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The proposed mechanism for the cause of favism is that these new compounds then undergo redox cycling and in the process deplete reduced glutathione, leading to the formation of free radicals and hydrogen peroxide that damage red blood cells in individuals deficient in G6PD

Metalloproteinase 3 (MMP3), MMP10, and MMP12 degrade the recombinant factor VIII, resulting in protein heterogeneity, denaturation, and attenuation of protein function 8

Larson AN, Ledonio CG, Brearley AM, Sucato DJ, Carreon LY, Crawford AH, et al

47 , 8596 (2015b)

However, few of these research are genuinely integrative

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