Multiplexed quantum sensing reveals coordinated thermomagnetic regulation of mitochondria

Mitochondria convert metabolic energy into heat and an electrochemical proton-motive force, yet how these outputs are coordinated in living cells remains poorly understood. Here we employ multiplexed nanodiamond quantum sensors containing nitrogen-vacancy centers to simultaneously monitor temperature and magnetic noise in single primary cells from adult mice. These dual-mode measurements suggest that intracellular ferric iron stores dynamically couple to thermogenesis through mitochondrial proton pumping. Pharmacological uncoupling of the proton gradient increases intracellular temperature, accompanied by a reduction in Fe³⁺-dependent magnetic noise, consistent with ferric-to-ferrous iron reduction. Conversely, genetic disruption of complex I in Ndufs4⁻/⁻ cells, which model Leigh syndrome, decreases intracellular temperature, but iron-rich splenocytes maintain thermal output, indicating iron-driven compensation. Our findings suggest an intrinsic thermomagnetic feedback mechanism linking mitochondrial bioenergetics and iron redox state, providing a new framework to understand primary mitochondrial diseases as disorders of cellular thermomagnetic homeostasis.