Rutgers Cancer Institute of New Jersey
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The herb pokeroot grows wild in many parts of North America. The name comes from a Native American word, "pocan," a term that indicates any plant used to provide a red-colored dye. Pokeroot is a source of a blood-red pigment. Medicinally, it was used as an “alterative,” a substance that supposedly removes toxins from the body and restores overall health. Like other alteratives, pokeroot was used for the treatment of cancer, skin conditions, and many other diseases attributed to toxins. Pokeroot causes vomiting and diarrhea, and these effects were also traditionally considered salutary.1 However, in modern times, it has become clear that pokeroot causes vomiting and diarrhea because it is toxic; it should not be used at all.
Pokeroot itself is not sold in the United States. However, substances found in pokeroot have shown promise for drug development. One of these, “pokeroot antiviral protein,” has shown potential as a treatment for HIV and other viral infections.2-10
Note, however, that these findings on one ingredient of pokeroot do not indicate that the whole herb is useful for HIV infection.
Another substance in pokeroot, “pokeweed mitogen,” forces cells to divide, a property that has led to a great deal of scientific investigation.11-18
These mitogenic effects are potentially quite dangerous, and are more an argument against the use of pokeroot than for it.
Other pokeroot constituents have shown potential anti-inflammatory, diuretic, and blood pressure–lowering effects.19
We recommend against using pokeroot in any dosage.
Pokeroot is a toxic herb. Ingestion can lead to symptoms such as nausea, vomiting (sometimes with blood), diarrhea, rapid heart rate, a dangerous fall in blood pressure, difficult breathing, confusion, and death.19,20 Symptoms may develop with one-time use or insidiously over time. Fresh root is more toxic than dried root. The juice of pokeweed berries is more toxic still, and can cause severe damage to blood cells even when it is only applied to the skin.21-24 Pokeroot should definitely not be used by pregnant or nursing women or young children.
1. Stolberg M. The miraculous effects of taking laxatives. Success and failure of pre-modern medical treatment from the patients' perspective. Wurzbg Medizinhist Mitt. 2003;22:167–77.
2. Picard D, Kao CC, Hudak KA, et al. Pokeweed antiviral protein inhibits brome mosaic virus replication in plant cells. J Biol Chem. 2005;280:20069–75.
3. Uckun FM, Rustamova L, Vassilev AO, et al. CNS activity of pokeweed anti-viral protein (PAP) in mice infected with lymphocytic choriomeningitis virus (LCMV). BMC Infect Dis. 2005;5:9.
4. Parikh BA, Baykal U, Di R, et al. Evidence for retro-translocation of pokeweed antiviral protein from endoplasmic reticulum into cytosol and separation of its activity on ribosomes from its activity on capped RNA. Biochemistry. 2005;44:2478–90.
5. D'Cruz OJ, Waurzyniak B, Uckun FM, et al. Mucosal toxicity studies of a gel formulation of native pokeweed antiviral protein. Toxicol Pathol. 2004;32:212–21.
6. D'Cruz OJ, Waurzyniakt B, Uckun FM, et al. A 13-week subchronic intravaginal toxicity study of pokeweed antiviral protein in mice. Phytomedicine. 2004;11:342–51.
7. Parikh BA, Tumer NE. Antiviral activity of ribosome inactivating proteins in medicine. Mini Rev Med Chem. 2004;4:523–43.
8. Hudak KA, Bauman JD, Tumer NE, et al. Pokeweed antiviral protein binds to the cap structure of eukaryotic mRNA and depurinates the mRNA downstream of the cap. RNA. 2002;8:1148–59.
9. Parikh BA, Coetzer C, Tumer NE, et al. Pokeweed antiviral protein regulates the stability of its own mRNA by a mechanism that requires depurination but can be separated from depurination of the alpha-sarcin/ricin loop of rRNA. J Biol Chem. 2002;277:41428–37.
10. Turpin JA. Considerations and development of topical microbicides to inhibit the sexual transmission of HIV. Expert Opin Investig Drugs. 2002;11:1077–97.
11. Yamaguchi K, Uechi M, Katakura Y, et al. Mitogenic properties of pokeweed lectin-D isoforms on human peripheral blood lymphocytes: non-mitogen PL-D1 and mitogen PL-D2. Biosci Biotechnol Biochem. 2004;68:1591–3.
12. Yan S, Marguet D, Dobers J, et al. Deficiency of CD26 results in a change of cytokine and immunoglobulin secretion after stimulation by pokeweed mitogen. Eur J Immunol. 2003;33:1519–27.
13. Barabas E, Kemeny B, Gonzalez R, et al. A comparison of the lymphoproliferative capacity of pokeweed mitogen (PWM) and phytohaemagglutinin (PHA) in CCR-5 wild-type and heterozygous HIV-infected and uninfected subjects. Int J STD AIDS. 2002;13:691–7.
14. Wang S, Panter KE, Evans RC, et al. The effects of pokeweed mitogen (PWM) and phytohemagglutinin (PHA) on bovine oocyte maturation and embryo development in vitro. Anim Reprod Sci. 2001;67:215–20.
15. Wimer BM, Mann PL. Mitogen immunotherapy for HIV infections exemplified by phytohemagglutinin and pokeweed mitogen. Cancer Biother Radiopharm. 2001;15:629–44.
16. Wimer BM, Mann PL. Apparent pokeweed mitogen cure of metastatic gum melanoma in an older dog. Cancer Biother Radiopharm. 2000;15:201–5.
17. Sjoberg O, Kurnick J. Conditions for induction of specific and polyclonal antibody production by Cowan 1 bacteria and by pokeweed mitogen. Scand J Immunol. 1998;11:47–51.
18. Lazarus DD, Trimble LA, Moldawer LL, et al. The metabolic effects of pokeweed mitogen in mice. Metabolism. 1998;47:75–82.
19. Newall CA, Anderson LA, Phillipson JD. Herbal Medicines: A Guide for Health-Care Professionals. London: The Pharmaceutical Press. 1996:215–217.
20. Roberge R, Brader E, Martin ML, et al. The root of evil—pokeweed intoxication. Ann Emerg Med. 1986;15:470–3.
21. Barker BE et al. Haematological effects of pokeweed. Lancet 1967;1:437.
22. Barker BE et al. Peripheral blood plasmacytosis following systemic exposure to Phytolacca americana (pokeweed). Pediatrics. 1966;38:490–493.
23. Barker BE et al. Mitogenic activity in Phytolacca americana (pokeweed). Lancet. 1965;1:170.
24. Yamaguchi K, Uechi M, Katakura Y, et al. Mitogenic properties of pokeweed lectin-D isoforms on human peripheral blood lymphocytes: non-mitogen PL-D1 and mitogen PL-D2. Biosci Biotechnol Biochem. 2004;68:1591–3.
Last reviewed December 2015 by EBSCO CAM Review Board Last Updated: 12/15/2015