studies, mostly in vitro and in animal models, have shown that alpha-tocopheryl succinate can reduce mitochondrial oxidative stress, protect against mitochondrial dysfunction, and even induce apoptosis in cancer cells through mitochondrial pathways. However, most of this research is preclinical and mechanistic, focusing on cellular models rather than direct clinical outcomes in humans. There is limited evidence from human studies demonstrating that alpha-tocopheryl succinate supplementation directly improves mitochondrial function or clinical outcomes related to mitochondrial health. While the antioxidant properties of Vitamin E are well documented and suggest a theoretical benefit for mitochondrial protection, the translation of these findings into validated clinical interventions remains incomplete. Therefore, the use of alpha-tocopheryl succinate for mitochondrial support is primarily justified by scientific rationale and early experimental data, but robust clinical validation is currently lacking.