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Whatever its involved mechanisms, increased robustness of human cells could account for the requirement of more mutations to generate cancers in humans than in mice [58]

The collaboration of pathways like DHODH and mitochondrial GPX4 in specific tissues, such as in neuroprotection post-injury [81], highlights the organized defense against high-dose radical stress, underscoring that pathological radical ROS levels pivot cell fate from growth to irreversible death

In the APP NL-F mouse model of -amyloidosis, increased tonic GABA tone was observed even before the development of plaques 276