Indium (III) induces isolated mitochondrial permeability transition by inhibiting proton influx and triggering oxidative stress.

While Indium's toxicity to organs is realized, its effects on mitochondria are still under investigation. Mitochondrial permeability transition (MPT) is widely accepted in mitochondrial dysfunction approaches and its importance in metal-induced mitochondrial degradation has been proposed. Since mitochondria are respiratory organelles, their interaction with free In is analyzed to access structural and functional changes. Spectral methods and multimode plate reader was used to detect mitochondrial swelling, membrane potential, membrane fluidity, and inner membrane permeability. Flow cytometry was employed to detect mitochondrial reactive oxygen species (ROS) generation and transmission electron microscopy to image mitochondria. And oxygen electrode was used to measure respiratory rate, microcalorimetry to monitor long-term real-time mitochondrial metabolism. In at a concentration up to 1mM induces mitochondrial swelling, membrane depolarization and inhibits the protons transportation. In-induced mitochondrial swelling and membrane depolarization is protected by MPT inhibitors and -SH protectors, but the influence on protons transportation is not protected. In addition, In is able to accelerate the ROS production and inhibit the electron transition and respiratory chain while it stimulates long-term metabolism. Our findings show that In induces MPT by inhibiting the proton channels located in the inner mitochondrial membrane and by stimulating mitochondrial oxidative stress.