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In summary, our study demonstrates that S-allyl-L-cysteine (SAC) alleviates UC by suppressing ferroptosis and oxidative damage in colonic epithelial cells through the Keap1/Nrf2/GPX4 signaling axis-mediated regulation of glutathione (GSH) metabolism

Results Competition induced a significant increase in lipid peroxidation, nitric oxide and carbon monoxide

Standard oral glutathione shows only 0.7% bioavailability due to gastrointestinal degradation

This model also generates testable predictions

Supports collagen formation, immune function, tissue repair, and energy production via L-carnitine synthesis.* Free-Form Delivery Immediately available for absorption without requiring protein digestion