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Together, these currently preliminary observations raise the possibility that redox signaling functions in interorganellar and intercellular ways between the redox factories of eukaryotic cells: mitochondria, peroxisomes and the ER

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This leads to the formation of protein clumps in dopamine neurons and nitric oxide-driven damage to vital mitochondrial components [5]

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Accordingly, in glucose-deprived conditions, tumor cells utilize mitochondria as glucose sensor by increasing mROS-dependent oxidative stress and post-translationally regulating the expression of monocarboxylate transporter 1, whose functional activity of lactate transport is dependent on pH gradient