Watercress Wins the Battle Against Cancer


Watercress, or Nasturtium officinale, is a member of the Brassicaceae family that includes
cruciferous vegetables such as broccoli, kale and cauliflower.

Its membership in this group suggests that watercress has some of the positive health effects of this nutritionally outstanding group of vegetables.

Watercress is a good source of folate and vitamin C. In comparison with other green vegetables, it is relatively high in the omega-3 fatty acid alpha-linolenic acid.1 Investigation of watercress' antioxidant properties has revealed free radical scavenging activities, an ability to decrease cellular lipid peroxidation, and more.2

Lung Cancer

In 1970, researchers noted that watercress had an inhibitory effect on cell division in some experimental tumors.3 In 1993, the Annals of the New York Academy of Sciences reported the findings of a team at the American Health Foundation of an inhibitory effect for the beneficial watercress compound phenethyl isothiocyanate (PEITC) against lung tumor formation induced by the nitrosamine compound NNK that occurs in tobacco.4

One reason for watercress' anticancer benefit may be its DNA-protective property. A randomized study of 30 smokers and 30 nonsmokers who consumed 85 grams watercress daily for eight weeks in addition to their regular diet found that the addition of watercress significantly reduced DNA damage as measured in white blood cells known as lymphocytes in comparison with damage measured during a control phase of the study.5 Watercress intake was associated with an increase in plasma beta-carotene and lutein, indicating increased antioxidant status.

Breast and Prostate Cancers

In a study of the effects of watercress or broccoli extract on human breast cancer cells treated with a tumor promoter, both extracts suppressed matrix metalloproteinase 9, an enzyme involved in invasiveness.6

Isothiocyanates like PEITC are released from glucosinolates in watercress when it is ingested. PEITC's presence in the body can be quantified by measurement of a metabolic byproduct formed by conjugation with N-acetyl-cysteine (NAC), although newer methods have been developed.7

A study of human prostate cancer cells revealed that exposure to the NAC conjugate of phenethyl isothiocyanate (PEITC-NAC) resulted in inhibition of cell proliferation and tumorigenesis.8 In immunodeficient mice that received human prostate cancer tumor grafts, supplementation with PEITC-NAC significantly reduced tumor size over nine weeks of treatment in all of the animals that received the compound. At the end of the study, tumor weight of PEITC-NAC-treated mice was half that of unsupplemented mice. PEITC-NAC supplementation was found to cause cell cycle arrest and induce apoptosis (programmed cell death).

An interesting point was brought up in an article published in the Asian Pacific Journal of Cancer Prevention concerning the high rate of colorectal cancer in New Zealand.9 The authors observe that the native Maori population — who consume more calories, red meat, saturated fat and alcohol, have more obesity, and consume fewer fruits and vegetables per day than non-Maoris — have nearly half the incidence of colorectal cancer. They do, however, consume two protective foods: sow thistle and watercress.

Colon Cancer and Leukemia

In an experiment in which female rats were given the carcinogen DMBA, a 20% watercress diet decreased the percentage of animals with mammary tumors and the average number of tumors per rat.10 In another rat study, PEITC reduced the formation of precursors of colorectal polyps known as aberrant crypt foci following the administration of a carcinogen.11 One of the protective mechanisms of PEITC's are the induction of phase II enzymes that enhance carcinogen biotransformation.12

Two other watercress isothiocyanates (7-methylsulfinylheptyl isothiocyanate and 8-methylsulfinyloctyl isothiocyanate) have been found to be even more potent phase II enzyme inducers.

In human colon cancer cells, watercress extract inhibited DNA damage induced by genotoxins, delayed the cell cycle and inhibited invasion, indicating a significant ability to protect against the three stages of carcinogenesis: initiation, proliferation and metastasis.13 In a mouse model of familial adenomatous polyposis (an inherited condition characterized by the development of numerous, potentially malignant colon polyps), animals that received a diet supplemented with PEITC had fewer and smaller polyps compared to those that received a standard diet. The growth inhibitory effect was thought to be associated with apoptosis and cell cycle arrest.14

PEITC could also be effective against leukemia. In human chronic myeloid leukemia cells, PEITC suppressed cell growth and induced apoptosis.15 Similar results have been observed in a study of human glioma cells treated with PEITC.16

While the contents of this post have focused on watercress' association with cancer protection, research has uncovered other favorable properties for this vegetable. If the British tea-time tradition of watercress sandwiches doesn't appeal to you, toss some in a salad or look for a supplement that lists watercress extract on its label.

References:

  1. Pereira C et al. Int J Vitam Nutr Res. 2001 Jul;71(4):223-8.
  2. Ozen T. Acta Pol Pharm. 2009 Mar-Apr;66(2):187-93.
  3. Cruz A. Hospital (Rio J). 1970 Mar;77(3):943-52.
  4. Chung FL et al. Ann N Y Acad Sci. 1993 May 28;686:186-201.
  5.  Gill CI et al. Am J Clin Nutr. 2007 Feb;85(2):504-10.
  6. Rose P et al. Toxicol Appl Pharmacol. 2005 Dec 1;209(2):105-13.
  7. Chung FL et al. Cancer Epidemiol Biomarkers Prev. 1992 Jul-Aug;1(5):383-8
  8.  Chiao JW et al. Carcinogenesis. 2004 Aug;25(8):1403-8.
  9. Thomson B et al. Asian Pac J Cancer Prev. 2002;3(4):319-324.
  10. Shwaireb M et al. Oncol Rep. 1995 Jul;2(4):689-92.
  11. Chung FL et al. Carcinogenesis. 2000 Dec;21(12):2287-91.
  12. Rose P et al. Carcinogenesis. 2000 Nov;21(11):1983-8.
  13. Boyd LA et al. Nutr Cancer. 2006;55(2):232-41.
  14. Khor TO et al. Mol Carcinog. 2008 May;47(5):321-5.
  15. Wang Y et al. Mol Med Rep. 2014 Jul;10(1):543-9.
  16. Su JC et al. Int J Clin Exp Pathol. 2015 Apr 1;8(4):4269-76.

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