Wasabi is best known for its presence alongside sushi in Japanese restaurants. But be careful, this
lovely green condiment is pungent!
Antimicrobial Benefits of Wasabi
Interestingly, wasabi and allyl isothiocyanate, the compound responsible for wasabi’s taste, have been found to inhibit the bacterium V. parahaemolyticus in tuna meat, indicating that its use as an accompaniment to sushi and sashimi adds more than flavor.1
Wasabi roots, stems, and leaves have also shown activity against the ulcer-causing bacterium H. pylori.2 While the bacterial activity of the leaves was higher than that of the roots, its leaves have a lower amount of allyl isothiocyanate, leading researchers to conclude that other components in wasabi have an antibacterial action. Subsequent research in animals infected with H. pylori and exposed to physical stress found a reduction in resultant oxidative DNA damage in the stomach and peripheral red blood cells in association with the administration of wasabi leaf extract.3
Of ten foods tested, including banana, coriander, mustard, and mugwort, wasabi had the strongest antibacterial activity against the intestinal bacterium Escherichia coli.4 The researchers identified 6-(methylsulfinyl)hexyl isothiocyanate (6-MITC) as wasabi’s active compound, and found that related compounds in other cruciferous plants were active against E. coli and Staphylococcus aureus (staph infection).
Anticancer Effects of Wasabi
One of the first studies to investigate wasabi was a rat study in which male animals received drinking water that contained MNNG, which induces gastric cancer.5 Some of the animals also received diets that contained 10% wasabi powder for 40 weeks. Among the 30 animals that received the carcinogen alone, nine animals developed stomach or duodenal cancers, in comparison with two rats among the group that also received wasabi. “These results indicated that glandular stomach carcinogenesis induced by MNNG was suppressed by the administration of wasabi,” the authors concluded.
6-MITC significantly inhibited mutation in the skin cells of mice that received a topical application of the carcinogen DMBA.6 6-MITC was also shown to suppress the growth of two mouse tumor cell lines.
In rats given 1,2-dimethylhydrazine (DMH) to induce the formation of premalignant lesions known as aberrant crypt foci and beta-catenin-accumulated crypts in the colon, the addition of 6-MITC to the diet during the initiation phase was associated with a reduction in the number of aberrant crypt foci as well as a decrease in those of larger size compared to treatment with DMH alone.7 6-MITC was also associated with a decrease in beta-catenin-accumulated crypts. A study involving colon cancer cells treated with wasabi extract resulted in the induction of autophagy and apoptosis (programmed cell death), which was verified in animals that received transplanted cancerous tumors.8
Apoptosis was also the inhibitory mechanism in a study involving human monoblastic leukemia cells, which the researchers attributed to its 6-MITC content.9 6-MITC also induced apoptosis in a stomach cancer cell line. Other research found an inhibitory effect for 6-MITC against the growth and survival of breast cancer and melanoma cell lines.10
In mice inoculated with either of two types of triple negative breast cancer cells, orally administered 6-MITC decreased tumor weight in mice that received one cell line and reduced tumor volume in both cell lines.11In vitro, 6-MITC induced apoptosis in both lines (as well as an estrogen receptor positive line), while downregulating nuclear factor-kappa beta (NF-kB). 6-MITC and a derivative compound have also shown inhibitory effects against the growth of human pancreatic cancer cells.12
Identification of wasabi as the most potent inducer of glutathione S-transferase (GST, a phase II detoxification enzyme involved in protection against carcinogenesis) following an extensive screening of vegetable extracts led to the identification of 6-MITC as wasabi’s major GST inducer.13 Researchers Yasujiro Morimitsu and colleagues concluded that 6-MITC “may be a chemoprotector against tumors evoked by a number of chemical carcinogens and can be regarded as a readily available promising new cancer chemopreventive agent.”
Other Protective Properties of Wasabi
In addition to wasabi’s anticarcinogenic properties, Dr. Morimitsu reports an ability to inhibit platelet aggregation, indicating a potential role in the prevention of cardiovascular disease.14 He was also a contributor to research that screened a number of Brassica vegetables for their ability to promote the formation of neurites in rat cells, which found that wasabi had the strongest activity and that 6-MITC was one of wasabi’s major enhancers of neuritogenesis.15 In a mouse model of Parkinson’s disease, 6-MITC showed neuroprotective effects, attributable to a reduction in apoptotic cell death and activation of glutathione-dependent antioxidant systems.16
Wasabi has shown antioxidant and superoxide scavenging properties.17 In mouse cells, 6-MITC inhibited cyclooxygenase-2 (COX-2) expression induced by lipopolysaccharide and interferon-gamma, indicating an anti-inflammatory effect.18,19 In human umbilical vein endothelial cells, 6-MITC suppressed cell adhesion and lowered inflammation.20
Additionally, in a mouse model of atopic dermatitis, wasabi rhizome extract added to the diet reduced scratching behavior as well as levels of histamine, IgE and other plasma factors.21
It has been suggested that some of the wasabi served in Japanese restaurants is not true wasabi, but is actually horseradish. While horseradish has its own health benefits, make sure you obtain true wasabi if you seek to avail yourself of its protective effects. The rhizome (stem of a plant that is usually found underground) of wasabi is also available as a dietary supplement.
- Hasegawa N et al. Int J Food Microbiol. 1999 Aug 1;49(1-2):27-34.
- Shin IS et al. Int J Food Microbiol. 2004 Aug 1;94(3):255-61.
- Sekiguchi H et al. Biosci Biotechnol Biochem. 2010;74(6):1194-9.
- Ono H et al. Biosci Biotechnol Biochem. 1998 Feb;62(2):363-5
- Tanida N et al. Nutr Cancer. 1991;16(1):53-8.
- Fuke Y et al. Cytotechnology. 1997 Nov;25(1-3):197-203.
- Kuno T et al. Oncol Lett. 2010 Mar;1(2):273-278.
- Hsuan SW et al. Eur J Nutr. 2016 Mar;55(2):491-503.
- Watanabe M et al. Phytochemistry. 2003 Mar;62(5):733-9.
- Nomura T et al. Cancer Detect Prev. 2005;29(2):155-60.
- Fuke Y et al. Nutr Cancer. 2014;66(5):879-87.
- Chen YJ et al. Evid Based Complement Alternat Med. 2014;2014:494739.
- Morimitsu Y et al. J Biol Chem. 2002 Feb 1;277(5):3456-63.
- Morimitsu Y et al. Biofactors. 2000;13(1-4):271-6.
- Shibata T et al. J Neurochem. 2008 Dec;107(5):1248-60.
- Morroni F et al. Brain Res. 2014 Nov 17;1589:93-104.
- Kinae N et al. Biofactors. 2000;13(1-4):265-9.
- Uto T et al. Biochem Pharmacol. 2005 Dec 5;70(12):1772-84.
- Uto T et al. Oncol Rep. 2007 Jan;17(1):233-8.
- Okamoto T et al. J Nat Med. 2014 Jan;68(1):144-53.
- Nagai M et al. J Nutr Sci Vitaminol (Tokyo). 2009 Apr;55(2):195-200.