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NNMT inhibition reduces consumption of nicotinamide (and of S-adenosylmethionine) by blocking the enzyme that would otherwise methylate them

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In gene expression profiling, GHK-Cu treatment of human fibroblasts upregulated superoxide dismutase (SOD1, SOD2, SOD3) and glutathione-related genes while suppressing NF-kB-driven inflammatory signaling [3]

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The increased oxygen consumption leads to a higher generation of superoxide radicals that require neutralization (548)