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The addition of nicotinamide precursor NAM in mitochondrial respiration-impaired cells restores the lysosomal function and limits the increased proinflammatory profile

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These observations suggest that the actions of DSIP on substance P, beta-endorphin, and corticosterone are indicative of a wider array of biochemical modifications, proposing that DSIP may trigger a cascade of molecular events that may facilitate its stress-modulatory functions