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Inflammatory bowel disease (IBD) is associated with the production of reactive species that target cysteine redox switches in proteins, thereby affecting gene regulation, DNA damage, ion transport, intermediary metabolism, and mitochondrial function. Precursors of reactive species are derived from organic and inorganic compounds and their cofactors, including amino acids, vitamins, oxygen, nitrite, and sulfate. Nutrition and the gut microbiome fuel this process to a significant extent. The production of reactive species in IBD is reflected by a reduction in systemic free thiols, the major components of the antioxidant machinery. Systemic free thiols are amenable to nutritional or therapeutic intervention. This opens up future avenues for therapeutic modulation of redox status in IBD.
Bourgonje et al. (Tue,) studied this question.