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Mechanistically, SLC25A39 deficiency induced mitochondrial dysfunction, characterized by excessive mitochondrial reactive oxygen species (ROS), reduced membrane potential, diminished adenosine triphosphate (ATP) synthesis, aberrant mitochondrial permeability transition pore (mPTP) opening, and cytochrome c release

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The mitochondrial glutaminase enzymes initiate glutaminolysis by catalyzing the hydrolysis of glutamine to glutamate, satisfying the metabolic requirements of aggressive cancers and thus representing potential therapeutic targets

L-PAM depleted GSH, but GSH rapidly recovered in a L-PAM-resistant MM cell line unless also treated with BSO