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Thus, disruption of mitochondrial iron homeostasis may amplify oxidative injury to mitochondrial proteins, lipids, and DNA, compromise ATP generation, and ultimately trigger energy stress that converges on ferroptotic cell death

During high-light stress, mitochondria facilitate the re-oxidation of excess reducing equivalents produced in plastids, thereby preventing over-reduction of the plastidic electron transport chain and limiting ROS overproduction

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The gene transcription factor cyclic AMP-responsive element binding protein: role in positive and negative affective states of alcohol addiction