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Under oxidative stress, excessive ROS such as OH directly attack DNA, causing single-strand or double-strand breaks, activating PARP-1, consuming NAD and ATP, and generating poly(ADP-ribose), resulting in mitochondrial membrane potential loss and the release of apoptosis-inducing factor, ultimately resulting in cell death [252]

Researchers track this mechanism to evaluate its downstream impact on limiting postprandial glucose spikes in metabolic disease models

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Diabetes Care, 29 (11), 23652370