Sulforaphane is a naturally occurring isothiocyanate found in cruciferous vegetables, such as broccoli, and has been studied for its effects on various cellular processes, including mitochondrial function. Several preclinical studies (in vitro and animal models) have shown that sulforaphane can activate the Nrf2 pathway, a key cellular defense mechanism that upregulates the expression of antioxidant enzymes and protects against oxidative stress. Mitochondria, as the main producers of cellular energy and significant sources of reactive oxygen species (ROS), benefit from enhanced antioxidant defenses, which can reduce mitochondrial dysfunction and cellular damage.

Research indicates that sulforaphane can improve mitochondrial biogenesis (the creation of new mitochondria) and function by modulating signaling pathways associated with oxidative stress and inflammation. For example, studies have reported that sulforaphane treatment increases mitochondrial membrane potential, ATP production, and reduces mitochondrial ROS in cell culture and animal models. However, human clinical data supporting these effects are still limited, with only a few small pilot trials and indirect evidence available.

In summary, while there is robust mechanistic and preclinical evidence suggesting sulforaphane may support mitochondrial health, direct clinical validation in humans is currently modest. Therefore, the use of sulforaphane for mitochondrial support is primarily justified by scientific investigation, but the strength of evidence is moderate rather than conclusive.