“Detoxification” is mainly liver plus renal/biliary excretion using these:

Glutathione (GSH)

  1. N-acetylcysteine (NAC)
  2. Cysteine
  3. Glycine
  4. Glutamate
  5. Methionine
  6. S-adenosylmethionine (SAMe)
  7. Serine
  8. Taurine
  9. UDP-glucuronic acid
  10. Glucuronic acid
  11. Sulfate
  12. Sulfur-containing amino acids
  13. Vitamin B2 (riboflavin)
  14. Vitamin B3 (niacin)
  15. Vitamin B6 (pyridoxal phosphate)
  16. Vitamin B9 (folate)
  17. Vitamin B12 (cobalamin)
  18. Vitamin C (ascorbate)
  19. Vitamin E (tocopherols)
  20. Selenium
  21. Zinc
  22. Magnesium
  23. Molybdenum
  24. Alpha-lipoic acid
  25. Coenzyme Q10
  26. NADPH
  27. Flavin adenine dinucleotide (FAD)
  28. Flavin mononucleotide (FMN)
  29. Heme iron-containing cytochrome P450 enzymes

More science: major detox pathways

Phase I

  • Oxidation
  • Reduction
  • Hydrolysis
  • Mainly catalyzed by cytochrome P450 enzymes
  • Often makes compounds more reactive, so Phase II is important afterward

Phase II

  • Glutathionation
  • Glucuronidation
  • Sulfation
  • Acetylation
  • Methylation
  • Amino acid conjugation
  • Glycine conjugation
  • Taurine conjugation

Phase III

  • Transporters remove conjugated compounds from cells into bile or urine
  • Important transporters include:
    • P-glycoprotein (ABCB1)
    • MRP2 (ABCC2)
    • BCRP (ABCG2)

Key biochemical notes

  • NADPH is required to keep antioxidant systems working and supports reductive metabolism.
  • FAD and FMN are essential for flavoproteins involved in redox reactions.
  • UDP-glucuronic acid is the activated donor for glucuronidation.
  • Sulfate is needed for sulfation reactions.
  • Glutathione is the major intracellular thiol antioxidant and a major conjugating molecule.
  • Methionine/folate/B12/B6 support methylation and one-carbon metabolism.
  • Taurine and glycine are important for conjugating bile acids and certain xenobiotics.

Full references

  1. Klaassen, C. D. (Ed.). (2013). Casarett & Doull’s Toxicology: The Basic Science of Poisons (8th ed.). McGraw-Hill Education.
  2. Nelson, D. L., & Cox, M. M. (2021). Lehninger Principles of Biochemistry (8th ed.). W. H. Freeman.
  3. Zanger, U. M., & Schwab, M. (2013). Cytochrome P450 enzymes in drug metabolism: Regulation of gene expression, enzyme activities, and impact of genetic variation. Pharmacology & Therapeutics, 138(1), 103–141. https://doi.org/10.1016/j.pharmthera.2012.12.007 (opens in new tab)
  4. Guengerich, F. P. (2008). Cytochrome P450 and chemical toxicology. Chemical Research in Toxicology, 21(1), 70–83. https://doi.org/10.1021/tx700079z (opens in new tab)
  5. Lu, S. C. (2013). Glutathione synthesis. Biochimica et Biophysica Acta, 1830(5), 3143–3153. https://doi.org/10.1016/j.bbagen.2012.09.008 (opens in new tab)
  6. DeLeve, L. D., & Kaplowitz, N. (2014). Glutathione metabolism and its role in hepatotoxicity. Pharmacology & Therapeutics, 109(1–2), 131–149. https://doi.org/10.1016/j.pharmthera.2005.01.010 (opens in new tab)
  7. Tukey, R. H., & Strassburg, C. P. (2000). Human UDP-glucuronosyltransferases: Metabolism, expression, and disease. Annual Review of Pharmacology and Toxicology, 40, 581–616. https://doi.org/10.1146/annurev.pharmtox.40.1.581 (opens in new tab)
  8. Stipanuk, M. H. (2004). Sulfate, transsulfuration, and taurine metabolism in health and disease. Advances in Experimental Medicine and Biology, 566, 87–107. https://doi.org/10.1007/0-387-26206-7_5 (opens in new tab)
  9. Townsend, D. M., Tew, K. D., & Tapiero, H. (2003). The importance of glutathione in human disease. Biomedicine & Pharmacotherapy, 57(3–4), 145–155. https://doi.org/10.1016/S0753-3322(03)00043-X (opens in new tab)
  10. Hayes, J. D., & Dinkova-Kostova, A. T. (2014). The Nrf2 regulatory network provides an interface between redox and intermediary metabolism. Trends in Biochemical Sciences, 39(4), 199–218. https://doi.org/10.1016/j.tibs.2014.02.002 (opens in new tab)

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