Sources and Composition
Watercress is the common name for the herb Nasturtium officinale (of the family Brassicaceae) which is a commonly consumed vegetable with a peppery taste. It is one of many herbs to be used against scurvy, due to its Vitamin C content. Due to it belonging to the Brassicaceae family, it is known as a cruciferous vegetable (similar to broccoli and cauliflower).
A vegetable in the same family as broccoli, commonly used as a vegetable (usually in salads, due to its leafy composition) and carried many of the same properties as well as a peppery taste
Watercress tends to contain:
- Gluconasturtiin, a glucosinolate at 0.06–0.21µmol/g dry weight which is the thioglucoside conjugate of β-phenylethyl isothiocyanate (PEITC) that is itself found at 23.7-29.7μmol/g dry weight
- Glucobrassicin (0.01-0.02µmol/g dry weight)
- 4-methoxyglucobrassicin (0.06–0.18µmol/g dry weight)
- 6-Methylsulfinylhexyl (0.2-0.3µmol/g dry weight), 7-methylsulfinylheptyl (3.9-7.5µmol/g dry weight), and 8-methylsulfinyloctyl (2.1-4.3µmol/g dry weight) isothiocyanates
- 7-Methylthioheptyl (1.2-2.5µmol/g) and 8-Methylthiooctyl (0.7-1.3µmol/g) isothiocyanates
- β-Carotene (5.919mg/100g wet weight) with no detectable α-Carotene
- Lutein (10.713mg/100g wet weight), no detectable Lycopene nor β-Cryptoxanthin
- Apigenin and glycosides
- Kaempferol (mostly glucosides, diglucosides, and some glycones with rhamnose)
- Quercetin (glucorhamnoside and diglucorhamnoside)
- Vitamin C at 104mg/100g fresh weight
While S-(N-β-Phenylethylthiocarbomyl)glutathione (PTCG) has been found to spontaneously and metabolically form from other glucosinates in watercress, without occurring naturally. The concentration in this particular study merely being 12.5nM and less than 1% of total hydrolysed β-phenylethyl glucosinolate (a minor metabolite). It may be formed from PEITC, as this study noted that PEITC was not found in tested extracts.
In general, watercress carries the same bioactives as other plants in the same family (Brassicaceae) although due to the gluconasturtiin content it contains a relatively high level of the isothiocyanate known as PEITC
While the essential oil (volatile compounds) include:
- Myristicin (57.6% of the leaves and not detected in stems or flowers)
- α-terpinolene (8.9% of the leaves, 15.2% and 19.7% of the stems and flowers)
- Limonene (6.7% of the leaves, but 11.8% and 43.6% of the stems and flowers)
- β-Caryophyllene (13.1% stems, 6.6% of the flowers, and 4.3% leaves)
- Caryophyllene oxide (37.2% of the stem, 6.7% of the flower, 4.2% of the leaves)
- p-cymene-8-ol (17.6% of the stem, 7.6% of the flower, 3.1% of the leaves)
- Neophytadienen (1.6% of the flowers, 1.5% of the leaves, and 0.8% of the stems)
The essential oil is a surprisingly good source (percentage wise) of Myristicin, the hallucinogenic substance in nutmeg; this may not be high enough overall to induce a trip, however
By weight, the essential oil is approximately 1.5% (stems), 1.2% (leaves) and 1.0% (flowers) and, when isolated, the essential oil does not contain polyphenolics nor flavonoids.
An extract (80:20 aqueous:ethanolic) of watercress has a polyphenolic content of 96.6+/-3.5mg/g as gallic acid equivalents (9.6%) and total flavonoid content of 62.3+/-2.4mg/g as catechin equivalents (6.2%; 64% of the phenolics). Comparatively speaking, Watercress appears to be one of the highest common sources of Lutein (including parsley and spinach) although the most common dietary source are tomatoes; β-Carotene is also higher in watercress than most tested common vegetables excluding carrots. This content of polyphenolics, relative to other Brassicaceae vegetables of leafy composure (mizuna and rocket) watercress has a higher phenolic content and a higher Vitamin C content.
It has been estimated that, due to the gluconasturiin content, consumption of approximately an ounce of watercress results in exposure to approximately 2-6mg of PEITC in humans and that consumption of 80g watercress has been noted to increase serum PEITC to 297nM on average (large range of 61-656nM) at a Tmax generally between 90-185 minutes, while 100g watercress has been noted to increase serum PEITC to 928nM.
Watercress consumption is able to increase circulating levels of PEITC, although in an unreliable manner
In hypercholesterolemic rats, 500mg/kg watercress daily for 30 days has been noted to reduce triglycerides (43%), LDL-C (49%), and total cholesterol (37%) while increasing HDL-C (16%); a beneficial influence on liver enzymes was noted as well, with reductions of ALT (39%), AST (42%), and ALP (40%). These effects were thought to be secondary to its antioxidant properties, and have been seen with a hydroalcoholic extract in rats fed a high fat diet, where oral ingestion of 500mg/kg of this watercress extract for 30 days normalized total cholesterol, LDL-C, and triglycerides with a small spike in HDL-C with a similar benefit to liver enzyme levels.
Animal evidence to suggest (surprisingly potent) anti-cholesterol and anti-triglyceride effects in rats fed a high fat diet, which is thought to be secondary to antioxidant effects in liver tissue. Currently no human evidence
Interactions with Oxidation
The antioxidant potential of watercress is shown in a concentration dependent manner against lipid peroxidation (EC50 273.5μg/mL, underperfoming relative to catechin at 10.1μg/mL), iron chelation (538.6μg/mL, underperforming relative to EDTA at 5μg/mL), DPPH free radical scavenging (114.7μg/mL, underperforming to Vitamin C at 3.5μg/mL), ABTS+ inhibition (60.8μg/mL, underperforming to Trolox at 11.2μg/mL), nitric oxide inhibition (395.2μg/mL, somewhat comparable to catechin at 332.1μg/mL), and hydrogen peroxide scavenging activity (312.4μg/mL, somewhat comparable to Vitamin C at 106.2μg/mL). Concentrating watercress for the ethanolic extract increases potency of the antioxidant parameters, but not enough to surpass reference compounds.
The essential oil components also possesses antioxidant properties, with that of the leaves (IC50 87.0+/-0.9µg/mL) being more potent than the stem or flower in a DPPH assay (but less potent than the reference compound BHT at 18.0+/-0.3µg/mL).
Compounds in watercress appear to have direct anti-oxidant properties, although they are not remarkably potent in vitro relative to reference compounds
15 days of supplementation of 0.5-1g/kg of watercress to rats was unable to induce genomic damage inherently but showed some protection against cyclophosphamide-induced genotoxicity as assessed by bladder histological changes; the protective effects were also replicated in vitro in a concentration-dependent manner. This DNA protective effect has been noted in vitro elsewhere.
May protect DNA from oxidative damage
An increase in antioxidant capacity of the blood has been noted in rats with high cholesterol consuming 500mg/kg of watercress daily for 30 days, where the increase in hepatic lipid peroxidation and subsequent decrease in hepatic glutathione were not only normalized but the correction surpassed control (with the hypercholesterolemic rats given watercress having less lipid peroxidation and more glutathione than non-hypercholesterolemic control rats). Similar trends were noted for Catalase, SOD, and glutahione reductase and peroxidase.
8 weeks of consumption of 85g watercress daily has been noted to influence anti-oxidant enzymes in humans, although the effect was only noted in red blood cells (not white blood cells) and the small increase in gluthione peroxidase and SOD were limited GSMT1*0 genotype (of which 44/60 persons had). This genotype is associated with having a more profound anti-cancer association with cruciferous vegetables which is thought to be due to a slower excretion rate of isothiocyanates and thus prolonged circulating levels; This study noted that the other genotypes had a trend towards enhanced glutathione peroxidase and SOD, but that the increases were not statistically significant.
These observations have been noted earlier in healthy adults consuming 85g watercress daily, and have been noted to be more significant in smokers relative to nonsmokers.
Two studies have confirmed some bioactivity of daily watercress consumption in regards to antioxidative parameters, with one noting a reduction in DNA damage in lymphocytes (white blood cells) while the other noted a genotype-dependent induction of anti-oxidant enzymes
Interactions with Cancer Metabolism
Glucosinolates are thought to confer chemoprotective effects via modulating phase I and II enzymes (enzymes involved in drug bioactivation and excretion).
Induction of Quinone reductase is observed with S-(N-β-Phenylethylthiocarbomyl)glutathione (PTCG) although at concentrations 400-fold higher than found in the food product; 7-Methylsulfinylheptyl and 8-methylsulfinyloctyl isothiocyanates were found to induce the enzyme 2-fold at 0.2µM and 0.5µM (similar potency to other sulfated isothiocyanates including 4-methylsulfinylbutyl isothiocyanate (sulforaphane)).
Appears to induce quinone reductase, with a few bioactives capable of doing so with similar potencies to sulforaphane
PEITC has been shown previously to inhibit the protein known as 4E-BP1 which may mediate some anti-cancer activity (via suppressing activities of HIF), and this has been shown to occur in vivo in women, where consumption of 80g watercress increased serum PEITC to 297nM and suppressed 4E-BP1 phosphorylation in lymphocytes of tested persons at 6-8 hours after ingestion although the degree of suppression was fairly unreliable.
Appears to inhibit 4E-BP1, which has been noted in a small sample of humans following oral ingestion of 80g watercress
Nicotine is a stimulatory alkaloid found most commonly in cigarettes and stop smoking aids.
Watercress consumption has been found to increase the urinary metabolites 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNAL) and its glucuronide. This was thought to be due to either an increase in glucuronidation or an inhibition of CYP1A2 (aromatase).
Three days of consumption of two ounces (56.8g) of watercress at each meal has failed to significantly change urinary nicotine and continine levels, which is thought to be due to minimal inhibition of CYP2A6.