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2.6. GM Rice
The kind that Express soybean gylcinin gene (40-50 mg gylcinin/g protein) has
been developed and is claimed to contain 20% more protein. However, the increased
protein contenet was probably due to a decrase in moisture rather than true increase in
protein putting a questionmark over the significance of this GM crop.
2.6.1. Designing Golden Rice
Rice (Oryza sativa) is a global food staple. It is eaten often and in high amounts.
Rice is usually processed to remove the husk and natural oil to leave the rice endosperm
(rice grain) for long term storage and use. The oil-rich aleurone layer is removed so that
the rice will not become rancid in storage. The rice endosperm is the edible part. While
rice is a staple food for many populations, essential nutrient content is low. Therefore, it
is a good candidate for ectopic production of β-carotene.
Rice endosperm does not naturally produce β-carotene; instead, it produces
geranylgeranyl diphosphate (GGPP) which is an early precursor of β-carotene.
Therefore it was necessary to use recombinant genetic techniques, not conventional
breeding, to develop a rice endosperm that would produce β-carotene. To convert
geranylgeranyl diphosphate to β-carotene, four additional plant enzymes were needed:
phytoene synthase, phytoene desaturase, carotene desaturase, and lycopene β-cyclase.
These enzymes were identified and their genes were isolated from various plants and
bacterium.
The phytoene desaturase and β-carotene desaturase were circumvented by using
a bacterial enzyme, carotene desaturase, that gave the combined result. The entire βcarotene biosynthesis pathway (three genes on three vectors) were transformed into rice
endosperm using Agrobacterium. The result were yellow endosperms and gained the
name Golden Rice. The yellow color was from the β-carotene formed in the endosperm.
It had refined the technique and were able to transform the β-carotene biosynthesis
pathway by either single- or co-transformations of cDNA constructs. 2 were used genes
from daffodil Narcissus psuedonarcissus (phytoene synthase and lycopene β-cyclase)
and 1 gene from a bacterium Erwinia uredovora (carotene desaturase).
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The resulting Golden Rice yielded 1.6 – 2.0 µg β-carotene/g of dry rice. With a
conversion factor of 6 µg of β-carotene to 1 µg of retinol, 200 g/day of rice would yield
70 µg/day of retinol which is not enough to fulfill the recommended daily allowance of
retinol.
Since this crop is still relatively new, further research can improve the system
and increase the levels of β-carotene produced in the rice. There have also been
considerations for crossing Golden Rice with a rice producing high iron because βcarotene helps increase the bioavailability of iron.
2.6.1.1. Golden-Iron Rice”: The Rice Of The Future
A successful example is the genetic modification of rice in order to enhance its
Vitamin A and iron content. Humans make Vitamin A from Beta-carotene, which is
found in most plants. B-carotene is one of the many carotenoids, which are yellow,
orange, and red pigments that are important in the photosynthetic membranes of all
plants. Rice in its naturally milled form does not contain B-carotene or any of its
immediate precursors. However, immature rice endosperm does synthesize the
carotenoid precursor geranylgeranyl diphosphate (GGPP) which can be converted into
B-carotene. This conversion involves the use of three essential enzymes that are not
found in the rice kernel. Scientists were able to insert the three genes encoding for these
enzymes into the rice kernel and modify it to properly use the enzymes and produce Bcarotene.The three enzymes are phytoene synthase and lycopene beta-cyclase from
daffodil, and phytoene desaturase from Erwinia uredovora bacterium.Beta-carotene is
made through the general isoprenoid synthetic pathway, which is shown in figure a.
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Figure a
Figure
b
Two molecules of GGPP are combined together to form phytoene using
phytoene synthase. Phytoene is then desaturated, using phytoene desaturase enzyme to
make lycopene. Lycopene is further cyclized, using lycopene Beta-cyclase, to make
Beta-carotene. The rice grains containing Beta-carotene are golden or saffron-coloured
as seen in figure b .
2.6.1.2. Increasing The Iron Content Of Rice
People with a high rice diet are very likely to experience iron deficiency since
rice contains a molecule called phytate. Phytate entraps 95% of the dietary iron and so
keeps the human body from absorbing it. To increase the iron content of rice, three
genes were introduced into the rice genome. The first gene encodes for the enzyme
phytase, which breaks down the phytate molecule. This enzyme can also withstand
high temperatures and so will not be denatured when the rice is cooked. The second
gene encodes for the iron storage protein called ferritin which doubles the iron level in
rice grains. The final gene encodes for a protein, which is rich in the amino acid
cysteine and helps in the iron absorption in the human digestive system.
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The final “golden-iron” rice strain was engineered by cross breeding the iron
rich rice strain with the B-carotene one to form hybrids that contained all of the new
genes.
In sum six new genes were combined with the rice genome to make the
modified rice as illustrated in figure c
It is estimated that only 300g of cooked
engineered-rice per day will be enough to provide the daily vitamin A requirement.
Figure c
2.6.1.3. Iron Fortification of Rice with the Soybean Ferritin Gene
Rice was also modified in another study to increase its iron content by the
addition of the soybean ferritin gene to the rice genome . As the chart below shows, the
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iron content of the modified seeds (Figure d) was as much as three times greater than
the original seeds.
The researchers concluded that it maybe possible to produce
“Ferritin rice” as an iron supplement in the human diet. The iron content in a meal size
portion, which is approximately 6mg of iron (Fe) per 150g of dry weight of ferritin rice,
may be sufficient to provide 30-50% of the daily adult iron requirement, which is 1315mg.
Ferritin, an iron-storage protein in animals, plants and bacteria, forms a large
complex that stores up to 4500 iron atoms. The soybean ferritin gene was transferred
into rice by Agrobacterium-mediated transformation . To accumulate iron specifically in
the seed which is the part of the plant that is eaten, the ferritin gene was linked to the
rice seed-storage protein glutelin promoter, GluB-1. Ferritin specifically accumulated in
the rice seed endosperm, resulting in a 3-fold increase in its iron content in comparison
to the untransformed rice.
Figure d
Tissues accumulating ferritin stain dark brown
(Unmodified
rice in middle and modified on right)
IRON CONTENT IN RICE TISSUES EXPRESSING FERRITIN
cDNA(micrograms-Fe/gram-dryweight)
Seed
Leaf
Stem
Root
Modified
38.1
104.8
162.8
962.1
Unmodified
14.3
119.3
170.0
956.0
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2.6.1.4. Benefits: Golden Rice as a vitamin A supplement
For the general population, Golden Rice can be beneficial because it serves as a
source of supplementary vitamin A and β-carotene. High intake of specific vitamins and
minerals, such as carotenoids, vitamin A and β-carotene, have been linked with
reducing risk of coronary artery disease, specific cancers, and macular degeneration. βcarotene is an antioxidant; therefore, it can help the protect the body from destructive
free-radical reactions.
Malnutrition is a global problem. As of 1995, 800 million people in the world
have diets are inadequate in macronutrients (carbohydrates, lipid, and protein) and
micronutrients (minerals and vitamins) . The major deficiencies include vitamin A, iron,
iodine, and vitamin E.
Specifically, vitamin A deficiency causes blindness, premature death, and
xerophthalmia (thickening on conjunctiva). Even people in the industrialized nations
suffer from vitamin and mineral deficiencies due to poor diets . Therefore, a food staple
such as rice, which is widely consumed globally, can serve as a means to address the
vitamin A deficiency. Once the Golden Rice has been enhanced and developed, it can
be cultivated, grown, and widely dispersed to eliminate vitamin A Deficiency.
2.6.2. Elevating vitamin A content by plant genetic engineering
Vitamin A (retinol) is an essential vitamin used in the retina to create pigment;
therefore, it promotes good day and night vision. Vitamin A deficiency can cause visual
impairment which can ultimately lead to blindness. It can also cause keratinization of
the mucous membranes and soft tissue such as the lungs, GI and urinary tracts. Vitamin
A deficiency is a problem in developing countries. Plants synthesize provitamin A
carotenoids, such as β-carotene, which are converted to retinol in the human body.
Natural sources of β-carotene include green leafy vegetables, yellow vegetables, and
broccoli. However, when these vegetables are cooked or processed, their nutritional
levels decline. Formed vitamin A is found as retinol in meats, milk, cheese, and butter.
High levels (5 times RDA, 800-1000 RE) of vitamin A is toxic and can lead to coma or
respiratory failure. However, it requires even higher levels of intake of β-carotene to be
toxic to the body because the provitamin has to be converted to vitamin A. The
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conversion of β-carotene to vitamin A is not fast enough to cause toxicity. β-carotene is
not toxic and can be stored by body . Therefore, researchers decided to use β-carotene
as a means to increase dietary vitamin A.
Plant genetic engineering has been developed in rice, canola seed, and tomato to
increase the levels of provitamin A cartenoids in the end food product. Golden rice has
been developed which has 1.6 µg of β-carotene / g of dry rice . canola seeds were
developed that had a 50 fold increase in cartenoids, consisting of mainly alpha and βcarotene. Transgenic tomato fruit (crtI) had a two fold increase in carteniods for a total
of 5 mg of β-carotene or 800 retinol equivalents per fruit; therefore, one ripe crtI tomato
fruit contained 45% of the RDA, while the control had 23% of the RDA for retinol.
Golden rice has the most potential to have an impact on vitamin A deficiency globally
because rice is a staple food in many populations.
2.6.2.1. Beta carotene
Beta-carotene is a member of a class of substances called carotenoids. Betacarotene, similar to the other carotenoids, is a natural fat-soluble pigment found
principally in plants, algae (Dunaliella salina, Dunaliella bardawil) and photosynthetic
bacteria, where it serves as an accessory light-gathering pigment and to protect these
organisms against the toxic effects of oxygen. Carotenoids are polyisoprenoids which
typically contain 40 carbon atoms and an extensive system of conjugated double bonds.
They usually show internal symmetry and frequently contain one or two ring structures
at the ends of their conjugated chains. Beta-carotene contains a cyclic structure at each
end of its conjugated chain. The structural formula for beta-carotene is:
Beta-Carotene
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Carotenoids are the principal pigments responsible for the red, orange, yellow
and green colors of vegetables and fruits. Beta-carotene is responsible for the color of
carrots.
Beta-carotene along with alpha-carotene, lycopene, lutein, zeaxanthin and betacryptoxanthin are the principal dietary carotenoids. Three of these carotenoids, alphacarotene, beta-carotene and beta-cryptoxanthin, can serve as dietary precursors of
retinol (all-trans retinol, vitamin A). Collectively, these carotenoids are called
provitamin A carotenoids or provitamin A. Dietary carotenoids that are not converted
into retinol (lutein, zeaxanthin, lycopene) are referred to as nonprovitamin A
carotenoids.
Beta-carotene occurs naturally as all-trans beta-carotene and 9-cis beta-carotene.
Smaller amounts of 13-cis beta-carotene are also found naturally. Synthetic betacarotene consists mainly of all-trans beta-carotene with smaller amounts of 13-cis betacarotene and even smaller amounts of 9-cis beta-carotene. Carrots are the major
contributors of beta-carotene in the diet. Beta-carotene is also found in cantaloupe,
broccoli, spinach and collard greens. Palm oil, which is used as a food colorant, is rich
in beta-carotene as well as alpha-carotene. Dietary intake of beta-carotene in the
American diet ranges from 1.3 to 2.9 milligrams daily. The consumption of five or more
servings of fruits and vegetables per day—which is recommended by a number of
federal agencies and other organizations, including the National Cancer Institute—
would provide 3 to 6 milligrams daily of beta-carotene.
Beta-carotene is considered a conditionally essential nutrient. Beta-carotene
becomes an essential nutrient when the dietary intake of retinol (vitamin A) is
inadequate. It is unclear whether beta-carotene has any biological function for humans
other than as a precursor for vitamin A. There is some evidence that beta-carotene may
play a beneficial role in human nutrition beyond its provitamin A function. Betacarotene has antioxidant activity, at least in vitro, and it may enhance intercellular
communication and may have immunomodulatory and anticarcinogenic activities in
certain circumstances. However, the evidence for a unique role in human nutrition
beyond its provitamin A function is, to date, not compelling.
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The absorption efficiency of beta-carotene and the other carotenoids from food
sources is highly variable. For this reason, it has been difficult to define a general
numerical factor for converting provitamin A carotenoids to vitamin A. There are two
systems of units which are currently used which do not agree with each other and which
have caused confusion. In the first system, 1 IU (international unit) is equal to 0.6
micrograms of all-trans beta-carotene or 1.2 micrograms of mixed other provitamin A
carotenoids. In this system, which is the one generally used for nutritional labeling, 3
milligrams of beta-carotene is equal to 5,000 IU. The U.S. RDA for vitamin A is 5,000
IU. The second system uses retinol equivalents in place of international units. In the
second system, one retinol equivalent (RE) is defined as one microgram of all-trans
retinol (vitamin A), six micrograms of all-trans beta-carotene or 12 micrograms of other
provitamin A carotenoids. In the first system, two micrograms of all-trans beta-carotene
are defined as being equal to one microgram of all-trans retinol. In the second system,
six micrograms of dietary all-trans beta-carotene are assumed to be nutritionally
equivalent to one microgram of all-trans retinol. It is clear that these two systems do not
agree with each other. In any case, all-trans carotene, as found in nutritional
supplements, should be converted according to the first system. That is, two micrograms
of all-trans carotene are equal to one microgram of all-trans retinol (vitamin A) or 3.33
IU.
2.6.2.1.1. Actıons
Beta-carotene
may
have
antioxidant
activity.
It
may
also
have
immunomodulatory, anticarcinogenic and antiatherogenic activities in some cases.
2.6.2.1.2. Mechanısm Of Actıon
Beta-carotene has been found to have antioxidant activity in vitro. It has been
demonstrated to quench singlet oxygen (O2), scavenge peroxyl radicals and inhibit lipid
peroxidation. The mechanism of beta-carotene's antioxidant activity is not clearly
understood. Some, but not all, studies have shown a difference in the in vitro activities
of the beta-carotene isomers. One study showed that 9-cis beta-carotene—a naturally
occurring form of beta-carotene—protected methyl linoleate from oxidation more
efficiently than all-trans beta-carotene. However, another study demonstrated that 9-cis
beta-carotene and all-trans beta-carotene had equal antioxidant activities when assessed
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by enhanced human neutrophil chemiluminescence. Whether beta-carotene has
significant antioxidant activity in vivo is unclear. Results from some human studies
have shown improvement of measures of antioxidant activity (decreased copperinduced LDL oxidation, decreased DNA strand breaks and oxidized pyrimidine bases in
lymphocytes, decreased serum lipid peroxide levels, decreased breath pentane,
decreased serum malondialdehyde, increased red blood cell copper/zinc-superoxide
dismutase activity) in those receiving relatively high intakes of beta-carotene. Studies of
those receiving relatively low to modest levels of beta-carotene have shown no changes
or inconsistent changes in the same antioxidant activities. Administration of betacarotene to cystic fibrosis subjects was found to decrease serum malondialdehyde, in
one study. Beta-carotene may have antioxidant activity in some with conditions of
increased oxidative stress. Retinol itself appears to have low antioxidant activity.
Therefore, possible in vivo antioxidant activity of beta-carotene is unlikely to be a
consequence of its conversion to retinol.
Beta-carotene has demonstrated some immunomodulatory effects. In healthy
male nonsmokers, beta-carotene supplementation (15 mg/day) was found to
significantly
increase
the
percentage
of
monocytes
expressing
the
major
histocompatibility complex class II molecule HLA-DR, to increase the expression of the
adhesion molecules, intercellular adhesion molecule-1 and leukocyte functionassociated antigen-3, and to increase ex vivo secretion of tumor necrosis factor (TNF)alpha by blood monocytes. Beta-carotene supplementation has also been found to
enhance natural killer cell activity in elderly men, to increase lymphocyte response to
mitogens in healthy male cigarette smokers and to increase the CD4 lymphocyte count
in some subjects with AIDS. The mechanism of the possible immunomodulatory
activity of beta-carotene is not known. It is thought that the possible immunomodulatory
activity may be independent of beta-carotene's role as a precursor of retinol.
Beta-carotene has been found to inhibit the growth of some malignant cells,
including human prostate cancer cells, in vitro. The mechanism of this activity is not
well understood. It is speculated that beta-carotene may increase cellular differentiation,
down-regulate epidermal growth factor receptors, reduce adenyl cyclase activity,
enhance expression of gap junctional proteins and protect against oxidative damage.
The ability of beta-carotene to modulate the carcinogenic process, at least in vitro, may
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be due, in part, to its conversion to retinoids. In this regard, there is evidence that betacarotene may be converted to retinol and other related metabolites (e.g., retinoic acid) in
human prostate cell lines.
Several observational epidemiological studies have shown an inverse association
between dietary beta-carotene intake and a number of cancers, in particular lung cancer.
Intervention trials, however, have not found beta-carotene to be protective against lung
cancer. In fact, two intervention trials, the Alpha-Tocopherol, Beta-Carotene (ATBC)
Cancer Prevention Study (the "Finnish study"), and the Carotene and Retinol Efficacy
Trial (CARET), both reported an unexpected increase in the number of lung cancer
cases in the groups that received supplemental beta-carotene. The subjects in the ATBC
and CARET studies were smokers. In the case of these studies, the mechanism, not of
the possible anticarcinogenic activity of beta-carotene, but of its possible
procarcinogenic activity, at least for smokers, requires elucidation. Several possible
explanations have been proposed to explain the unexpected increase in lung cancer in
these studies. Beta-carotene may act as a prooxidant when present in high
concentrations in an oxidative environment such as the lungs of smokers in the
advanced promotional stage of the neoplastic process. (Beta-carotene may be effective
in the prevention of lung cancer if chronically present before or during the phases of
initiation and early promotion of the process). Supplemental beta-carotene is known to
inhibit the absorption of the carotenoid lutein which itself may have chemopreventive
activity. Beta-carotene may have a co-carcinogenic effect. Beta-carotene has been found
in the rat lung to produce a booster effect on phase I carcinogen-bioactivating enzymes,
including activators of polycyclic aromatic hydrocarbons (PAHs). Finally, oxidative
metabolites of beta-carotene may diminish retinoid signaling and eventually enhance
carcinogenesis. The mechanism of the possible effect of beta-carotene in enhancing
lung cancer in smokers remains a mystery. The general opinion is that the effect is
related to prooxidant activity of beta-carotene or oxidative metabolites of beta-carotene
in the context of increased partial pressure of oxygen in smokers’ lungs.
Beta-carotene may have anticarcinogenic activity in the case of prostate cancer.
In the Physicians' Health Study, it was found that men with low baseline beta-carotene
levels at the beginning of the study experienced a decreased risk of developing prostate
cancer when supplemented with 50 milligrams of beta-carotene every other day. The
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mechanism of this possible anticarcinogenic effect is unclear. A review of the
postulated mechanisms of possible anticarcinogenic activity in certain circumstances is
as follows: beta-carotene may be metabolically converted to retinoids which modulate
the gene expression of factors linked to differentiation and cell proliferation via retinoic
acid. Beta-carotene may modulate the activity of enzymes that metabolize xenobiotics.
The carotenoid has been found to increase the levels of phase II detoxifying enzymes
such as glutathione S-transferase mu (GST-mu) and glutathione peroxidase. Betacarotene's possible immunomodulatory activity may also play a role. Its possible
antioxidant activity may result in prevention of oxidative damage to DNA and
inhibition of lipid peroxidation as well as regulation of the expression of genes sensitive
to the intracellular redox state that may be involved in carcinogenesis. Beta-carotene
may modulate the gene expression of connexin 43 resulting in the induction of gap
junctions with a consequent inhibition of neoplastic transformations. Finally, in animals,
beta-carotene has been found to modulate the gene expression of the enzyme HMGCoA reductase. This would inhibit the endogenous synthesis of cholesterol resulting in
possible inhibition of cell proliferation and malignant transformation.
Epidemiological studies and some, but not all, intervention studies suggest an
inverse association between coronary artery disease and beta-carotene intake. The
possible antiatherogenic activity of beta-carotene may be accounted for, in part, by its
possible antioxidant activity. Humans supplemented with beta-carotene, but not
lycopene, were found to have low-density lipoproteins that were less oxidized than did
controls using endothelial cell-initiated autoxidation
2.6.2.1.3. Beta carotene Chemical Formula:
β-carotene
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Synonyms
β-carotene
Description
Beta carotene is one of the orange dyes found in most green leaves, and in
carrots. When leaves lose their chlorophyll in the fall, carotene is one of the colors left
over in the leaf.
Uses
Beta carotene is used in foods to provide color (margarine would look as white
as shortening without it). Another similar molecule, annatto is used in cheeses, and
another famous carotenoid dye, saffron is used to color rice and other foods.
Beta carotene is sometimes added to products for its anti-oxidant effects, to keep
fats from going rancid.
The body turns it into Vitamin A, and beta carotene is sometimes added to foods
or vitamin supplements as a nutrient.
The same long chains of conjugated double bonds (alternating single and double
bonds) that give the carotenes their colors are also the reason they make good antioxidants. The can mop up oxygen free radicals and dissipate their energy.
Chemistry lesson
Annother colorful carotene is lycopene.
lycopene
This is the red molecule that gives ripe tomatoes their color.
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Notice the alternating double and single bonds between the carbon atoms. These
are called "conjugated" bonds, or "resonance" bonds. The electrons in those bonds are
not locked onto one atom, but spend their time bouncing from atom to atom. This gives
the effect of something in between a double bond and a single bond, more of a one and
a half bond.
The long chain of conjugated bonds acts like a wire, allowing the electrical
energy to move from one side of the molecule to the other. The energy can slosh around
like water in a bathtub.
Normally it takes quite a bit of energy to move an electron away from an atom.
X-rays, or high-energy ultraviolet light can move an electron into a higher orbit in an
atom, but ordinary visible light does not have enough energy.
A molecule of lycopene can absorb blue light because the electrons are not
orbiting a single atom, they are sloshing around orbiting many atoms, and the energy
needed to move them is a lot less than in a smaller molecule, or one without conjugated
bonds.
Each end of the jump rope is a "node", a place where the rope doesn't move. It is
possible to get a jump rope to have three nodes, as you may have done as a child. It acts
like there are two jump ropes, each one half the length of the other.
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The energy sloshing around in the lycopene molecule can do the same thing.
Absorbing a photon of green light makes it act as if the molecule were two molecules,
each half as long.
The molecule has absorbed the green light. White light that is missing its green
light looks red. Beta carotene absorbs blue light, so it looks orange.
Another class of colored compounds are the anthocyanins. These molecules give
color to flowers, blueberries, apples, and red cabbage. Anthocyanins are in the group of
compounds known as flavenoids.
Anthocyanins can change their color, depending on how acid or alkaline they are.
Cyanidin 3-glucoside
In neutral conditions, the molecule has no charge. It absorbs yellow light, and
appears purple. Notice all of the alternating single and double bonds.
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In an acid (pH less than 3), the acid donates a hydrogen nucleus, and the
molecule becomes positive. The bond next to the oxygen becomes a double bond, and
the molecule now absorbs green light, so it appears red.
In an alkaline solution, the molecule donates a hydrogen nucleus, and a hydroxyl
group becomes an oxygen atom with a negative charge. The molecule now absorbs
orange light, and appears blue
2.6.2.2. Lycopen Chemical Formula:
Description
Lycopene is the red pigment that gives tomatoes their color. It is also found in
watermelons, and pink grapefruit.
Uses
Lycopene is a good anti-oxidant, and a food coloring.
It is used as a nutrient in supplement tablets for its anti-oxidant properties.
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It is in the class of carotenoids, along with another colorful molecule beta carotene.
2.6.2.4. Annatto Chemical Formula:
Bixin
Norbixin
Synonyms
Bixin carotenoids
Description
Annatto is a colored pigment extracted from the Central and South American
plant Bixa orellana.
The color comes from the resinous outer covering of the seeds of the plant, and
is composed of the carotenoid pigments bixin and norbixin, and their esters.
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The central portion of those molecules is the same as that of the molecule βcarotene, and the yellow orange color of annatto comes from the same physical
chemistry origins as the orange color of β-carotene.
Uses
Annatto is used in foods to provide color in cheese, butter, margarine, and
microwave popcorn. It is often used as a substitute for the expensive herb saffron. It
also has anti-oxidant properties.
The seeds are also used as a flavoring in the form of a powder or a paste, but the
main use is as a coloring agent.
Because annatto binds well to the proteins in dairy foods, it is often used to add
color to milk products such as butter, cheese, or puddings.
2.6.2.5. Safron Chemical Formula:
18
β-gentobiose crocetin
Synonyms
β-gentobiose crocetin,
Saffron carotenoids
Description
Saffron is one of the most expensive spices used today. It is the tiny stigmata at
the center of the Crocus flower Crocus sativa. Each tiny stigma is plucked from the
flower by hand.
The dye molecule in saffron is the carotenoid β-gentobiose crocetin. It is related
to β-carotene, and you can see the relationship in the center of the molecule. That center
portion is the carotenoid pigment crocetin:
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Crocetin
On either side of the crocetin molecule is a disaccharide molecule called βgentobiose, and the result is the molecule that gives saffron its yellow color.
Uses
Saffron is a spice, added sometimes for flavor, but mostly for the yellow color it
imparts to foods.
Because of its expense, saffron is often replaced in recipes by another
carotenoid, annatto or the unrelated dye molecule in turmeric.
Like the other carotenoid dyes, saffron is an anti-oxidant, but its expense makes
it unsuitable as a preservative or dietary supplement
2.6.3. Hazards: Concerns for Genetically Modified foods
Despite the potential of plant genetic engineering to increase nutritional value
and other benefits, GM foods continue to be a controversial topic in the public arena.
Concerns include increased toxicity, decreased nutritional value, gene transfer, and
allergencity of the GM food. Some think exogenous genes can insert in a way that
silences an endogenous gene that would can cause a decreased nutritional value of the
progeny plant. Conversely, the gene can interrupt a promoter region causing a gene to
be over active and cause increased toxicity in the plant. A study suggest that these
situations are rare. It demonstrated that plant toxins and antinutrients are similar in GM
plants and their parent plants. There is also concern that genes from the GM crops can
transfer in to the soil or other plants and that genes can transfer into human cells while a
person is digesting GM foods. Allergencity of GM foods is a valid and real concern for
GM foods. Allergencity is not easily predictable. A gene extracted from one source may
not be allergenic; however, in the transgenic product the novel gene can cross react with
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other proteins or be over expressed and cause an allergic response in the consumer.
Since allergens cannot be reliably predicted by physio-chemical characteristics or level
of expression, GM foods should be rigorously tested before approval for mass
production and sale of the product. Overall, there is not much research showing
evidence that GM foods are hazardous to consumers; however, a systematic protocol
should be developed by the existing food regulation organizations (FDA, USDA, EPA)
to evaluate the safety of new GM food products.
Furthermore, the general population should be educated about GM foods to
dispel the myths and increase knowledge. Long-term studies need to be conducted
concerning the potential hazards and impact of GM crops on human health and the
environment. While there are concerns about the safety of GM foods, the potential they
have for improving health and nutrition currently allows for the benefits to outweigh the
hazards.
2.6.4. Protein Fortification of Rice with the Soybean Glycinin Gene
The most widespread form of malnutrition throughout the world is proteinenergy malnutrition (PEM) due to inadequate food intakes and protein-poor diets. The
key to tackling this problem is improving human protein intakes efficiently and cheaply.
Rice, one of the worlds most common staple crops, lacks certain amino acids,
including lysine. Unlike many vegetables and fruits, the soybean storage protein,
glycinin, is a good source of protein and essential amino acids, particularly lysine.
Electroporation is used to insert the soybean glycinin gene between the promoter
and terminator of the rice glutelin gene of an important variety of Japanese rice,
"Matsuyamamii". As with all genetically modified foods, quality and safety are prime
concerns of consumers. studied the composition and digestibility of their transgenic rice
by compositional and in vitro digestion analyses. They analysed about 60 components
that are nutritionally and physiologically important in rice.
Significant differences between the composition of the transgenic rice and its
non-transgenic counterpart were not observed, except for the levels of protein, amino
acids and moisture. The transgenic rice had about 20% more protein as a result of
glycinin expression. Some essential amino acids which are lacking in normal rice were
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found in increased amounts in the transgenic rice. The moisture content of the rice had
decreased. In addition, glycinin was completely digested by the gastric and intestinal
juices . Further nutritional and toxicological studies are being carried out by this group
to confirm the safety of this transgenic rice.
Perhaps an increase in the protein content of rice by 20% does not seem much;
however, this can be significant when diets are very low in protein and rice is the main
food eaten. Genetic engineering can be beneficial to improving human nutrition
provided that the composition and quality of transgenic foods are analysed.
Iron deficiency is the most common nutrient deficiency that affects an estimated
30% of the world’s population (WHO, 1992). It is most prevalent in developing
countries and particularly affects young children and pregnant women. The lack of meat
in diets due to its cost and scarcity is a major factor and often iron tablet
supplementation is not economically feasible. Iron fortification of soil has been used;
however, it is also costly and can reduce crop productivity. An ideal method would be
to improve iron accumulation in staple crops commonly eaten in developing countries.
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