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Modulation of enzymes involved in NAD + consumption and synthesis In addition to NAD + precursor-based strategies, halting of processes linked to NAD + consumption or biosynthesis represents a complementary and therapeutically appealing approach to alter or restore NAD + homeostasis in context-specific applications
R Clinical implications of slow acetylation: Increased risk of isoniazid-induced hepatotoxicity and peripheral neuropathy (tuberculosis treatment) R Increased risk of sulfonamide hypersensitivity reactions R Increased risk of aromatic amine-related bladder cancer in occupational exposure settings (dye workers, rubber industry) R Drug-induced lupus from hydralazine and procainamide occurs almost exclusively in slow acetylators R Altered caffeine metabolism (slow acetylators clear caffeine more slowly via the NAT2 pathway) R NAT1 polymorphisms are less well characterized but the slow allele NAT1*14 has been associated with increased risk of cancers from dietary aromatic amines
Thus, the role of zinc and its regulatory mechanism in CRC requires further in-depth investigation
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