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Together, these observations lead to the conclusion that the formation of NAPQI by Cyp2E1 and the formation of protein adducts, especially on mitochondria, are initiating events leading to mitochondrial dysfunction and mitochondrial oxidant stress (Fig

in a study conducted using fat-free breast milk, supporting the presence of nocturnal increases [54, 55]

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In view of this, a more complex definition of oxidative stress, based on the disruption of redox signaling has been proposed (Jones 2006)

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