Potential nutraceuticals and their function & health benefits

1. ©Hazrat Ali
Dept. of Applied Nutrition and Food Technology
Islamic University, Bangladesh
Potential nutraceutical and their function, present in common foods in
Bangladesh
Hazrat Ali
Dept. Of Applied Nutrition and Food Technology
Islamic University, Bangladesh

2. ©Hazrat Ali
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1. Nutraceutical
1.1 Definition:
The term "Nutraceutical" was coined by combining the terms "Nutrition" and
"Pharmaceutical" in 1989 by Dr. Stephen De Felice. Founder and Chairman of
the Foundation for Innovation in Medicine (FIM), New Jersey, USA .
According to Dr. De Felice: A nutraceutical is any substance considered as a
food, or its part which, in addition to its normal nutritional value provides
health benefits including the prevention of disease or promotion of health. e.g.,
lycopene, beta carotene.
Health ministry of Canada defines it “As a product isolated or purified from
the food generally sold in medicinal form not assisted with food and demonstrated
to have a physiological benefit and provide protection against chronic disease.
1.2 Classification:
Potential Nutraceuticals - One which has promising approach towards
particular health or medicinal benefit.
Established Nutraceuticals – A Potential Nutraceutical becomes established
nutraceutical only after there are sufficient clinical use to demonstrate a benefit.
1.3 Potential health benefits
Over the years nutraceuticals have attracted considerable interest due to
their potential nutritional, safety and therapeutic effects. They could have a role
in a plethora of biological processes, including antioxidant defenses, cell
proliferation, gene expression, and safeguarding of mitochondrial integrity.
Therefore nutraceuticals may be used to improve health, prevent chronic
diseases, postpone the aging process (and in turn increase life expectancy), or just
support functions and integrity of the body. They are considered to be healthy
sources for prevention of life threatening diseases such as diabetes, renal and
gastrointestinal disorders, as well as different infections.
A wide range of nutraceuticals have been shown to impose crucial roles in
immune status and susceptibility to certain disease states. They also exhibit
diseases modifying indications related to oxidative stress including allergy,
Alzheimer's disease, cardiovascular diseases, cancer, eye conditions, Parkinson's
diseases and obesity.[1]
1.4 Global demand for nutraceuticals
The global nutraceutical market has experienced maximum growth in the last
decade. Although nutraceuticals as an industry emerged in the early 1990s, the

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world has witnessed its explosive growth in the first decade of this century. From
1999 to 2002 the industry grew at an annual average growth rate of 7.3 percent,
while in this century the rate doubled to 14.7 percent.
Today, global nutraceutical market is estimated at 117 billion USD.
Personalization and customization are current trends in the development of
nutraceuticals, especially in developed markets of the world. Investment in
research and development to find innovative approaches, verifying health claims
of the products and market research represent key strategies for the industry.[2]
Table 1: Potential nutraceuticals in Bagladeshi foods
Nutraceutical Sources
1 Capsaicin Peppers
2 Cinnamic acid Cinnamon
3 Cucurbitacin Pointed gourds, Pumpkins, and Cucumbers
4
Delphinidin
Rice, Onion, Eggplants, Wheat, Orange, Lentil,
Pea, Peppers, Soybean,
5
Eugenol
Guava, Clove buds, Cinnamon bark and leaves,
Tulsi leaves, Turmeric, Pepper, Ginger
6 Gallic acid Mango, Bell Peppers, Nuts, Tea
7 -Orzanol Rice
8 Linalool Coriander seeds
9
Lutein & Zeaxanthin
Peppers, Spinach, Pumpkin, String Bean/ Green
Bean, Carrots, Okra, Coriander seeds,
Cauliflower
10 Lycopene Watermelon, Tomato, Peppers, Guava, Papaya
11 Nasunin Brinjal/Eggplants,
12 Phytic Acid Rice, Wheat, Kidney Bean, Soybean
13 Polypeptide-p Bitter gourd
14 Sinigrin Cabbage, Cauliflower, Mustard

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2. Capsaicin
Capsaicin (8-methyl-N-vanillyl-6-nonenamide) is an active component of chili
peppers, which are plants belonging to the genus Capsicum. It is a
chemical irritant for mammals, including humans, and produces a sensation of
burning in any tissue with which it comes into contact. Capsaicin and several
related compounds are called capsaicinoids and are produced as secondary
metabolites by chili peppers, probably as deterrents against certain mammals
and fungi. Pure capsaicin is a hydrophobic, colorless, highly pungent, crystalline
to waxy solid compound.
Capsaicin is present in large quantities in the placental tissue (which holds
the seeds), the internal membranes and, to a lesser extent, the other fleshy parts
of the fruits of plants in the genus Capsicum. The seeds themselves do not
produce any capsaicin, although the highest concentration of capsaicin can be
found in the white pith of the inner wall, where the seeds are attached.[3]
2.1 Source: Peppers
2.2 Health benefits:
- May Be Helpful in Treating Cancer
- Decreases Incidence of Cluster Headaches
- Relieves Pain
- Treats Psoriasis
- Aids in Management of Diabetes
- May Lower Blood Pressure
2.2.1 May Be Helpful in Treating Cancer
Of the many benefits consuming capsaicin has to offer, few have been
reviewed as much as its powerful effect against cancer.
For example, various studies show capsaicin can effectively fight prostate
cancer, including a 2006 study at the UCLA School of Medicine, stating it has a
“profound antiproliferative effect” on this type of cancer. Researchers found that
taking capsaicin orally significantly stopped the spread of prostate cancer cells as
well as caused apoptosis (cell death) in more than one type of prostate cancer cell.
In a gerbil study, scientists also discovered capsaicin to be effective against H.
pylori-induced gastritis, an infection of the stomach lining caused by a bacteria
penetrating the inner mucous layer. This condition is of particular concern in
developing nations where living conditions are also cramped, where the H.
pylori bacteria is most common. Capsaicin, along with piperine, in this
study acted by decreasing inflammation caused by the virus, and it was

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determined, therefore, to be a useful way to potentially prevent the next step in
this bacterial infection: gastric cancer.
Another type of cancer capsaicin may be useful in fighting is breast cancer,
the second most fatal cancer in women. For some time, it’s been clear that
capsaicin has the ability to induce apoptosis in specific breast cancer cells, but
another breakthrough study was released in South Korea in late 2015 that found
capsaicin may also help kill an additional type of cell: breast cancer stem cells.
This discovery is especially important because the stem cells that remain
after the other cancer cells have died are the ones responsible for recurrences of
the disease.
Capsaicin has been researched at length in conjunction with its impact on
primary effusion lymphoma (PEL). This form of non-Hodgkin’s lymphoma is a
rare one associated with HIV.
2.2.2 Decreases Incidence of Cluster Headaches
One specific pain remedy that commonly includes the cream form of this
natural pain reliever is the treatment of cluster headaches. Different from
migraine or tension headaches, these recurring, specific headaches are described
by most as the worst pain they have ever experienced, with some women even
comparing it to the pain of childbirth.
While they’re rare, cluster headaches are debilitating and can last for six to
12 weeks. There are many lifestyle and dietary options that are useful in treating
them, including the application of capsaicin cream to the inside of a nostril on the
side of your head suffering the headache. By repeatedly applying the cream,
subjects found the frequency of their headaches decreased for up to 60 days after
ending this treatment option in a study conducted by the Institute of Internal
Medicine and Clinical Pharmacology at the University of Florence, Italy.
2.2.3 Relieves Pain
Capsaicin is a commonly known pain-relief agent. The reasons for this are
widely unknown, although scientists are uncovering more about the mechanisms
it uses to provide relief. It seems that, in large part, capsaicin provides analgesic
relief by activating the TRPV1 receptor, which then causes the brain to release a
neurotransmitter called “substance P.”
Especially in cream form, it’s been used for many years to treat pain related
to osteoarthritis, rheumatoid arthritis and fibromyalgia, as well as certain kinds
of joint pain.
More recently, researchers have been investigating a method of injecting
highly purified capsaicin into cartilage and tendons connected to a damaged
rotator cuff. While this did not speed the healing process as initially expected, it

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did significantly alter pain responses, making it a good candidate for pain
treatment for this condition.
2.2.4 Treats Psoriasis
In addition to treating pain, capsaicin has been long known for its ability to
treat various skin conditions, including the dry, itchy skin of psoriasis. Substance
P seems to be an effective treatment for this condition, as research shows that
continued application of capsaicin cream shows a dramatically decreased amount
of psoriasis breakout on the skin.
2.2.5 Aids in Management of Diabetes
Like many features of healthy foods, capsaicin is very useful when aiming to
prevent and treat diabetes. Consistently consuming foods high in this nutrient
has been proven to improve the blood sugar and insulin reactions in both men and
women, and also in women with gestational diabetes.
A painful condition associated with diabetes, diabetic neuropathy, may also
be treated with capsaicin cream to decrease pain responses.[4]
2.2.6 May Lower Blood Pressure
High blood pressure is a huge health risk worldwide. In fact, over 40% of
adults over 25 have high blood pressure.
Interestingly, animal studies have shown that the capsaicin in cayenne
peppers may reduce high blood pressure.
One study in mice with high blood pressure showed that the long-term
consumption of dietary spices containing capsaicin helped reduce blood pressure.
Another study showed that capsaicin helped relax blood vessels in pigs,
leading to lower blood pressure.[5]

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3. Cinnamic acid
Cinnamic acid is an organic compound with the formula C6H5CH=CHCOOH.
It is a white crystalline compound that is slightly soluble in water, and freely
soluble in many organic solvents. Classified as an unsaturated carboxylic acid, it
occurs naturally in a number of plants. It exists as both a cis and a trans isomer,
although the latter is more common.
It is obtained from oil of cinnamon, or from balsams such as storax. It is also
found in shea butter. Cinnamic acid has a honey-like odor; it and its more volatile
ethyl ester (ethyl cinnamate) are flavor components in the essential oil
of cinnamon, in which related cinnamaldehyde is the major constituent.[6]
3.1 Sources:
Cinnamon
3.2 Health benefits:
- Cinnamic acid act as anti-oxidant.
- May used as an anti-microial agent.
- Contains Anti-Inflammatory Properties.
- Protects Heart Health.

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4. Cucurbitacins
Cucurbitacin is any of a class of biochemical compounds that some plants —
notably members of the pumpkin and gourd family, Cucurbitaceae — produce
and which function as a defence against herbivores. Cucurbitacins are chemically
classified as triterpenes, formally derived from cucurbitane,
a triterpene hydrocarbon – specifically, from the unsaturated
variant cucurbit-5-ene, or 19(10→9β)-abeo-10α-lanost-5-ene. They often occur
as glycosides. They and their derivatives have been found in many plant families
(including Brassicaceae, Cucurbitaceae, Scrophulariaceae, Begoniaceae, Elaeocar
paceae, Datiscaceae, Desfontainiaceae, Polemoniaceae, Primulaceae, Rubiaceae,
Sterculiaceae, Rosaceae, and Thymelaeaceae), in some mushrooms (including
Russula and Hebeloma) and even in some marine mollusks.
Cucurbitacins may be a taste deterrent in plants foraged by some animals
and in some edible plants preferred by humans,
like cucumbers and zucchinis. In laboratory research, cucurbitacins
have cytotoxic properties and are under study for their potential biological
activities.[7]
4.1 Sources:
Pointed gourds, Pumpkins, and Cucumbers
4.2 Health benefits:
- They are potent cathartics and laxatives.
- May have anti-cancer activities.
- Possess anti-inflammatory and analgesic effects.
- Show antibacterial and anthelmintic properties.
- Have hepatoprotective, cardioprotective, and anti-diabetic effects.

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5. Delphinidin
Delphinidin (also delphinidine) is an anthocyanidin, a primary plant pigment,
and also an antioxidant. Delphinidin gives blue hues to flowers in the
genera Viola and Delphinium. It also gives the blue-red color of the grape that
produces Cabernet Sauvignon, and can be found in cranberries and Concord
grapes as well as pomegranates, and bilberries.
Delphinidin, like nearly all other anthocyanidins, is pH-sensitive, i.e.
a natural pH indicator, and changes from red in basic solution to blue
in acidic solution.[8]
5.1 Sources:
Rice, Onion, Eggplants, Wheat, Orange, Lentil, Pea, Peppers, Soybean
5.2 Health benefits:
- Exhibit antiproliferative and apoptotic effects in human breast cancer
cells.[9]
- Exhibit Antioxidant and Anti-Inflammatory Effects.[10]
5.2.1 Anti-cancer activity of delphinidin
For the determination of anticancer activity, effect of delphinidin on
established breast cancer cell lines of various molecular subtypes were
determined. Delphinidin inhibited proliferation, blocked anchorage-independent
growth, and induced apoptosis of ER-positive, triple negative, and
HER2-overexpressing breast cancer cell lines. MAPK (mitogen-activated protein
kinase) signaling was partially reduced in triple negative cells and ER-negative
chemically transformed MCF10A cells after treatment with delphinidin.
Anthocyanins have gained much attention due to their wide range of potential
health-promoting effect. Mechanisms responsible for the cytoprotective actions of
delphinidin and other anthocyanins were investigated. All the tested flavonoids
were found to counteract peroxynitrite-induced apoptotic effects on endothelial
cells through the inhibition of several crucial signaling cascades. Furthermore
epidemiological studies revealed that delphinidin has a beneficial effect on
various stages of carcinogenesis. In another study, the extent of DNA damage by
delphinidin is not affected by the expression of tyrosyl-DNA-phosphodiesterase 1,
indicating that the induction of DNA strand breaks is not predominantly
topoisomerase-mediated. However, the DNA-damaging properties of delphinidin

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were decreased by the addition of catalase to the cell culture medium,
counteracting delphinidin-mediated hydrogen peroxide formation. In another
study, delphinidin inhibits tumor promoter-induced transformation and
cyclooxygenase-2 (COX-2) expression in JB6 promotion-sensitive mouse skin
epidermal (JB6 P+) cells by directly targeting Raf and mitogen-activated protein
kinase (MEK). The activation of activator protein-1 and nuclear factor-kappaB by
TPA were found to be dose dependently, moreover it is inhibited by delphinidin
treatment.
Effect of delphinidin in human colon cancer HCT116 cells was investigated.
Delphinidin exhibited decreased cell viability, induction of apoptosis, cleavage of
PARP, activation of caspases-3, -8, and -9, increase in Bax with a concomitant
decrease in Bcl-2 protein and G2/M phase cell cycle arrest. In another study,
Effect of anthocyanidins in primary (Caco-2) and metastatic (LoVo and LoVo/ADR)
colorectal cancer cell lines was investigated. Delphinidin showed cytotoxic effect
on metastatic cells. Effects of anthocyanins in different modes of cell death in
different cancers were investigated. Delphinidin could induce apoptosis in
leukemia cells thereby promoting growth retardation in hepatocellular carcinoma
cells. Effects of delphinidin on UVB-induced COX-2 upregulation and underlying
molecular mechanism were investigated. Delphinidin suppressed UVB-induced
COX-2 expression in JB6 P+ mouse epidermal cells. COX-2 promoter activity and
PGE (2) production were also suppressed by delphinidin treatment within
non-cytotoxic concentrations. Effect of delphinidin treatment to human PCa
LNCaP, C4-2, 22Rnu1, and PC3 cells was investigated and found that it exhibited
dose-dependent inhibition of cell growth without affecting normal human
prostate epithelial cells. Delphinidin induces apoptosis and cell cycle arrest in
androgen refractory human PCa 22Rnu1 cells and the effects are concomitant
with inhibition of NfkappaB.
5.2.2 Anti-inflamatory activity of delphinidin
Delphinidin (isolated from Punica granatum L) specifically inhibited the
Histone acetyltransferase (HAT) activities of p300/CBP. It also inhibited p65
acetylation in MH7A cells, a human rheumatoid arthritis synovial cell line.
Delphinidin treatment inhibited TNF -stimulated increases in NF-к B function
and expression of NF-к B target genes in these cells. Delphinidin suppressed
lipopolysaccharide-induced pro-inflammatory cytokine expression in Jurkat T
lymphocytes, demonstrating that HATi efficiently suppresses cytokine-mediated
immune responses.
5.2.3 Antioxidant activity of delphinidin
Effects of delphinidin against oxidized low-density lipoprotein (oxLDL)
-induced damage in human umbilical vein endothelial cells (HUVECs) was
investigated. Delphinidin was found to markedly restore the oxLDL-induced
viability loss in HUVECs in a concentration-dependent manner. In another study,
density functional theory calculations were done to evaluate the antioxidant
activity of delphinidin. One-step H atom transfer rather than sequential proton

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loss-electron transfer or electron transfer-proton transfer would be the most
favored mechanisms for explaining the antioxidant activity of delphinidin in
nonpolar solvents as well as in aqueous solution. Delphindin enhanced the levels
of p27, suppressed by hydrogen peroxide in the tested cell line. Hydrogen
peroxide and delphinidin seem to regulate intracellular levels of p27 through the
regulating HIF-1 level that is in turn, governed by its upstream regulators
comprising of PI3K/Akt/mTOR signaling pathway. In another study,
anthocyanidins showed significant scavenging activity against different free
radicals including delphinidin that was found to be the most active in the tested
concentration.
5.2.4 Hepatoprotective activity of delphinidin
The hepatoprotective effects of delphinidin in carbon tetrachloride (CCl (4))
-induced liver fibrosis in mice was investigated. Delphinidin has successfully
attenuated oxidative stress, increased matrix metalloproteinase-9
andmetallothionein I/II expression and restored hepatic architecture. The
therapeutic effect of delphinidin is mainly attributed to hepatic stellate cells
(HSC) inactivation and down-regulation of fibrogenic stimuli with strong
enhancement of hepatic regenerative power.
5.2.5. CNS activity of delphinidin
Neuroprotective effects of delphinidin against abeta-induced toxicity were
investigated. Delphinidin rescued PC12 cells from abeta by attenuating the
elevation of intracellular calcium levels and tau phosphorylation. Effect of
delphinidin isolated from Vaccinium myrtillus on retinal ganglion cells (RGCs)
against retinal damage were investigated in-vitro and in-vivo. Delphinidin
significantly inhibited SIN-1-induced neurotoxicity and radical activation in
RGC-5 and inhibited lipid peroxidation in mouse forebrain homogenates in a
concentration dependant manner. Neuronal SNARE proteins mediate
neurotransmitter release at the synapse by facilitating the fusion of vesicles with
the presynaptic plasma membrane. SNARE zippering can be modulated in the
midways by wedging with small hydrophobic molecules where as delphinidin and
cyanidin inhibited N-terminal nucleation of SNARE zippering.
5.2.6. Effect of delphinidin on enzymes and other metabolic pathways
The effect of delphinidin on human Glyoxalase I (GLO I) were investigated
and exhibited the most potent inhibitory effect on human Glyoxalase I (GLO I)
revealing its potential for the development of novel GLO I inhibitory anticancer
drugs. Delphinidin affects the catalytic activity of topoisomerase-II alpha in a
redox-independent manner. Delphinidin also diminished the DNA-damaging
properties of topoisomerase II poisons in HT29 cells without affecting the level of
sites sensitivity to formamidopyrimidine-DNA-glycosylase. Delphinidin was
found to have Schistosoma mansoni NAD (+) catabolizing enzyme (SmNACE)
inhibitory potential in a sensitive and robust fluorometric high-throughput
screening assay. Delphinidin inhibited TNF-alpha-induced COX-2 expression in

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JB6 P+ mouse epidermal (JB6 P+) cells in another study. Delphinidin inhibited
the TNF-alpha-induced phosphorylations of JNK, p38 MAP kinase, Akt, p90RSK,
MSK1, and ERK, and subsequently blocked the activation of the eukaryotic
transcription factors AP-1 and NF-kappaB. Effect of delphinidin (Dp) using
soybean lipoxygenase-1 and human neutrophil granulocyte 5-lipoxygenase were
investigated and found that Dp 3-O-glucoside (Dp3glc) and Dp 3-O-galactoside
(Dp3gal) revealed the most effective soybean lipoxygenase-1 inhibition. Alpha
isoform of estrogen receptor (ERalpha) deficient mice were used to determine the
endothelium-dependent vasorelaxation effect of delphinidin. Delphinidin is able
to induce endothelial vasodilation in aorta from ERalpha Wild-Type but not from
Knock-Out mice, by activation of nitric oxide (NO) pathway in endothelial cells.
Competitive radioligand binding assays to identified delphinidin as ligands with
moderate affinity to human cannabinoid receptor 1 were also investigated in
another study. In another study, anthocyanins and anthocyanidins were exposed
to the human efflux transporters multidrug resistance protein 1 (MDR1) and
breast cancer resistance protein (BCRP), using dye efflux, ATPase and, for BCRP,
vesicular transport assays. Results showed that delphinidin interacted with the
BCRP transporter. In another study, delphinidin was found to strongly inhibit
the protein tyrosine kinase activity of receptor tyrosine kinases at low micromolar
concentrations. In another study, photometric assay was used to screen the
inhibitory ability of delphinidin against phospholipase enzyme.
Antiangiogenic properties and antioxidant activities of delphinidin form
Vaccinium myrtillus were investigated. These anthocyanidins
concentration-dependently inhibited vascular endothelial growth factor
(VEGF)-induced tube formation in a co-culture of human umbilical vein
endothelial cells (HUVECs) and fibroblasts. Effect of delphinidin as a inhibitors
of spermidine-induced pro-Plasma hyaluronan-binding protein (PHBP)
autoactivation were investigated and was found to be potent and selective, and
did not inhibit heparin-induced pro-PHBP. In another study, delphinidin chloride
showed instability in the Dulbecco’s modified Eagle’s medium (DMEM), RPMI
1640 (RPMI) and Minimal Essential Medium Eagle (MEM)) culture media’s. The
absorption and metabolism of the 3-monoglucosides of delphinidin in healthy
human subjects were investigated to examine the effect of red wine extract on
plasma antioxidant status and on monocyte chemoattractant protein 1 production.
In another study, a scheme of genetic control of anthocyanidin biosynthesis in
sweet pea flowers is proposed by the Gene E1 is involved in the biosynthesis of
trihydroxylated delphinidin. In another study it was found that delphinidin had a
strong interaction with soybean seed ferritin.[11]

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6. Eugenol
Eugenol is an allyl chain-substituted guaiacol, a member of
the allylbenzene class of chemical compounds. It is a colorless to pale yellow,
aromatic oily liquid extracted from certain essential oils especially from clove
oil, nutmeg, cinnamon, basil and bay leaf. It is present in concentrations of
80–90% in clove bud oil and at 82–88% in clove leaf oil. Eugenol has a pleasant,
spicy, clove-like scent. The name is derived from Eugenia caryophyllata, the
former Linnean nomenclature term for cloves.[12]
6.1 Sources:
Guava, Clove buds, Cinnamon bark and leaves, Tulsi leaves, Turmeric,
Pepper, Ginger.
6.2 Health benefits:
6.2.1 As an antiseptic and anti-inflammatory:
As Eugenol is antiseptic and anti-inflammatory, it is used in dentistry to
destroy the germs and relieve the pain in teeth and gums during tooth extractions,
fillings and root canal treatment. It is combined with zinc peroxide to form a
filling in root canal treatment and is also used as a local anesthetic in dentistry.
According to the study titled,” Anti-inflammatory and antinociceptive activities of
eugenol in experimental animal models”, it had been found that eugenol has
anti-inflammatory and peripheral antinociceptive activities. The
anti-inflammatory activity was evaluated by carrageenan-induced paw edema
tests in rats.
6.2.2 Anti-microbial and antifungal properties:
Eugenol possesses antimicrobial and antifungal properties and so it fights
against bacteria and reduce the growth of various fungi including Candida
albicans. So it is used to fight numerous fungal infections in the skin, ears and
vagina. Further, it is also mainly responsible for the antifungal activity of clove
oil.
According to a study named,” Eugenol (an essential oil of clove) acts as an
antibacterial agent against Salmonella typhi by disrupting the cellular
membrane”, the antibacterial property of Eugenol against the bacteria
Salmonella typhi was evaluated. Eugenol when treated on Salmonella typhi
completely inactivated the bacteria within 60 minutes of exposure.

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In the study “Antimicrobial activities of Eugenol and Cinnamaldehyde
against the human gastric pathogen Helicobacter pylori”, it was found
that Eugenol is very efficient against the bacteria Helicobacter pylori, which is
responsible for gastric diseases such as gastritis, peptic ulcer and gastric
malignancy.
According to the study titled “Investigation on mechanism of antifungal
activity of eugenol against Trichophyton rubrum”, the antifungal activity of
eugenol against Trichophyton rubrum was examined and it was found that
eugenol inhibited the growth of Trichophyton rubrum, mycelia growth and
conidial germination.
Thus, eugenol is effective against Trichophyton rubrum which is responsible
for dermatophytosis.
6.2.3 Anti-cancer properties:
In the research article, “Eugenol Enhances the Chemotherapeutic Potential of
Gemcitabine and Induces Anticarcinogenic and Anti-inflammatory Activity in
Human Cervical Cancer Cells “, it was made clear that Eugenol exhibits
anticancer properties.
6.2.4 Anti-ulcerogenic properties:
In the study” Preventive effect of eugenol on PAF and ethanol-induced gastric
mucosal damage”, the anti-ulcerogenic effect of eugenol was examined and it was
found that eugenol pretreatment inhibits platelet activating factor and ethanol
that were induced on Gastric ulcers. Eugenol reduces the number of ulcers and
the gravity of lesions.
6.2.5 Anti-oxidant properties:
Eugenol is a very effective fat-soluble anti-oxidant which inhibits the fat
peroxide to accumulate in red blood cells and helps the anti-oxidant enzymes of
the body to act at normal level.
In the research article” Assessment of antioxidant activity of eugenol in vitro
and in vivo”, the antioxidant activity of eugenol was examined and it was found
that it exhibits antioxidant activity by granting protection against free radical
mediated lipid peroxidation.
6.2.6 Prevents Cardio-vascular diseases:
Due to its strong antimicrobial properties, Eugenol is one of the efficient blood
purifiers. It inhibits the abnormal clotting of blood platelets and it protects the
body from cardio-vascular diseases.[13]

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7. Gallic acid
Gallic acid (also known as 3,4,5-trihydroxybenzoic acid) is
a trihydroxybenzoic acid with the formula C6H2(OH)3CO2H. It is classified as
a phenolic acid. It is found in gallnuts, sumac, witch hazel, tea leaves, oak bark,
and other plants.[1] It is a white solid, although samples are typically brown
owing to partial oxidation. Salts and esters of gallic acid are termed "gallates".[14]
7.1 Sources:
Mango, Bell Peppers, Nuts, Tea
7.2 Health benefits:
7.2.1 Antimicrobial activity
Structure-activity relationship studies of phenolic acids show that some
parameters such as the basic chemical structure, the position, and the number of
hydroxyl groups as well as their substituents on the phenolic ring, and the
esterification of the carboxyl group, can affect the antimicrobial activity.
Generally, hydroxycinnamic acids have higher antibacterial activity compared
with hydroxybenzoic acids. Hydroxybenzoic acids with a lower degree of
hydroxylation in phenol groups, highly methoxylated phenol groups, highly
oxidized phenol groups, or ester derivatives with long alkyl chains showed higher
antibacterial activities in comparison with their parent structures. On the other
hand, hydroxybenzoic acids with more free –OH groups on the phenol ring were
found more potent against the human immunodeficiency virus (HIV) and
hepatitis C virus (HCV).
From the mechanistic point of view, gallic acid can inhibit motility, adherence
and biofilm formation of Pseudomonas aeruginosa, Staphylococcus
aureus, Streptococcus mutans, Chromobacterium violaceum, and Listeria
monocytogenes. The compound can also disrupt the integrity of the cell
membrane in Gram-positive and Gram-negative bacteria and change the charge,
hydrophobicity, and permeability of the membrane surface. Gallic acid can
interfere with the membrane permeability of Campylobacter jejuni and elevate
the antibiotic accumulation in the microorganism. Moreover, it can disintegrate
the outer membrane of Gram-negative bacteria via chelation of divalent cations.
In addition to its effects on the bacterial cell membrane, there are some
reports on the inhibitory activity of gallic acid against bacterial dihydrofolate

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reductase and its excitatory activity on topoisomerase IV-mediated DNA cleavage
in different bacteria. Alkyl gallates can also penetrate the bacterial cell
membrane and interfere with the electron transport chain and cellular
respiration.
Some ester derivatives of gallic acid, i.e., octyl gallate, use the hydrophilic
catechol part as a hook to bind to the polar surface of the cell membrane and
enter the lipid bilayer using the hydrophobic alkyl part. Subsequently, they act as
a nonionic surfactant and interfere with the selective permeability of cell
membrane in fungi.
Gallic acid can inhibit HIV-1 integrase, HIV-1 transcriptase, HIV-1 protease
dimerization, HCV attachment and penetration, HCV replication, HCV serine
protease, the herpes simplex virus (HSV)-1 and HSV-2 attachment and
penetration. It also causes disruption in Haemophilus influenza A and B
particles.
In connection with protozoa, gallic acid can bind to the glutamate-gated
chloride channels in the nervous system of Caenorhabditis elegans and initiates
the hyperpolarization of the cell membranes and excitation of muscles. These
events finally result in worm paralysis and death.
Gallic acid, alkyl gallates and chitosan-based formulations of gallic acid can
potentiate the antimicrobial activity of other antibiotics, including erythromycin,
gentamicin, norfloxacin, ciprofloxacin, ampicillin, penicillin, and oxacillin via
synergism.
7.2.2 Anticancer activity
In normal physiological conditions, the cells of a healthy organism are
programmed for collaboration and coordination, thereby disruption in cells can
evoke different life-threatening diseases, such as cancer. At the cellular level,
cancer is defined as an unusual increase of cell division, the resistance of the
produced cells to death, and their tendency to invade and metastasize.
The cancerous cells disturb the normal functions of other cells by invasion or
metastasis. No matter where the origin of the problem is, the overall quality of
life is overshadowed by cancer. According to the official reports of health- and
wellness-related organizations, the magnitude of personal and social
consequences of cancer is very significant and the investigation of new drugs to
control this problem continues.
Gallic acid can exert its cytotoxic and antitumor effect via modulation of
antioxidant/pro-oxidant balance. In some cases, the compound can control the
reactive oxygen species (ROS)-induced carcinogenesis through increasing the
activity of superoxide dismutase (SOD), catalase (CAT), glutathione reductase
(GR), and glutathione peroxidase (GPx) and/or by reducing the lipid peroxidation
and ROS production. In other cases, gallic acid can induce the cell cycle arrest,

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autophagy, and apoptosis via activating the caspases pathway and ROS
generation. In addition, it can inhibit the invasion and metastasis by decreasing
the matrix metalloproteinase expression and activity.
Moreover, some derivatives of gallic acid, such as isobutyl
gallate-3,5-dimethyl ether and methyl gallate-3,5-dimethyl ether, are able to
reduce the tumor size and increase the survival rate in in vivo models of cancer
(44). Gallic acid regulates the cell-cycle-related proteins such as cyclin A, cyclin
D1, and cyclin E, and slow down the cell division by induction of the p27KIP
enzyme and inhibition of CDK activity. In the case of hepatocellular carcinoma,
gallic acid decreased the tumor size and the serum level of tumor marker
enzymes such as aspartate transaminase (AST), alanine transaminase (ALT),
lactate dehydrogenase (LDH), alkaline phosphatase (ALP), and gamma-glutamyl
transferase (GGT) by inhibiting the proliferation of hepatic cells.
7.2.3 Gastrointestinal diseases
Gallic acid protects the mucosal layer of the gastrointestinal tract from ulcer
via different mechanisms by reducing the acid secretion, inducing the release of
endogenous antioxidant agents and defensive factors (i.e. SOD, CAT, endothelial
nitric oxide synthase (e-NOS) and prostaglandin E2 (PGE2)), as well as
decreasing oxidative stress and lipid peroxidation. In addition, gallic acid has
been associated with several other beneficial pathways including reduction of the
expression of pro-inflammatory mediators (i.e., tumor necrosis factor (TNF)-α and
inducible nitric oxide synthase (i-NOS)), up-regulation of the pro-angiogenesis
factors (i.e., Von Willebrand factor (vWF) VIII, mucosal hepatocyte growth factor
(HGF) and vascular endothelial growth factor (VEGF)), promotion of angiogenesis,
and inhibition of the expression of apoptosis parameters (i.e., caspase-3 and
caspase-9).
Gallic acid interferes with various intra-cellular inflammatory pathways that
induce ulcerative colitis. The compound inhibits the expression of nuclear
transcription factors, such as nuclear factor (NF)-κB and signal transducer and
activator of transcription 3 (STAT3), and down-regulates their inflammatory
downstream targets. It also reduces the expression and/or activity of
pro-inflammatory cytokines and inflammatory proteins, including TNF-α,
interferon-γ (INF-γ), interleukin (IL)-1β, IL-6, IL-17, IL-21, IL-23, cyclooxygenase
(COX)-2, and i-NOS, and decreases the expression and infiltration of neutrophils
and CD68+ macrophages into the colon.
Gallic acid inhibits the lipid peroxidation and malondialdehyde production by
inducing transcription factors (i.e., Nrf2) and its cytoprotective downstream
targets including NAD(P)H quinone dehydrogenase 1 (NQO1) and
UDP-glucuronosyltransferase (UDP-GT).
Beside the gastroprotective activity, gallic acid ameliorates the hepatotoxic
effects of xenobiotic agents by acting as an antioxidant compound that scavenges
free radicals, such as ROS, and improves the capacity of antioxidant defense

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systems including SOD, GST, GPx, CAT, GSH, and cytochrome P450-dependent
detoxifying enzymes.
7.2.4 Cardiovascular diseases
Myocardial ischemia is defined as a condition that is caused by an imbalance
between oxygen supply and demand of the myocardium, of which coronary artery
atherosclerosis is known to be the main cause. To decrease the risk of myocardial
infarction, the ischemia can be treated using different surgical methods and/or
pharmacological agents.
Gallic acid pretreatment decreases the harmful oxidative consequences of
myocardial infarction in the context of its antioxidant potency, either by
increasing the activity of antioxidant enzymes, such as SOD, CAT, GST, and GPx
and/or by elevation of the level of non-enzymatic antioxidant agents, such as GSH,
vitamin C, and vitamin E. All of these activities can inhibit the detrimental
effects of free radicals on the integrity and function of myocytes membranes, and
consequently, the concentration of serum cardiac biomarkers, including cardiac
troponin T (cTnT) and creatine kinase-MB (CK-MB) decreases after infarction.
7.2.5 Metabolic diseases
Obesity, diabetes mellitus, and hyperlipidemia are the most prevalent
metabolic disorders among adults. The ability to store the excess energy in
adipocytes and release it in the future is vital for survival. However, genetic
susceptibility, excessive energy intake and sedentary lifestyle may provoke
increased adipose storage and further cause metabolic disorders.
In metabolic disorders, gallic acid inhibits diet-induced hyperglycemia and
hypertriglyceridemia, reduces the size of adipocytes, and protects pancreatic
β-cells by inducing the expression of peroxisome proliferator-activated receptor-γ
(PPAR-γ), a nuclear transcription factor that induces differentiation and insulin
sensitivity in adipocytes. Gallic acid also increases the cellular glucose uptake via
stimulation of the phosphatidylinositol 3-kinase (PI3K)/p-Akt signaling pathway
and translocation of insulin-stimulated glucose transporters, such as GLUT4,
GLUT2, and GLUT1.
The compound prevents the diet-induced oxidative stress by stimulating
various enzymatic and non-enzymatic antioxidant defenses. Gallic acid can
up-regulate the hepatic glycolysis enzymes, such as hexokinase, aldolase, and
phosphofructokinase, and down-regulate the hepatic gluconeogenesis enzyme,
named fructose-1,6-bisphosphatase, in rodents fed a high fructose diet.
7.2.6 Neuropsychological diseases
Alzheimer’s disease is a cognitive neurodegenerative problem, which
commonly results in dementia in elderly individuals. Insidious memory loss and
progressive dementia over the years are the major clinical presentations of

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patients. In this disease, the atrophy of the brain starts from the temporal lobe
and spreads to the parietal and frontal lobes. In the microscopic scale, plaques of
amyloid-β (Aβ) molecules and fibrillary tangles of hyperphosphorylated tau
filaments are visible in the nervous system.
The protective effect of gallic acid on nerve cells is a controversial issue. On
the one hand, gallic acid decreases the Aβ-induced toxicity in cultured cortical
neurons of rats via inhibiting Ca2+
release from the endoplasmic reticulum into
the cytoplasm or Ca2+
influx, inhibiting ROS generation and apoptosis. The
compound restores the streptozotocin (STZ)-induced cerebellar oxidative stress
and cognitive impairment in rats by scavenging free radical molecules such as
ROS, inhibiting lipid peroxidation, and stimulating the activity of endogenous
antioxidant agents, such as SOD, CAT, and GPx. Gallic acid is also able to
reverse the scopolamine-induced amnesia in mice, probably through inhibiting
oxidative stress and decreasing acetylcholinesterase (AChE) enzyme activity in
the brain.
On the other hand, gallic acid decreases the viability of PC-12 rat
pheochromocytoma cells in the H2O2-induced toxicity model. In this manner,
gallic acid increases the rate of apoptosis via stimulation of the c-Jun N-terminal
kinase (JNK) protein, down-regulation of Bcl-2 protein, inducing poly
(ADP-ribose) polymerase cleavage, or even increasing intracellular Ca2+
and ROS
generation.[15]

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8. -Orzanol
-Oryzanol is a mixture of lipids derived from rice (Oryza sativa). -Oryzanol
occurs mainly in the fat fraction of rice bran and rice bran oil.
Originally thought to be a single chemical compound, it is now known to be a
mixture of ferulic acid esters of phytosterols and triterpenoids, particularly
cycloartenyl ferulate, 24-methylenecycloartanyl ferulate, and campesteryl
ferulate, which together account for 80% of -oryzanol.[16]
Major constituents of -Oryzanol[16]
Names Chemical structure Molecular formula
Cycloartenyl ferulate
Oryzanol A
C40H58O4
24-Methylenecycloartanyl
ferulate
Oryzanol C
C41H60O4
Campesteryl ferulate C38H56O4
8.1 Source:
Rice
8.2 Mechanisms of Action
Researchers believe that gamma oryzanol could decrease cholesterol by:
 Decreasing the uptake of cholesterol by gut cells.
 Decreasing HMG-CoA reductase activity. HMG-CoA reductase is an
enzyme that promotes cholesterol production.
 Blocking the formation of micelles, which are small aggregates of
molecules that often contain cholesterol.
Researchers further believe that this supplement could lower inflammation by:

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 Decreasing NF-kB – the master-regulator of inflammation.
 Decreasing inflammatory molecules PGE2, COX-2, TNF-alpha, and IL-6.
 Lowering CRP – a marker of chronic low-grade inflammation.
8.3 Health benefits:
8.3.1 Blocks the uptake of cholesterol
Gamma oryzanol blocks the uptake of cholesterol by gut cells, as it
decreases HMG-CoA reductase, an enzyme that promotes cholesterol production.
This supplement also increases cholesterol removal by bile acids.
In 30 men with high cholesterol, rice bran oil, with varying amounts of
gamma oryzanol, was able to lower total and LDL cholesterol levels. However,
there was little difference between the cholesterol-lowering effects of the high and
low gamma oryzanol-containing rice bran oil.
Gamma oryzanol decreased total cholesterol and LDL cholesterol levels in 20
schizophrenia patients with high cholesterol.
In another study, this supplement lowered cholesterol and improved fat
metabolism in rats fed a high-cholesterol diet.
The compound was effective in lowering LDL-cholesterol levels and
increasing HDL-cholesterol in rats. Low HDL and high LDL-cholesterol increase
the risk of heart disease.
Gamma oryzanol decreased cholesterol levels in hamsters with high
cholesterol.
It also lowered cholesterol absorption by 20% and increased cholesterol
removal by bile acids in rats.
8.3.2 Muscle Strength
A study of 30 healthy participants found that gamma oryzanol improved
bench press and leg curl results, showing that the supplement may have
improved muscle strength during resistance training.
However, another study on 22 weight-trained men showed that nine weeks of
gamma oryzanol supplementation did not influence performance.
8.3.3 Atherosclerosis
Rice bran enzymatic extract (containing gamma oryzanol) lowered cholesterol
and prevented atherosclerotic plaque development in atherosclerosis-prone mice
on a high-fat diet.

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This compound decreased cholesterol and reduced “aortic fatty streaks” in
hamsters. Fatty streaks are the first visible damage in the hardening of the
arteries.
However, it was ineffective in treating the hardening of the arteries
(atherosclerosis) in rabbits.
8.3.4 Diabetes
Gamma oryzanol improved glucose levels in mice by improving the function
and survival of pancreatic beta cells (cells that release insulin).
This compound directly acts on pancreatic cells to enhance glucose-stimulated
insulin release.
Also, it directly enhances glucose uptake by fat cells (adipocytes).
This supplement effectively prevented the decrease of adiponectin levels in
mice. Low adiponectin is a risk factor for diabetes.
Gamma oryzanol increased insulin sensitivity in rats with type 2 diabetes.
When pregnant mice are fed a high-fat diet, their offspring develop insulin
resistance. Gamma oryzanol given to pregnant mice prevented the development
of insulin resistance in the offspring.
8.3.5 Obesity
A study performed on rats suggests that gamma oryzanol can combat obesity
by blocking dopamine receptors (D2R) in the brain (striatum). These receptors
are part of the brain reward system. They are increased by a high-fat diet,
resulting in hedonic overeating.
This compound reduced the preference for dietary fats, and
reduced obesity and fat accumulation in rats fed a high-fat and high-fructose
diet.
It also decreased the production of fat cells (adipocytes).
8.3.6 Skin Health
When delivered under the skin via an injection, gamma oryzanol protected
against skin-aging and improved wrinkles in 15 people and UV radiation-exposed
rats.
Also, when it was incorporated into a cream and applied to the skin, it
hydrated and lightened the skin.

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8.3.7 Osteoporosis
This compound increased bone density and calcium content in a rat model of
osteoporosis (female rats that had their ovaries removed).
Another study found that it increased bone formation-related genes in rats
(SP7/OSX, POSTN, RUNX2, and COL1 and.
8.3.8 Inflammation
In rats, gamma oryzanol decreased inflammatory mediators such as PGE2,
TNF-alpha, and IL-6.
This supplement reduced lung inflammation in rats with sepsis.
It also decreased IL-6 and a marker of chronic low-grade inflammation, CRP,
in rats with metabolic syndrome.
Gamma oryzanol also decreases other inflammatory parameters, such
as COX-2 and Nf-kB.
8.3.9 Anaphylaxis
Anaphylaxis is an extreme allergic reaction characterized by swelling and
difficulty breathing.
A component of gamma oryzanol called cycloartenol ferulate was able to
reduce mast cell degranulation (mast cells release histamine and other
inflammatory agents), which decreased the anaphylaxis reaction in rats.
8.3.10 Hair Growth
A rice bran extract containing gamma oryzanol promoted hair growth and the
formation of new hair follicles in mice.
8.3.11 Immune Response
This supplement increased cytokines IL-8 and CCL2 and enhanced the
activity of macrophages ( a type of white blood cell) important for the innate
immune responses.
8.3.12 Heavy Metal Toxicity
This compound protected mice against cadmium-induced testicular toxicity
and oxidative stress.
8.3.13 Ulcers
In a couple of studies, gamma oryzanol prevented stress-induced ulcers in rats .

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8.3.14 Cancer Research
Gamma oryzanol inhibited colon tumor growth in mice, probably by:
 Increasing natural killer (NK) cell activity
 Increasing cytokines TNF-alpha, IL-1beta, and IL-6
 Reducing blood supply to the tumor
Cycloartenol ferulate, a component of gamma oryzanol, reduced the growth of
skin tumors in mice.
Gamma oryzanol inhibited the growth of human prostate cancer cells.[17]

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9. Linalool
Linalool refers to two enantiomers of a naturally
occurring terpene alcohol found in many flowers and spice plants. These have
multiple commercial applications, the majority of which are based on its pleasant
scent (floral, with a touch of spiciness).The word linalool is based on linaloe (a
type of wood) and the suffix -ol. It has other names such as β-linalool, linalyl
alcohol, linaloyl oxide, allo-ocimenol, and 3,7-dimethyl-1,6-octadien-3-ol.Over 200
species of plants produce linalool, mainly from the families Lamiaceae (mint and
other herbs), Lauraceae (laurels, cinnamon, rosewood), and Rutaceae (citrus
fruits), but also birch trees and other plants, from tropical to boreal climate zones.
Also some fungi produce this chemical.[18]
9.1 Sources:
Coriander seed
9.2 Health benefits:
9.2.1 Anti-Inflammatory and Pain Reducer: Linalool is useful for dampening
overractive responses to injury or sickness.
9.2.2 Anti-Epileptic: Linalool is "very powerful in it's anticonvulsant quality"
9.2.3 Stress Reducer: Linalool inhalation has been shown to act as an anxiolytic
(anxiety reducer) and may boost immune system performance.
9.2.4 Vampire Deterrent: Linalool can deter mosquitos with 93% efficiency.
9.2.5 Sedative: Linalool can improve sleep and increase energy the following
morning!
9.2.6 Anti-Microbial Modulator: Linalool may improve anti-microbial
properties.[19]

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10. Lutein & Zeaxanthin
Lutein
Lutein( from Latin luteus meaning "yellow") is a xanthophyll and one of 600
known naturally occurring carotenoids. Lutein is synthesized only by plants, and
like other xanthophylls is found in high quantities in green leafy vegetables such
as spinach, kale and yellow carrots. In green plants, xanthophylls act to
modulate light energy and serve as non-photochemical quenching agents to deal
with triplet chlorophyll (an excited form of chlorophyll), which is overproduced at
very high light levels, during photosynthesis.[20]
Zeaxanthin
Zeaxanthin is one of the most common carotenoid alcohols found in nature. It
is important in the xanthophyll cycle. Synthesized in plants and some
micro-organisms, it is the pigment that gives paprika (made from bell
peppers), corn, saffron, wolfberries, and many other plants and microbes their
characteristic color.[21]
10.1 Sources:
Peppers, Spinach, Pumpkin, String Bean/ Green Bean, Carrots, Okra,
Coriander seeds
10.2 Health benefits:
10.2.1 They’re Important Antioxidants
Lutein and zeaxanthin are powerful antioxidants that defend your body
against unstable molecules called free radicals.

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In excess, free radicals can damage your cells, contribute to aging and lead to
the progression of diseases like heart disease, cancer, type 2 diabetes and
Alzheimer’s disease.
Lutein and zeaxanthin protect your body’s proteins, fats and DNA from
stressors and can even help recycle glutathione, another key antioxidant in your
body.
Additionally, their antioxidant properties may reduce the effects of “bad” LDL
cholesterol, thus decreasing plaque build-up in your arteries and reducing your
risk of heart disease (1Trusted Source, 4Trusted Source, 5Trusted Source).
Lutein and zeaxanthin also work to protect your eyes from free radical
damage.
Your eyes are exposed to both oxygen and light, which in turn promote the
production of harmful oxygen free radicals. Lutein and zeaxanthin cancel out
these free radicals, so they’re no longer able to damage your eye cells.
These carotenoids seem to work better together and can combat free radicals
more effectively when combined, even at the same concentration.
10.2.2 Support Eye Health
Lutein and zeaxanthin are the only dietary carotenoids that accumulate in
the retina, particularly the macula region, which is located at the back of your
eye.
Because they’re found in concentrated amounts in the macula, they’re known
as macular pigments.
The macula is essential for vision. Lutein and zeaxanthin work as important
antioxidants in this area by protecting your eyes from harmful free radicals. It’s
thought that a reduction of these antioxidants over time can impair eye health.
Lutein and zeaxanthin also act as a natural sunblock by absorbing excess
light energy. They’re thought to especially protect your eyes from harmful blue
light.
10.2.3 Below are some conditions with which lutein and zeaxanthin may help:
 Age-related macular degeneration (AMD): Consumption of lutein and
zeaxanthin may protect against AMD progression to blindness.
 Cataracts: Cataracts are cloudy patches at the front of your eye. Eating foods
rich in lutein and zeaxanthin may slow their formation.
 Diabetic retinopathy: In animal diabetes studies, supplementing with lutein
and zeaxanthin has been shown to reduce oxidative stress markers that
damage the eyes.

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 Eye detachment: Rats with eye detachments who were given lutein injections
had 54% less cell death than those injected with corn oil.
 Uveitis: This is an inflammatory condition in the middle layer of the eye.
Lutein and zeaxanthin may help reduce the inflammatory process involved.
 The research to support lutein and zeaxanthin for eye health is promising,
but not all studies show benefits. For example, some studies found no link
between lutein and zeaxanthin intake and the risk of early onset age-related
macular degeneration.
10.2.4 May Protect Skin
Only in recent years have the beneficial effects of lutein and zeaxanthin
on skin been discovered.
Their antioxidant effects allow them to protect your skin from the sun’s
damaging ultraviolet (UV) rays.
A two-week animal study showed that rats who received 0.4% lutein- and
zeaxanthin-enriched diets had less UVB-induced skin inflammation than those
who received only 0.04% of these carotenoids.
Another study in 46 people with mild-to-moderate dry skin found that those
who received 10 mg of lutein and 2 mg of zeaxanthin had significantly improved
skin tone, compared to the control group.
Furthermore, lutein and zeaxanthin may protect your skin cells from
premature aging and UVB-induced tumors.[22]

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11. Lycopene:
Lycopene (from the neo-Latin Lycopersicum, the tomato species) is a bright
red carotenoid hydrocarbon found in tomatoes and other red fruits and
vegetables, such as red carrots, watermelons, grapefruits, and papayas, but it is
not present in strawberries or cherries. Although lycopene is chemically a
carotene, it has no vitamin A activity.[23]
11.1 Sources:
Watermelon, Tomato, Peppers, Guava, Papaya
11.2 Health benefits:
11.2.1 Heart Disease
Free radical damage plays a large role in heart disease. Antioxidants help in
general, but lycopene has unique potential among them.
In an observational study of 1,379 European men, high blood levels of
lycopene, but not other carotenoids, correlated with fewer heart attacks. In line
with this, low lycopene blood levels were associated with heart disease in an
observational study of 210 men.
Other observational trials suggest that higher lycopene intake may also be
protective against atherosclerosis, a central risk factor for heart disease and
stroke.
A meta-analysis of 12 studies concluded that the intake of 25 mg of lycopene
per day effectively reduces two major heart disease risk factors: “bad” (LDL)
cholesterol and high blood pressure.
In another meta-analysis of 21 trials, higher tomato intake was associated
with lower LDL cholesterol and improved blood vessel function. It also confirmed
the beneficial effects of lycopene intake on blood pressure.

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11.2.2 Prostate Cancer Prevention
Lycopene tends to accumulate in the prostate and may play a role in prostate
cancer prevention.
In an observational study of nearly 50K men, those with higher lycopene
intake were less likely to develop prostate cancer. The link was even stronger for
a deadly type of prostate cancer. Those who ate more tomatoes had higher
lycopene blood levels, which lowered their prostate cancer risk. And once again,
other carotenoids had no effect.
A large analysis of 17 studies concluded that increased tomato consumption is
linked to 15-20% lower rates of prostate cancer. The connection between lycopene
intake and cancer rates was weaker but still significant.
The largest meta-analysis of 26 studies and over 560,000 participants
confirmed an inverse association between lycopene intake and blood levels and
prostate cancer.
Some trials found no connection, but when the authors of the above analysis
excluded low-quality clinical trials, the connection was even stronger.
11.2.3 Breast Cancer Prevention
Eating tomatoes protected against digestive cancers (stomach, colon, and
throat) in an observational study of almost 6,000 people.
In another study of over 7,000 women, high blood levels of lycopene were
associated with lower rates of breast cancer. Other carotenoids like alpha- and
beta-carotene lacked this benefit.
On the other hand, some observational studies failed to make a connection
between lycopene intake/blood levels and breast cancer.
11.2.4 Brain Health and Cognition
Dietary lycopene combined with other herbs such as ginkgo improved
cognition in a study of 622 elderly people. But ginkgo itself enhances cognition,
making lycopene’s contribution unclear.
Another study paints a clearer picture: of 193 healthy older people, those with
higher blood levels of lycopene had better cognitive function.
Lycopene prevented early cognitive decline in rats with diabetes and
Parkinson’s disease. In both cases, it worked by reducing oxidative damage in the
brain.
In another rat study, lycopene improved depressive behavior by lowering
brain inflammation. It reduced injury to the hippocampus, the brain’s hub for
memory and emotions.

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11.2.5 Sunburn Protection
In a study of 22 people, eating 40 g tomato of paste (or roughly ~12 mg
lycopene) daily for 10 weeks reduced sunburn and skin damage by 40%.
According to another research group, tomato juice lowers sunburns by almost
50% – but lycopene only accounts for half of the effect.
11.2.6 Eyesight
People with an age-related vision disease called macular degeneration have
low lycopene levels. We know numerous other carotenoids improve eyesight;
while lycopene may do the same, research is still lacking to support the claim.
11.2.7 Pain & Inflammation
In a clinical trial of 102 patients, lycopene supplements reduced the
symptoms of chronic pelvic pain syndrome.
It relieved diabetic nerve pain in rats and mice by reducing inflammatory
compounds like TNF-alpha.
11.2.8 Bone Health
According to a study in 33 postmenopasual women, those with higher blood
lycopene levels from dietary intake also had less oxidative bone damage.
Researchers didn’t measure its effects on bone composition, though.
In a rat study, a lycopene-rich diet increased bone strength better than the
typical diet. Additionally, lycopene reduced bone cell death in test tubes.

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12. Nasunin
Nasunin, the antioxidant found in the purple skin of eggplants, is a potent
antioxidant and free radical scavenger that has been shown to protect cell
membranes from damage. Nasunin helps eliminate the buildup of plaque in the
blood vessels, keeping your heart and the cardiovascular system healthy. Roast
eggplant slices in the oven with some olive oil to reap this benefit.[23]
12.1 Sources:
Brinjal/Eggplants
12.2 Health benefits:
- Act as anti-oxidant.
- May Reduce the Risk of Heart Disease.
- May Promote Blood Sugar Control.
- Could Help With Weight Loss.
- May Have Cancer-Fighting Benefits.

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13. Phytic Acid
Phytic acid is a six-fold dihydrogenphosphate ester of inositol (specifically, of
the myo isomer), also called inositol hexakisphosphate (IP6) or inositol
polyphosphate. At physiological pH, the phosphates are partially ionized,
resulting in the phytate anion.
The (myo) phytate anion is a colorless species that has significant nutritional
role as the principal storage form of phosphorus in many plant tissues,
especially bran and seeds. It is also present in many legumes, cereals, and grains.
Phytic acid and phytate have a strong binding affinity to the dietary
minerals, calcium, iron, and zinc, inhibiting their absorption.[24]
13.1 Sources:
Rice, Wheat, Kidney Bean, Soybean
13.2 Health benefits:
13.2.1 It is an Antioxidant
Phytic acid has protected against alcohol-related liver injury by blocking free
radicals and elevating antioxidant potentials.
The anti-oxidative action of phytic acid is as a result of inhibiting Xanthine
Oxidase and by ‘preventing a formation of ADP-iron-oxygen complexes’ [5]. It was
also able to protect DNA from free radicals.
Roasting/cooking foods with phytic acid improved antioxidant ability.

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13.2.2 Reduces Inflammation
Phytic acid was found to decrease the inflammatory cytokines IL-8 and IL-6,
especially in colon cells.
13.2.3 Induces Autophagy
Phytic Acid was found to induce autophagy.
Autophagy is a cellular process for degrading and recycling junk proteins.
It has recently been recognized as a principal response to cellular stress and
an important regulator of neuronal function and survival.
It plays a role in the destruction of pathogens inside our cells.
As a ‘quality control’ process, autophagy is believed to be particularly
beneficial in neurodegenerative disorders – Alzheimer’s, Parkinson’s, ALS and
Huntington’s. This is because these disorders are, in part, characterized by the
accumulation of misfolded disease-causing proteins.
Research suggests that autophagy is required for the lifespan-prolonging
effects of caloric restriction and for much of the health benefits of exercise.
Inhibiting mTOR increases autophagy, which is part of the
reason mTOR inhibition increases longevity.
13.2.4 Has Potential For Treating Multiple Cancers
Phytic acid was found to be anti-cancer against bone, prostate, ovarian,
breast, liver, colorectal, leukemia, sarcomas and skin cancers.
Mechanism: suppressing the expression of matrix metalloproteinases (MMPs)
[19] and telomerase.
13.2.5 Reduces Blood Glucose Levels
Studies show that phytate reduces blood glucose levels in mice and rats.
It works in part by slowing the rate of starch digestibility.
13.2.6 It is Neuroprotective
Neuroprotective effects of Phytic acid were found in a cell culture model of
Parkinson’s disease.
It was found to protect against 6-Hydroxydopamine-Induced dopaminergic
neuron apoptosis, which causes Parkinson’s.

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By inducing autophagy, it can also protect against Alzheimer’s and other
neurodegenerative diseases.
13.2.7 Reduces Triglycerides and Increases high-density lipoproteins (HDL)
Studies have found phytate reduces triglycerides and increases HDL
cholesterol (the good one) in rats.
13.2.8 Repairs DNA
It was found that phytic acid can enter cells and help DNA repairs breaks in
the strands. This is a potential mechanism by which phytate prevents cancer.
13.2.9 Increases Bone Mineral Density
Phytate consumption had a protective effect against osteoporosis. Low
phytate consumption is a risk factor for osteoporosis.
Adequate consumption of phytate may play an important role in the
prevention of bone mineral density loss in postmenopausal women.
13.2.10 Protects Human Skin From UVB Exposure
UVB radiation damages skin cells, which can cause skin damage, cancer and
suppression of the immune system.
Studies show that phytic acid protects cells from UVB-induced destruction
and mice from UVB-induced tumors.
13.2.11 Can Protect The Gut From Toxins
Phytic acid supplementation increased gut transit time and resulted in more
efficient absorption of nutrients (via ‘surface amplification’).
Phytate also protects intestinal cells from certain toxins – at least in pigs.
13.2.12 Helps Prevent Kidney Stones
In rats treated with phytic acid, calcifications in their kidneys were reduced,
which suggests a potential for preventing kidney stones.
Another animal study found that it inhibited the formation of calcium oxalate
stones.
In a study on humans, phytate urinary levels in a group of active calcium
oxalate stone formers were studied and compared with those found in healthy
people. Urinary phytate was significantly lower for stone formers.

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Low phytate levels may be why kidney stones are more of a problem in the
paleo world.
13.2.13 Binds to Heavy Metals, Mycotoxins, Uranium, Iron, Manganese
Phytic acid is one of a few chelating therapies used for uranium removal.
Phytic Acid reduces the toxicity of mycotoxins, which may be explained by its
antioxidant activity.
It also binds to heavy metals, iron, and manganese. Iron and manganese are
nutrients that we normally get too much of, but not always. If we do have an
excess, then that can have ill effects on our health.
13.2.14 Decreases Uric Acid/Helps Gout
By inhibiting the enzyme xanthine oxidase, phytic acid blocks the buildup of
uric acid and can help prevent gout.
13.2.15 It is Anti-HIV
Phytate was able to inhibit the replication of HIV-1 in cell lines. PA was only
beneficial on an early replicative stage of HIV-1-infection.
13.2.16 Increases The Bioavailability of Flavones
Phytate is a potential absorption enhancer for pharmaceuticals/supplements.
The oral bioavailability of isorhamnetin, kaempferol, and quercetin was
enhanced by the co-administration of phytate.
The main mechanisms are related to their enhanced aqueous solubility and
permeability in the presence of phytate.[25]

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14. Polypeptide-p
Bitter melon is one of the most commonly used vegetable that contains
polypeptide-p and is used to control diabetes naturally. Polypeptide-p or p-insulin
is an insulin-like hypoglycemic protein, shown to lower blood glucose levels in
gerbils, langurs and humans when injected subcutaneously. The p-insulin works
by mimicking the action of human insulin in the body and thus may be used as
plant-based insulin replacement in patients with type-1 diabetes.
14.1 Sources:
Bitter gourd
14.2 Health benefits:
- Helps in maintaining blood sugar levels.
- Lowers bad cholesterol levels.
- Helps in weight loss.
- Boosts immune system.

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15. Sinigrin
Sinigrin is a glucosinolate that belongs to the family of glucosides found in
some plants of the family Brassicaceae such as Brussels sprouts, broccoli, and the
seeds of black mustard (Brassica nigra). Whenever sinigrin-containing plant
tissue is crushed or otherwise damaged, the enzyme myrosinase degrades
sinigrin to a mustard oil (allyl isothiocyanate), which is responsible for
the pungent taste of mustard and horseradish. Seeds of white mustard, Sinapis
alba, will give a much less pungent mustard because this species contains a
different glucosinolate, sinalbin.
The chemical name of sinigrin is allylglucosinolate or
2-propenylglucosinolate.[26]
15.1 Sources:
Cabbage, Cauliflower, Mustard
15.2 Health benefits:
15.2.1. Anticancer Activity
The potential of sinigrin to prevent the growth of cancer cells have been well
established. Allyl isothiocyanate-rich mustard seed powder (MSP-1), was stably
stored as its glucosinolate precursor (sinigrin) in MSP-1. On addition of
water,sinigrin was readily hydrolyzed by endogenous myrosinase.
Sinigrin, itself, was not bioactive, but hydrated MSP-1 caused apoptosis and
G2/M phase arrest in bladder cancer cell lines in vitro. In an orthotopic rat
bladder cancer model, it inhibited bladder cancer growth and blocked muscle
invasion. The Jie research group studied the anti-proliferative activities of
sinigrin in a model of carcinogen-induced hepatotoxicity in rats. It was found that
sinigrin signifificantly inhibited the proliferation of liver tumor cells and the
number of surface tumors in the rat liver was lessened. Sinigrin also induced
apoptosis of liver cancer cells through up-regulation of the p53 and
down-regulation of the Bcl-2 family members and caspases. Their fifindings
indicated that the liver functions were gradually restored after treatment with

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sinigrin and it did not cause any liver toxicity. Cell cycle analysis showed that
sinigrin caused cell cycle arrest in the G0/G1 phase. The results illustrated that
sinigrin displayed anti-proliferative activity in carcinogen-induced
hepatocarcinogenesis in rats and indicated the potential of sinigrin as an
anti-cancer agent against liver cancer.
In another study, Ethiopian mustard (Brassica carinata A. Braun) and its
glucosinolate sinigrin were tested in the in vitro HL60 (human promyelocytic
leukaemia cell line) and in vivo Drosophila melanogaster systems to determine
the anti-mutagenic and anti-proliferative properties.
The antitumor activity of the B. carinata and, its major glucosinolates,
sinigrin was determined by measuring the relative inhibitory capacity of tumors
growing in HL60 cells. B. carinata showed a dose-response curve with a high
tumoricide activity in HL60 cells (IC50 value of 0.28 mg¨ mL´1).
Single sinigrin to the cell medium did not produce cytotoxic effects. When
sinigrin was hydrolyzed by the enzyme myrosinase by addition to it, exhibited
anti-proliferative activity (hydrolyzed sinigrin IC50 = 2.71 µM). They also studied
the anti-genotoxicity and the results obtained contributed to the health
properties of B. carinata and sinigrin in DNA protection. The percentage of
inhibition of B. carinata and sinigrin when are assayed against H2O2. The
addition of plant samples to the flfly food produced anti-mutagenic effects. Both of
them showed a high desmutagenic and recombinogenic potency. The lowest
concentrations assayed for B. carinata plant samples showed more anti-genotoxic
effects than those of higher (78.46% clone inhibition). For sinigrin, the highest
anti-genotoxic effect displayed percentage of inhibition of clone formation of
84.61%. Investigations were conducted on the inhibition of
dimethylhydrazine-induced aberrant crypt foci and induction of apoptosis in the
rat colon, following oral administration of the glucosinolate sinigrin to rats for
three months. An increase in apoptosis in colonic crypts was displayed, when
exposed to the carcinogen. There was no signifificant induction of apoptosis in
rats when sinigrin, alone, was fed; however, sinigrin administered after
dimethylhydrazine suppressed the induction of aberrant crypt foci. This may be
due to increased apoptotic deletion of damaged stem cells in the crypts of rats
with treated sinigrin.
The activity of sinigrin indole-3-carbinol (I3C) on DNA methylation in target
tissues of tobacco-specifific nitrosamine
4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) tumorigenesis, and also
the effect of dietary sinigrin on NNK tumorigenicity were assessed in a two-year
bioassay in F344 rats. The study reported that sinigrin decreased
7-methylguanine formation in hepatic DNA, but had no effect on
7-methylguanine levels of lung or nasal mucosa DNA. I3C increased
7-methylguanine levels in hepatic DNA, but decreased DNA methylation in lung
and nasal mucosa.

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The bioassay, suggested that sinigrin had no effects on NNK tumorigenesis in
the target tissues, but sinigrin plus NNK displayed signifificant incidence of
pancreatic tumors than in the NNK treated alone. This study concluded that,
absence of any inhibitory effect of sinigrin on NNK hepatic cells tumorigenesis,
could be due factors other than DNA methylation and O6-methylguanine repair
which can be considered in evaluating the effects of dietary compounds on NNK
hepatic tumorigenesis, and also stated that the contrary effects on NNK-induced
hepatic DNA-methylation by sinigrin and I3C shows the complexities of dietary
modulation of carcinogenesis.
In another study, the effects of sinigrin and indole-3-carbinol (I3C) on the
hepatocarcinogenesis induced by diethyl-nitrosamine (DEN) were studied in male
ACI/N rats. When rats where treated with diethyl-nitrosamine and diet
containing 1200 ppm. Sinigrin and rats fed with rats where treated with
diethyl-nitrosamine and diet containing 1000 ppm. (I3C), the incidences of
iron-excluding altered foci, liver cell tumors, and the tumor multiplicity were
signifificantly smaller than when rats when treated only with
diethyl-nitrosamine. This study suggested that sinigrin and indole-3-carbinol
inhibited the hepatocarcinogenesis induced by diethyl-nitrosamine when
delivered concurrently with the carcinogen.
The inhibitory effects of indole-3-carbinol (I3C) and sinigrin during initiation
and promotion phases of 4-Nitroquinoline 1-oxide-induced rat tongue
carcinogenesis were demonstrated in male ACI/N rats. Both I3C and sinigrin
treated during initiation and post initiation phase suppressed preneoplastic and
neoplastic lesions of the tongue epithelium induced by 4-nitroquinoline-1-oxide. It
also caused signifificant decreased in the number and area of silver-stained
nucleolar organizer regions protein, they are known as indices of cell proliferation
effects. The results indicated that I3C and sinigrin inhibited rat tongue
carcinogenesis in both the initiation and post initiation phases, followed by
treatment with 4-nitroquinoline-1-oxide. They suggested that the mechanism by
which by which I3C and sinigrin displayed their inhibitory actions on tongue
carcinoma was not clear but it could be related to the actions these compounds on
the metabolic activation, formation of DNA adduct, detoxifification of
4-nitroquinoline-1-oxide or formation of radicals.
Few speculations for the mechanisms of the anti-carcinogenesis activity of
glucosinolates have been recognized. The mechanism of the anti-carcinogenesis
activity of glucosinolates is unknown.
Blocking effects are believed to involve modulation of enzymes, which can
reduce exposure of target tissues to DNA damage. Isothiocyanates have shown to
induce the activity of phase II enzymes, including glutathione S-transferase and
quinone reductase, in the small intestinal mucosa and liver, and also to block
chemical carcinogenesis. Increased consumption of brassica vegetables induces
glutathione S-transferase in humans and increased protection against cancer.

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Another speculated mechanism of anti-carcinogenesis is suppression of tumor
development following the initiation of pre-cancerous cells. Other mechanisms of
suppression are the deletion of initiated cells from genetically-damaged tissue by
apoptosis.
Recently, our research group tested the effect of sinigrin on melanoma cells
(A-375) and in normal human keratinocytes (HaCaT). We also investigated the
use of a vesicular carrier system called phytosomes, to encapsulate sinigrin and
determine whether the phytosome complex could enhance the effects of sinigrin
on melanoma cells. Our results indicated that sinigrin alone, at higher
concentration, displayed about 46% toxicity, whilst the sinigrin-phytosome
complex inhibited cytotoxicity by 74%.
These fifindings suggested that the sinigrin-phytosome complex did enhance
the cytotoxic effects of sinigrin. It was noteworthy that sinigrin and its phytosome
complex displayed minimal toxicity towards HaCaT cells. When the anticancer
effects of sinigrin were studied by other researchers, it was noticed they exhibited
strong anticancer activity. Although the phytosome formulation increased its
activity at higher concentration, sinigrin did not exhibit much cytotoxic effect
towards A-375 melanoma cells.
15.2.2. Anti-Inflflammatory Activity
Sinigrin’s effect on the production of inflflammatory mediators in
lipopolysaccharide (LPS)-activated RAW 264.7 macrophages, have been
examined by Lee. They investigated the anti-inflflammatory effects of sinigrin on
nitrite oxide (NO) and pro-inflflammatory cytokine production by utilizing
colorimetric and ELISA assay. By using Western blot assays the researchers also
examined the expression of MAPK, NLRP-3, and p65. The results indicated that
sinigrin did not reduced the NO production, but sinigrin inhibited the levels of
tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). Sinigrin blocked
phosphorylation of JNK and p38, but not ERK. Sinigrin treatment signifificantly
suppressed the expression of p65 and NLRP-3. These results revealed sinigrin
has potential anti-inflflammatory activity, which may result from the inhibition
of MAPK phosphorylation, expression of NLRP-3 and p65, and also lowers the
production of pro-inflflammatory mediators.
The effectiveness of sinigrin against atherosclerosis (chronic inflflammatory
disease) in ApoE-defificient mice was studied. Sinigrin exhibited signifificant
repressive effects on the expression of VCAM-1 and ICAM-1 in ApoE mice. It also
mitigated the level of oxLDL, HDL, LDH, triglyceride, and cholesterol in serum.
The serum levels of sterol-regulatory element binding protein-2 (SREBP-2),
oxidized low-density lipoprotein receptor-1 (LOX-1), and liver X receptors (LXRs)
were reduced by sinigrin; it also decreased the serum levels of IL-6 and TNF-α. It
can, therefore, be concluded that sinigrin has anti-atherosclerotic activity.
Lee and Lee studied the effect of sinigrin on the expression of the vascular cell
adhesion molecule-1 (VCAM-1) in TNF-α-induced vascular smooth muscle cells

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(VSMCs). The data suggested that sinigrin suppressed the nuclear translocation
of NF-κB induced by TNF-α. Through the suppression of NF-κB signaling
pathways, sinigrin inhibited the TNF-α-stimulated VCAM-1 expression. The
result from the two above studies, it can be concluded that sinigrin acts as an
anti-atherosclerosis therapeutic agent.
15.2.3. Antibacterial Activity
Glucosinolate hydrolysis products are potent inhibitors of bacterial activity.
Sinigrin is not usually antimicrobial; when it is enzymatically hydrolyzed to form
allyl isothiocyanate it exhibited potent antimicrobial activity against food
spoilage and pathogenic organisms. Allyl isothiocyanate showed minimum
inhibitory concentrations as 25 µL/L at pH 4.5 with greater antimicrobial activity
at low pH value than at high pH 8.5 against Escherichia coli O157:H7. This
indicated a gradual reduction of the antimicrobial activity when the pH was
raised. Hence, it was suggested that allyl isothiocyanate could work better in
more acid foods. The speculated mechanism of the antimicrobial activity of
isothiocyanates could be related to intracellular inactivation of
sulphydryl-enzymes; this was concluded from the observations, where proteins
and sulphydryl compounds were able to suppress the antimicrobial effects of
diverse isothiocyanates. The thioredoxin system is known for its essential role in
DNA synthesis. It has shown the capability of allyl isothiocyanate in crossing the
plasma membrane and reaching the cytoplasm of prokaryotic and eukaryotic cells.
Hence, suggesting that the antibacterial activity of allyl isothiocyanate could be
related to the inhibition of DNA synthesis.
Allyl isothiocyanate is known to inhibit the catalysis of thioredoxin reductase
and acetate kinase, which are responsible for important metabolic reactions in
bacteria. Thus, it can be proposed that allyl isothiocyanate have many targeted
antimicrobial activity, as they can cause enzymatic inhibition and membrane
damage.
The antimicrobial activity of residual endogenous plant myrosinase in
Oriental and yellow mustard powders and a deoiled meal (which contained more
glucosinolate than unextracted mustard powder of each type of mustard), against
E. coli O15:H7 during dry-fermented sausage ripening was investigated. It was
noticed that when 4% (w/w) deodorized yellow mustard powder containing
myrosinase from hot mustard was added to the sausages, ripening required
between 18 and 24 d to reduce E. coli O157:H7 numbers. The 2% (w/w) deoiled
yellow mustard meal treatment containing myrosinase activity was as potently
antimicrobial as 4% yellow mustard powder and took 21 d to obtain the reduction.
A signifificant difference in bactericidal activity was noticed between yellow and
Oriental mustard treatments, where yellow mustard was more antimicrobial.
This may be due to the yellow mustard contained higher glucosinolate levels
than Oriental mustard. It was believed that myrosinase activity contributed to
the high antimicrobial actions of mustard when used in sausage against E. coli
O157:H7 through its hydrolysis of glucosinolates.

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In a study by Herzallah and Holley, evaluated the use of carboxymethyl
cellulose (CMC) nanoparticulate on the antimicrobial activity of CMC fifilms
containing sinigrin against E. coli O157:H7 on fresh beef. The study indicated
that the fifilms with nanoparticulation that contain sinigrin in oriental mustard
signifificantly exhibited more antimicrobial activity than fifilms without
nanoparticulation. Hence it was concluded that the nanopartiulation of CMC
signifificantly enhanced the antimicrobial effects of the fifilms having sinigrin.
Sinigrin and its degradation products, such as allyl isothiocyanate, allyl
cyanide (AC), 1-cyano-2,3-epithiopropane (CETP), and allyl thiocyanate (ATC),
were tested for antibacterial activity on nine species of bacteria and eight species
of yeasts. The results gained from this study indicated that sinigrin, AC, and
CETP at 1000 ppm were not inhibitory to any bacteria or yeast growth and allyl
isothiocyanate was the most inhibitory of the sinigrin hydrolysis products.
Brabban and Edwards reported that sinigrin was found to be innocuous to all
the organisms being tested but its hydrolysis products exhibited inhibitory effects
of growth. In this investigation rapemeal, containing potentially toxic compounds;
glucosinolates, was examined as a substrate for the growth of micro-organisms.
Before its hydrolysis the initial inhibitory sinigrin concentration was found to be
species-dependent with Bacillus subtilis being the most resistant (80 µg¨ mL´1 )
and Saccharomyces cerevisiae (40 µg¨ mL´1 ) the most sensitive one. Three
Gram-positive organisms tested were found to be more resistant to hydrolysis
products than other micro-organisms. It was observed in rapemeal media growth
inhibition was dependent on the glucosinolate content of the rapemeal. In an
investigation by Lara-Lledo and their group, the ability of Listeria
monocytogenes to convert glucosinolates present in deodorized oriental and
yellow mustard, as well as pure sinigrin, into their respective isothiocyanates
during in vitro study and on sliced bologna vaccum-packed with polyvinyl
polyethylene glycol graft copolymer packaging fifilms. During broth tests with
deodorized (myrosinase-inactivated) mustard extracts or with purifified sinigrin
inhibition was only displayed when exogenous myrosinase was added. It was
noticed that when pure sinigrin, oriental or yellow mustard extracts were
incorporated in fifilms containing 3%, 5%, and 6% (w/w) of the corresponding
glucosinolate and used to package bologna inoculated with L monocytogenes., the
pathogen was found in bologna packed with the oriental mustard extract. The
yellow mustard extract exerted less inhibition and the pure sinigrin did not show
antimicrobial activity.
15.2.4. Antifungal Activity
The potential of members of the Brassicaceae family have been shown to
produce signifificant quantities of antifungal compounds in roots. The results
indicated the glucosinolate-mediated resistance to fungi in the roots of Brassica
species. Investigations by Ocampo, have indicated that extracts from the roots of
various Brassica species and reactions of the glucosinolate sinigrin with
myrosinase inhibited the germination of Glomus mosseae spores.

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The fungitoxicity of allyl-isothiocyanate vapour against Penicillium
expansum, the agent of blue mould on pears, was studied and it was observed
that the use of allyl-isothiocyanate produced from pure sinigrin (Brassica juncea)
was effective and an alternative to synthetic fungicides against P. expansum.
15.2.5. Antioxidant Activity
The Ippoushi research group have demonstrated the sinigrin antioxidant
activity. It is known that allyl isothiocyanate is produced from sinigrin and this
suppresses nitric oxide production and the induction of inducible nitric oxide
synthase in lipopolysaccharide-activated J774.1 macrophages.
Myrosinase, in cruciferous vegetables, is not activated at the time of processes
of cooking and, therefore, cannot produce allyl isothiocyanate from sinigrin, thus
sinigrin is mainly taken by human beings and not allyl isothiocyanate. They tried
to demonstrate the in vivo suppressive effect of sinigrin administration on nitric
oxide formation induced lipopolysaccharide administration. Their study was
performed to assay the levels of urinary nitrate + nitrite and allyl isothiocyanate
in rats. The results indicated that the intake of sinigrin signifificantly reduced
urinary levels of nitrate + nitrite, an index of nitric oxide production in
lipopolysaccharide treated rats. It also revealed that sinigrin has antioxidative
properties and lowers the level of reactive nitrogen species. Generally reactive
oxygen species and reactive nitrogen species are known to be involved in the
multistage carcinogenesis process.
15.2.6. Wound Healing Activity
The wound healing properties of sinigrin were not previously studied. Our
research group recently, for the fifirst time, revealed that sinigrin has the
potential to also cure wounds. The in vitro wound healing activity was tested on
normal human keratinocytes (HaCaT). Sinigrin was also formulated using a
vesicular system called phytosome. The fifindings suggested that the
sinigrin-phytosome complex enhanced the wound healing actions of sinigrin. The
effects of sinigrin and its phytosome formulations were studied at two different
concentrations. It was observed that, at lower concentration of 0.07 mg/mL, the
sinigrin–phytosome complex displayed 79%, whilst sinigrin showed only 50% of
wound closure. At the higher concentration 0.14 mg/mL the sinigrin–phytosome
complex completely cured the wound (100%), whereas the sinigrin alone
displayed only 71% wound healing. These results confifirmed the wound healing
activity of sinigrin, which was also augmented by encapsulation in the phytosome
delivery system.[27]

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