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Plant hormones (also known as phytohormones) are chemicals that regulate plant growth. In
the United Kingdom, these are termed 'plant growth substances'.
Plant hormones are signal molecules produced within the plant, and occur in extremely
low concentrations. Hormones regulate cellular processes in targeted cells locally and, moved to
other locations, in other functional parts of the plant. Hormones also determine the formation
of flowers, stems, leaves, the shedding of leaves, and the development and ripening of fruit. Plants,
unlike animals, lack glands that produce and secrete hormones. Instead, each cell is capable of
producing hormones. Plant hormones shape the plant, affecting seed growth, time of flowering, the
sex of flowers, senescence of leaves, and fruits. They affect which tissues grow upward and which
grow downward, leaf formation and stem growth, fruit development and ripening, plant longevity, and
even plant death. Hormones are vital to plant growth, and, lacking them, plants would be mostly a
mass of undifferentiated cells. So they are also known as growth factors or growth hormones. The
term 'Phytohormone' was coined by Thimann in 1948[clarification needed].
Phytohormones are found not only in higher plants, but in algae too, showing similar functions,[1] and
in microorganisms, like fungi and bacteria, but, in this case, they play no hormonal or other
immediate physiological role in the producing organism and can, thus, be regarded as secondary
metabolites.[2]
Contents
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1Characteristics
2Classes of plant hormones
o 2.1Abscisic acid
o 2.2Auxins
o 2.3Cytokinins
o 2.4Ethylene
o 2.5Gibberellins
o 2.6Other known hormones
3Potential medical applications
4Hormones and plant propagation
o 4.1Seed dormancy
5References
6External links
Characteristics[edit]
Phyllody on a purple coneflower(Echinacea purpurea), a plant development abnormality where leaf-like
structures replace flower organs. It can be caused by hormonal imbalance, among other reasons.
The word hormone is derived from Greek, meaning set in motion. Plant hormones affect gene
expression and transcription levels, cellular division, and growth. They are naturally produced within
plants, though very similar chemicals are produced by fungi and bacteria that can also affect plant
growth.[3] A large number of related chemical compounds are synthesized by humans. They are used
to regulate the growth of cultivated plants, weeds, and in vitro-grown plants and plant cells; these
manmade compounds are called Plant Growth Regulators or PGRs for short. Early in the study of
plant hormones, "phytohormone" was the commonly used term, but its use is less widely applied
now.
Plant hormones are not nutrients, but chemicals that in small amounts promote and influence the
growth,[4] development, and differentiation of cells and tissues. The biosynthesis of plant hormones
within plant tissues is often diffuse and not always localized. Plants lack glands to produce and store
hormones, because, unlike animals — which have two circulatory systems
(lymphatic and cardiovascular) powered by a heart that moves fluids around the body — plants use
more passive means to move chemicals around the plant. Plants utilize simple chemicals as
hormones, which move more easily through the plant's tissues. They are often produced and used
on a local basis within the plant body. Plant cells produce hormones that affect even different
regions of the cell producing the hormone.
Hormones are transported within the plant by utilizing four types of movements. For localized
movement, cytoplasmic streaming within cells and slow diffusion of ions andmolecules between cells
are utilized. Vascular tissues are used to move hormones from one part of the plant to another;
these include sieve tubes or phloem that move sugarsfrom the leaves to the roots and flowers,
and xylem that moves water and mineral solutes from the roots to the foliage.
Not all plant cells respond to hormones, but those cells that do are programmed to respond at
specific points in their growth cycle. The greatest effects occur at specific stages during the cell's life,
with diminished effects occurring before or after this period. Plants need hormones at very specific
times during plant growth and at specific locations. They also need to disengage the effects that
hormones have when they are no longer needed. The production of hormones occurs very often at
sites of active growth within themeristems, before cells have fully differentiated. After production,
they are sometimes moved to other parts of the plant, where they cause an immediate effect; or they
can be stored in cells to be released later. Plants use different pathways to regulate internal
hormone quantities and moderate their effects; they can regulate the amount of chemicals used to
biosynthesize hormones. They can store them in cells, inactivate them, or cannibalise alreadyformed hormones by conjugating them with carbohydrates, amino acids, or peptides. Plants can also
break down hormones chemically, effectively destroying them. Plant hormones frequently regulate
the concentrations of other plant hormones.[5]Plants also move hormones around the plant diluting
their concentrations.
The concentration of hormones required for plant responses are very low (10−6 to 10−5 mol/L).
Because of these low concentrations, it has been very difficult to study plant hormones, and only
since the late 1970s have scientists been able to start piecing together their effects and relationships
to plant physiology.[6] Much of the early work on plant hormones involved studying plants that were
genetically deficient in one or involved the use of tissue-cultured plants grown in vitro that were
subjected to differing ratios of hormones, and the resultant growth compared. The earliest scientific
observation and study dates to the 1880s; the determination and observation of plant hormones and
their identification was spread-out over the next 70 years.
Classes of plant hormones[edit]
In general, it is accepted that there are five major classes of plant hormones, some of which are
made up of many different chemicals that can vary in structure from one plant to the next. The
chemicals are each grouped together into one of these classes based on their structural similarities
and on their effects on plant physiology. Other plant hormones and growth regulators are not easily
grouped into these classes; they exist naturally or are synthesized by humans or other organisms,
including chemicals that inhibit plant growth or interrupt the physiological processes within plants.
Each class has positive as well as inhibitory functions, and most often work in tandem with each
other, with varying ratios of one or more interplaying to affect growth regulation.[7]
The five major classes are:
Abscisic acid[edit]
Abscisic acid (also called ABA) is one of the most important plant growth regulators. It was
discovered and researched under two different names before its chemical properties were fully
known, it was called dorminand abscicin II. Once it was determined that the two compounds are the
same, it was named abscisic acid. The name "abscisic acid" was given because it was found in high
concentrations in newly abscissed or freshly fallen leaves.
This class of PGR is composed of one chemical compound normally produced in the leaves of
plants, originating from chloroplasts, especially when plants are under stress. In general, it acts as
an inhibitory chemical compound that affects bud growth, and seed and bud dormancy. It mediates
changes within the apical meristem, causing bud dormancy and the alteration of the last set of
leaves into protective bud covers. Since it was found in freshly abscissed leaves, it was thought to
play a role in the processes of natural leaf drop, but further research has disproven this. In plant
species from temperate parts of the world, it plays a role in leaf and seed dormancy by inhibiting
growth, but, as it is dissipated from seeds or buds, growth begins. In other plants, as ABA levels
decrease, growth then commences as gibberellin levels increase. Without ABA, buds and seeds
would start to grow during warm periods in winter and be killed when it froze again. Since ABA
dissipates slowly from the tissues and its effects take time to be offset by other plant hormones,
there is a delay in physiological pathways that provide some protection from premature growth. It
accumulates within seeds during fruit maturation, preventing seed germination within the fruit, or
seed germination before winter. Abscisic acid's effects are degraded within plant tissues during cold
temperatures or by its removal by water washing in out of the tissues, releasing the seeds and buds
from dormancy.[8]
In plants under water stress, ABA plays a role in closing the stomata. Soon after plants are waterstressed and the roots are deficient in water, a signal moves up to the leaves, causing the formation
of ABA precursors there, which then move to the roots. The roots then release ABA, which is
translocated to the foliage through the vascular system[9] and modulates the potassium and sodium
uptake within the guard cells, which then lose turgidity, closing the stomata.[10][11] ABA exists in all
parts of the plant and its concentration within any tissue seems to mediate its effects and function as
a hormone; its degradation, or more properlycatabolism, within the plant affects metabolic reactions
and cellular growth and production of other hormones.[12] Plants start life as a seed with high ABA
levels. Just before the seed germinates, ABA levels decrease; during germination and early growth
of the seedling, ABA levels decrease even more. As plants begin to produce shoots with fully
functional leaves, ABA levels begin to increase, slowing down cellular growth in more "mature" areas
of the plant. Stress from water or predation affects ABA production and catabolism rates, mediating
another cascade of effects that trigger specific responses from targeted cells. Scientists are still
piecing together the complex interactions and effects of this and other phytohormones.
Auxins[edit]
Main article: Auxin
The auxin indole-3-acetic acid
Auxins are compounds that positively influence cell enlargement, bud formation and root initiation.
They also promote the production of other hormones and in conjunction withcytokinins, they control
the growth of stems, roots, and fruits, and convert stems into flowers.[13] Auxins were the first class of
growth regulators discovered.[14] They affect cell elongation by altering cell wall plasticity. They
stimulate cambium, a subtype of meristem cells, to divide and in stems cause secondary xylem to
differentiate. Auxins act to inhibit the growth of buds lower down the stems (apical dominance), and
also to promote lateral and adventitious root development and growth. Leaf abscission is initiated by
the growing point of a plant ceasing to produce auxins. Auxins in seeds regulate specific protein
synthesis,[15] as they develop within the flower after pollination, causing the flower to develop a fruit to
contain the developing seeds. Auxins are toxic to plants in large concentrations; they are most toxic
to dicots and less so to monocots. Because of this property, synthetic auxin herbicides including 2,4D and2,4,5-T have been developed and used for weed control. Auxins, especially 1Naphthaleneacetic acid (NAA) and Indole-3-butyric acid (IBA), are also commonly applied to
stimulate root growth when taking cuttings of plants. The most common auxin found in plants
is indole-3-acetic acid or IAA. The correlation of auxins and cytokinins in the plants is a constant
(A/C = const.)[citation needed].
Cytokinins[edit]
The cytokinin zeatin, the name is derived fromZea, in which it was first discovered in immature kernels.
Cytokinins or CKs are a group of chemicals that influence cell division and shoot formation. They
were called kinins in the past when the first cytokinins were isolated from yeast cells. They also help
delay senescence of tissues, are responsible for mediating auxin transport throughout the plant, and
affect internodal length and leaf growth. They have a highly synergistic effect in concert with auxins,
and the ratios of these two groups of plant hormones affect most major growth periods during a
plant's lifetime. Cytokinins counter the apical dominance induced by auxins; they in conjunction with
ethylene promote abscission of leaves, flower parts, and fruits.[16] The correlation of auxins and
cytokinins in the plants is a constant (A/C = const.).[citation needed]
Ethylene[edit]
Ethylene
Ethylene is a gas that forms through the breakdown of methionine, which is in all cells. Ethylene has
very limited solubility in water and does not accumulate within the cell but diffuses out of the cell and
escapes out of the plant. Its effectiveness as a plant hormone is dependent on its rate of production
versus its rate of escaping into the atmosphere. Ethylene is produced at a faster rate in rapidly
growing and dividing cells, especially in darkness. New growth and newly germinated seedlings
produce more ethylene than can escape the plant, which leads to elevated amounts of ethylene,
inhibiting leaf expansion (see Hyponastic response). As the new shoot is exposed to light, reactions
by phytochrome in the plant's cells produce a signal for ethylene production to decrease, allowing
leaf expansion. Ethylene affects cell growth and cell shape; when a growing shoot hits an obstacle
while underground, ethylene production greatly increases, preventing cell elongation and causing
the stem to swell. The resulting thicker stem can exert more pressure against the object impeding its
path to the surface. If the shoot does not reach the surface and the ethylene stimulus becomes
prolonged, it affects the stem's natural geotropic response, which is to grow upright, allowing it to
grow around an object. Studies seem to indicate that ethylene affects stem diameter and height:
When stems of trees are subjected to wind, causing lateral stress, greater ethylene production
occurs, resulting in thicker, more sturdy tree trunks and branches. Ethylene affects fruit-ripening:
Normally, when the seeds are mature, ethylene production increases and builds-up within the fruit,
resulting in aclimacteric event just before seed dispersal. The nuclear protein Ethylene Insensitive2
(EIN2) is regulated by ethylene production, and, in turn, regulates other hormones including ABA
and stress hormones.[17]
Gibberellins[edit]
Main article: Gibberellins
Gibberellin A1
Main function: initiate mobilization of storage materials in seeds during germination, cause
elongation of stems, stimulate bolting in biennials stimulate pollen tube growth.
Gibberellins, or GAs, include a large range of chemicals that are produced naturally within plants
and by fungi. They were first discovered when Japanese researchers, including Eiichi Kurosawa,
noticed a chemical produced by a fungus called Gibberella fujikuroi that produced abnormal growth
in rice plants.[18] Gibberellins are important in seed germination, affecting enzyme production that
mobilizes food production used for growth of new cells. This is done by modulating chromosomal
transcription. In grain (rice, wheat, corn, etc.) seeds, a layer of cells called the aleurone layer wraps
around the endosperm tissue. Absorption of water by the seed causes production of GA. The GA is
transported to the aleurone layer, which responds by producing enzymes that break down stored
food reserves within the endosperm, which are utilized by the growing seedling. GAs
produce bolting of rosette-forming plants, increasing internodal length. They promote flowering,
cellular division, and in seeds growth after germination. Gibberellins also reverse the inhibition of
shoot growth and dormancy induced by ABA.[19]
Other known hormones[edit]
Other identified plant growth regulators include:

Brassinosteroids - are a class of polyhydroxysteroids, a group of plant growth regulators.
Brassinosteroids have been recognized as a sixth class of plant hormones, which stimulate cell
elongation and division,gravitropism, resistance to stress, and xylem differentiation. They
inhibit root growth and leaf abscission. Brassinolide was the first identified brassinosteroid and
was isolated from extracts of rapeseed (Brassica napus) pollen in 1979.[20]
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Salicylic acid — activates genes in some plants that produce chemicals that aid in the defense
against pathogenic invaders.
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Jasmonates — are produced from fatty acids and seem to promote the production of defense
proteins that are used to fend off invading organisms. They are believed to also have a role in
seed germination, and affect the storage of protein in seeds, and seem to affect root growth.

Plant peptide hormones — encompasses all small secreted peptides that are involved in cell-tocell signaling. These small peptide hormones play crucial roles in plant growth and development,
including defense mechanisms, the control of cell division and expansion, and pollen selfincompatibility.[21]

Polyamines — are strongly basic molecules with low molecular weight that have been found in
all organisms studied thus far. They are essential for plant growth and development and affect
the process of mitosis and meiosis.

Nitric oxide (NO) — serves as signal in hormonal and defense responses (e.g. stomatal closure,
root development, germination, nitrogen fixation, cell death, stress response).[22] NO can be
produced by a yet undefined NO synthase, a special type of nitrite reductase, nitrate reductase,
mitochondrial cytochrome c oxidase or non enzymatic processes and regulate plant cell
organelle functions (e.g. ATP synthesis in chloroplasts and mitochondria).[23]

Strigolactones - implicated in the inhibition of shoot branching.[24]

Karrikins - not plant hormones because they are not made by plants, but are a group of plant
growth regulators found in the smoke of burning plant material that have the ability to stimulate
the germination of seeds [25]

Triacontanol - a fatty alcohol that acts as a growth stimulant, especially initiating new basal
breaks in the rose family. It is found in alfalfa (lucerne), bee's wax, and some waxy leave
cuticles.
Potential medical applications[edit]
Plant stress hormones activate cellular responses, including cell death, to diverse stress situations in
plants. Researchers have found that some plant stress hormones share the ability to adversely
affect human cancer cells. For example, sodium salicylate has been found to suppress proliferation
of lymphoblastic leukemia, prostate, breast, and melanoma human cancer cells.[26] Jasmonic acid, a
plant stress hormone that belongs to the jasmonate family, induced death in lymphoblastic leukemia
cells. Methyl jasmonate has been found to induce cell death in a number of cancer cell lines.
Hormones and plant propagation[edit]
Synthetic plant hormones or PGRs are commonly used in a number of different techniques
involving plant propagation from cuttings, grafting, micropropagation, and tissue culture.
The propagation of plants by cuttings of fully developed leaves, stems, or roots is performed by
gardeners utilizing auxin as a rooting compound applied to the cut surface; the auxins are taken into
the plant and promote root initiation. In grafting, auxin promotes callus tissue formation, which joins
the surfaces of the graft together. In micropropagation, different PGRs are used to promote
multiplication and then rooting of new plantlets. In the tissue-culturing of plant cells, PGRs are used
to produce callus growth, multiplication, and rooting.
Seed dormancy[edit]
Main article: Seed dormancy
Plant hormones affect seed germination and dormancy by acting on different parts of the seed.
Embryo dormancy is characterized by a high ABA:GA ratio, whereas the seed has a high ABA
sensitivity and low GA sensitivity. In order to release the seed from this type of dormancy and initiate
seed germination, an alteration in hormone biosynthesis and degradation toward a low ABA/GA
ratio, along with a decrease in ABA sensitivity and an increase in GA sensitivity, must occur.
ABA controls embryo dormancy, and GA embryo germination. Seed coat dormancy involves the
mechanical restriction of the seed coat. This, along with a low embryo growth potential, effectively
produces seed dormancy. GA releases this dormancy by increasing the embryo growth potential,
and/or weakening the seed coat so the radical of the seedling can break through the seed coat.
Different types of seed coats can be made up of living or dead cells, and both types can be
influenced by hormones; those composed of living cells are acted upon after seed formation,
whereas the seed coats composed of dead cells can be influenced by hormones during the
formation of the seed coat. ABA affects testa or seed coat growth characteristics, including
thickness, and effects the GA-mediated embryo growth potential. These conditions and effects occur
during the formation of the seed, often in response to environmental conditions. Hormones also
mediate endosperm dormancy: Endosperm in most seeds is composed of living tissue that can
actively respond to hormones generated by the embryo. The endosperm often acts as a barrier to
seed germination, playing a part in seed coat dormancy or in the germination process. Living cells
respond to and also affect the ABA:GA ratio, and mediate cellular sensitivity; GA thus increases the
embryo growth potential and can promote endosperm weakening. GA also affects both ABAindependent and ABA-inhibiting processes within the endosperm.
Brassinosteroids (BRs) are a class of polyhydroxysteroids that have been recognized as a sixth
class of plant hormones. These were first explored nearly 40 years ago, when Mitchell et al. reported
promotion in stem elongation and cell division by the treatment of organic extracts of rapeseed
(Brassica napus) pollen.[1] Brassinolide was the first isolated brassinosteroid in 1979, when pollen
from Brassica napus was shown to promote stem elongation and cell divisions, and the biologically
active molecule was isolated.[1][2] The yield of brassinosteroids from 230 kg of Brassica napus pollen
was only 10 mg. Since their discovery, over 70 BR compounds have been isolated from plants.[3]
Contents
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1Biosynthesis
2Hormonal activity
3Agricultural uses
4Detection and chemical analysis
5References
6External links
Biosynthesis[edit]
The BR is biosynthesised from campesterol. The biosynthetic pathway was elucidated by Japanese
researchers and later shown to be correct through the analysis of BR biosynthesis mutants
in Arabidopsis thaliana, tomatoes, and peas.[4] The sites for BR synthesis in plants have not been
experimentally demonstrated. One well-supported hypothesis is that all tissues produce BRs, since
BR biosynthetic and signal transduction genes are expressed in a wide range of plant organs, and
short distance activity of the hormones also supports this.[5][6] Experiments have shown that long
distance transport is possible and that flow is in anacropetal direction, but it is not known if this
movement is biologically relevant.[5] Brassinosteroids are recognized at the cell membrane, although
they are membrane-soluble.
Hormonal activity[edit]
BRs have been shown to be involved in numerous plant processes:

Promotion of cell expansion and cell elongation;[5] works with auxin to do so.[7]

It has an unclear role in cell division and cell wall regeneration.[5]

Promotion of vascular differentiation; BR signal transduction has been studied during vascular
differentiation.[8]

Is necessary for pollen elongation for pollen tube formation.[9]

Acceleration of senescence in dying tissue cultured cells; delayed senescence in BR mutants
supports that this action may be biologically relevant.[5]

Can provide some protection to plants during chilling and drought stress.[5]
Extract from the plant Lychnis viscaria contains a relatively high amount of Brassinosteroids. Lychnis
viscaria increases the disease resistance of surrounding plants.[citation needed]
24-Epibrassinolide (EBL), a brassinosteroid isolated from Aegle marmelos Correa (Rutaceae), was
further evaluated for the antigenotoxicity against maleic hydrazide (MH)-induced genotoxicity
in Allium cepachromosomal aberration assay. It was shown that the percentage of chromosomal
aberrations induced by maleic hydrazide (0.01%) declined significantly with 24-epibrassinolide
treatment.[10]
BRs have been reported to counteract both abiotic and biotic stress in plants.[11][12] Application of
brassinosteroids to cucumbers was demonstrated to increase the metabolism and removal of
pesticides, which could be beneficial for reducing the human ingestion of residual pesticides from
non-organically grown vegetables.[13] In all Type of brassinosteroids 28-homoBL is the most effective
type of brassinosteroids. (sandeep kumar et al. 2010 Jour. of Indian bot society) Brassinosteroids
increased tolerance to high temperature in Brassica juncea L. (Kumar S. 2010) The ability of 28homobrassinolide to confer resistance to stress in Brassica juncea L. has also established (sandeep
kumar). Application of 24-epiBL have any protective role on shoot, root length, soluble protein,
proline content and peroxidases along with proline content PPO and IAA in seedlings of B. juncea L.
under seasonal stress (Geetika Sirhindi)
BRs have also been reported to have a variety of effects when applied to rice seeds (Oryza sativa
L.).Seeds treated with BRs were shown to reduce the growth inhibitory effect of salt stress.[14] When
the developed plants fresh weight was analyzed the treated seeds outperformed plants grown on
saline and non-saline medium however when the dry weight was analyzed BR treated seeds only
outperformed untreated plants that were grown on saline medium.[14] When dealing with tomatoes
(Lycopersicon esculentum) under salt stress the concentration of cholophyll a and cholophyll b were
decreased and thus pigmentation was decreased as well.[15] BR treated rice seeds considerably
restored the pigment level in plants that were grown on saline medium when compared to nontreated plants under the same conditions.[14]
Agricultural uses[edit]
BR might reveal to have a prominent interest in the role of horticultural crops. Based on extensive
research BR has the ability to improve the quantity and quality of horticultural crops and protect
plants against many stresses that can be present in the local environment.[16][17] With the many
advances in technology dealing with the synthesis of more stable synthetic analogues and the
genetic manipulation of cellular BR activity, using BR in the production of horticultural crops has
become a more practical and hopeful strategy for improving crop yields and success.[16]
BR could also help bridge the gap of the consumers' health concerns and the producers need for
growth. A major benefit of using BR is that it does not interfere with the environment because they
act in natural doses in a natural way.[17] Since it is a “plant strengthening substance” and it is natural,
BR application would be more favorable than pesticides and does not contribute to the co-evolution
of pests.[17]
In Germany, extract from the plant is allowed for use as a "plant strengthening substance."[citation needed]
Detection and chemical analysis[edit]
BRs can be detected by gas chromatography mass spectrometry and bioassays.[18]
Salicylic acid (from Latin salix, willow tree) is a monohydroxybenzoic acid, a type of phenolic
acid and a beta hydroxy acid. It has the formula C7H6O3. This colorless crystalline organic acid is
widely used in organic synthesis and functions as a plant hormone. It is derived from the metabolism
of salicin. In addition to serving as an important active metabolite of aspirin (acetylsalicylic acid),
which acts in part as a prodrug to salicylic acid, it is probably best known for its use as a key
ingredient in topical anti-acne products. The salts and esters of salicylic acid are known as
salicylates. The medicinal part of the plant is the inner bark.
It is on the WHO Model List of Essential Medicines, the most important medications needed in a
basic health system.[8]
Contents
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1Uses
o 1.1Medicine
o 1.2Chemistry
o 1.3Other uses
2Safety
3Plant hormone
4Production
5History
6Dietary sources
7Mechanism of action
8See also
9References
10External links
Uses[edit]
Medicine[edit]
Salicylic acid is known for its ability to ease aches and pains and reduce fevers.[9] These medicinal
properties, particularly fever relief, were discovered in ancient times. It is used as an antiinflammatory drug.[9]
In modern medicine, salicylic acid and its derivatives are constituents of some rubefacient products.
For example, methyl salicylate is used as a liniment to soothe joint and muscle pain and choline
salicylate is used topically to relieve the pain of mouth ulcers.
Cotton pads soaked in salicylic acid can be used to chemically exfoliate skin
As with other hydroxy acids, salicylic acid is a key ingredient in many skin-care products for the
treatment of seborrhoeic dermatitis, acne, psoriasis, calluses, corns, keratosis pilaris, acanthosis
nigricans, ichthyosis and warts.[9] The standard treatment for calluses is a 6% aspirin suspension
in petroleum jelly, applied on the callus for one hour and then removed with washing.[citation needed]
Salicylic acid works as a keratolytic, comedolytic and bacteriostatic agent, causing the cells of the
epidermis to shed more readily, opening clogged pores and neutralizing bacteria within, preventing
pores from clogging up again by constricting pore diameter and allowing room for new cell
growth.[9][10]
Because of its effect on skin cells, salicylic acid is used in some shampoos to treat dandruff.
Concentrated solutions of salicylic acid may cause hyperpigmentation on people with darker skin
types (Fitzpatrick phototypes IV, V, VI), without a broad spectrum sunblock.[11][12]
Bismuth subsalicylate, a salt of bismuth and salicylic acid, is the active ingredient in stomach relief
aids such as Pepto-Bismol, is the main ingredient of Kaopectate and "displays anti-inflammatory
action (due to salicylic acid) and also acts as an antacid and mild antibiotic".[13]
Salicylic acid is used in the production of other pharmaceuticals including 4-aminosalicylic
acidsandulpiridelandetimide (via Salethamide).
In 2016 salicylic acid — and (more potently) diflunisal, a cousin of aspirin — was shown to
suppress p300 and CREB-binding protein or CBP, proteins that help control gene expression in a
mouse model. The method of action was direct competition with acetyl-Coenzyme A, blocking
the acetylation of lysine residues on histone and non-histone proteins . Suppressing these proteins
can prevent cellular damage caused by inflammation.[14]
Chemistry[edit]
Salicylic acid has the formula C6H4(OH)COOH, where the OH group is ortho to the carboxyl group. It
is also known as 2-hydroxybenzoic acid. It is poorly soluble in water (2 g/L at
20 °C).[15] Aspirin (acetylsalicylic acid or ASA) can be prepared by the esterification of
the phenolic hydroxyl group of salicylic acid with the acetyl group fromacetic anhydride or acetyl
chloride. Salicylic acid can also be prepared using the Kolbe-Schmitt reaction.
Other uses[edit]
Salicylic acid is used as a food preservative, a bactericidal and an antiseptic.[16]
Sodium salicylate is a useful phosphor in the vacuum ultraviolet, with nearly flat quantum efficiency
for wavelengths between 10 and 100 nm.[17] It fluoresces in the blue at 420 nm. It is easily prepared
on a clean surface by spraying a saturated solution of the salt in methanol followed by evaporation.
Safety[edit]
As a topical agent and as a beta-hydroxy acid (and unlike alpha-hydroxy acids), salicylic acid is
capable of penetrating and breaking down fats and lipids, causing moderate chemical burns of the
skin at very high concentrations. It may damage the lining of pores if the solvent is alcohol, acetone
or an oil. Over-the-counter limits are set at 2% for topical preparations expected to be left on the face
and 3% for those expected to be washed off, such as acne cleansers or shampoo. 17% and 27%
salicylic acid, which is sold for wart removal, should not be applied to the face and should not be
used for acne treatment. Even for wart removal, such a solution should be applied once or twice a
day – more frequent use may lead to an increase in side-effects without an increase in efficacy.[18]
When ingested, salicylic acid has a possible ototoxic effect by inhibiting prestin.[19] It can induce
transient hearing loss in zinc-deficient rats. An injection of salicylic acid induced hearing loss, while
an injection of zinc reversed the hearing loss. An injection of magnesium in the zinc-deficient rats did
not reverse the induced hearing loss.[citation needed]
No studies examine topical salicylic acid in pregnancy. Oral salicylic acid is not associated with an
increase in malformations if used during the first trimester, but in late pregnancy has been
associated with bleeding, especially intracranial bleeding.[20] The risks of aspirin late in pregnancy are
probably not relevant for a topical exposure to salicylic acid, even late in the pregnancy, because of
its low systemic levels. Topical salicylic acid is common in many over-the-counter dermatological
agents and the lack of adverse reports suggests a low teratogenic potential.[21]
Salicylic acid overdose can lead to salicylate intoxication, which often presents clinically in a state
of metabolic acidosis with compensatory respiratory alkalosis. In patients presenting with an acute
overdose, a 16% morbidity rate and a 1% mortality rate are observed.[22]
Some people are hypersensitive to salicylic acid and related compounds.
The United States Food and Drug Administration (FDA) recommends the use of sun protection when
using skincare products containing salicylic acid (or any other BHA) on sun-exposed skin areas.[23]
Data support an association between exposure to salicylic acid and Reye's Syndrome. The National
Reye's Syndrome Foundation cautions against the use of these and other substances similar to
aspirin on children and adolescents. Epidemiological research associated the development of Reye's
Syndrome and the use of aspirin for treating the symptoms of influenza-like illnesses, chicken pox,
colds, etc. The U.S. Surgeon General, the FDA, the Centers for Disease Control and Prevention and
theAmerican Academy of Pediatrics recommend that aspirin and combination products containing
aspirin not be given to children under 19 years of age during episodes of fever-causing illnesses.[24]
Plant hormone[edit]
Salicylic acid (SA) is a phenolic phytohormone and is found in plants with roles in plant growth and
development, photosynthesis, transpiration, ion uptake and transport. SA also induces specific
changes in leaf anatomy and chloroplast structure.[which?] SA is involved in endogenous signaling,
mediating in plant defense againstpathogens.[25] It plays a role in the resistance to pathogens by
inducing the production of pathogenesis-related proteins.[26] It is involved in the systemic acquired
resistance (SAR) in which a pathogenic attack on one part of the plant induces resistance in other
parts. The signal can also move to nearby plants by salicylic acid being converted to the volatile
ester, methyl salicylate.[27]
Production[edit]
Salicylic acid is biosynthesized from the amino acid phenylalanine. In Arabidopsis thaliana it can be
synthesized via a phenylalanine-independent pathway.
Sodium salicylate is commercially prepared by treating sodium phenolate (the sodium salt of phenol)
with carbon dioxide at high pressure (100 atm) and high temperature (390 K) – a method known as
the Kolbe-Schmitt reaction. Acidification of the product with sulfuric acid gives salicylic acid:
It can also be prepared by the hydrolysis of aspirin (acetylsalicylic acid)[28] or methyl salicylate (oil
of wintergreen) with a strong acid or base.
History[edit]
Main article: History of aspirin
White willow (Salix alba) is a natural source of salicylic acid
Hippocrates, Galen, Pliny the Elder and others knew that willow bark could ease pain and
reduce fevers.[29] It was used in Europe and China to treat these conditions.[30] This remedy is
mentioned in texts from ancient Egypt, Sumer and Assyria.[31] TheCherokee and other Native
Americans used an infusion of the bark for fever and other medicinal purposes.[32]
In 2014, archaeologists identified traces of salicylic acid on 7th century pottery fragments found
in east central Colorado.[33] TheReverend Edward Stone, a vicar from Chipping Norton,
Oxfordshire, England, noted in 1763 that the bark of the willow was effective in reducing a
fever.[34]
The active extract of the bark, called salicin, after the Latin name for the white willow (Salix
alba), was isolated and named by theGerman chemist Johann Andreas Buchner in 1828.[35] A
larger amount of the substance was isolated in 1829 by Henri Leroux,
aFrench pharmacist.[36] Raffaele Piria, an Italian chemist, was able to convert the substance into
a sugar and a second component, which on oxidation becomes salicylic acid.[37][38]
Salicylic acid was also isolated from the herb meadowsweet (Filipendula ulmaria, formerly
classified as Spiraea ulmaria) by German researchers in 1839.[39] While their extract was
somewhat effective, it also caused digestive problems such as gastric
irritation, bleeding, diarrhea and even death when consumed in high doses.
Dietary sources[edit]
Unripe fruits and vegetables are natural sources of salicylic acid,
particularly blackberries, blueberries, cantaloupes, dates, grapes, kiwi
fruits, guavas, apricots, green pepper,olives, tomatoes, radish, chicory and mushrooms.[citation
needed]
Some herbs and spices contain high amounts, while meat, poultry, fish, eggs and dairy
products all have little to no salicylates.[40] Of the legumes, seeds, nuts and cereals,
only almonds, water chestnuts and peanuts have significant amounts.[41]
Mechanism of action[edit]
Salicylic acid works through several different pathways. It produces its anti-inflammatory effects
via suppressing the activity of cyclooxygenase (COX), an enzyme that is responsible for the
production of pro-inflammatory mediators such as the prostaglandins. It does this not by
direct inhibition of COX like most other non-steroidal anti-inflammatory drugs (NSAIDs) but
instead by suppression of the expression of the enzyme through a yet-unelucidated
mechanism.[42]
Salicylic acid activates adenosine monophosphate-activated protein kinase (AMPK) and this
action may play a role in the anticancer effects of the compound and its prodrugs aspirin
and salsalate. The antidiabeticeffects of salicylic acid are likely mediated by AMPK activation
primarily through allosteric conformational change that increases levels of phosphorylation.[43]
Salicylic acid also uncouples oxidative phosphorylation, which leads to increased ADP:ATP and
AMP:ATP ratios in the cell. As a consequence, salicylic acid may alter AMPK activity and work
as an anti-diabetic by altering the energy status of the cell. AMPK knock-out mice display an
anti-diabetic effect, demonstrating at least one additional, yet-unidentified action.[44]
Salicylic acid regulates c-Myc level at both transcriptional and post-transcription levels. Inhibition
of c-Myc may be an important pathway by which aspirin exerts an anti-cancer effect, decreasing
the occurrence of cancer in epithelial tissues.[45]
Jasmonate (JA) and its derivatives are lipid-based hormone signals that regulate a wide range of
processes in plants, ranging from growth and photosynthesis to reproductive development. In
particular, JAs are critical for plant defense against herbivory and plant responses to poor
environmental conditions and other kinds of abiotic and biotic challenges.[1] Some JAs can also be
released as volatile organic compounds (VOCs) to permit communication between plants in
anticipation of mutual dangers.[2]
The isolation of methyl jasmonate from jasmine oil derived from Jasminum grandiflorum led to the
discovery of the molecular structure of jasmonates and their name.[3]
Contents
[hide]






1Chemical structure
2Mechanism of signaling
3Function
4Role in pathogenesis
5Cross talk with other defense pathways
6References
Chemical structure[edit]
Jasmonic acid (JA)
Methyl JA
Structures of active jasmonate derivatives
Jasmonates (JA) are an oxylipin, i.e. a derivative of oxygenated fatty acid. It is biosynthesized from
linolenic acid in chloroplast membranes. Synthesis is initiated with the conversion of linolenic acid to
12-oxo-phytodienoic acid (OPDA), which then undergoes a reduction and three rounds of oxidation
to form (+)-7-iso-JA, jasmonic acid. Only the conversion of linolenic acid to OPDA occurs in
the chloroplast; all subsequent reactions occur in the peroxisome.[4]
JA itself can be further metabolized into active or inactive derivatives. Methyl JA (MeJA) is a volatile
compound that is potentially responsible for interplant communication. JA conjugated with amino
acid isoleucine (Ile) results in JA-Ile, which is currently the only known JA derivative needed for JA
signaling.[4] JA undergoes decarboxylation to give cis-jasmone.
Mechanism of signaling[edit]
Major components of the jasmonate pathway
In general, the steps in jasmonate (JA) signaling mirror that of auxin signaling: the first step
comprises E3 ubiquitin ligase complexes, which tag substrates with ubiquitin to mark them for
degradation by proteasomes. The second step utilizes transcription factors to effect physiological
changes. One of the key molecules in this pathway is JAZ, which serves as the on-off switch for JA
signaling. In the absence of JA, JAZ proteins bind to downstream transcription factors and limit their
activity. However, in the presence of JA or its bioactive derivatives, JAZ proteins are degraded,
freeing transcription factors for expression of genes needed in stress responses.[5]
Because JAZ did not disappear in null coi1 mutant plant backgrounds, protein COI1 was shown to
mediate JAZ degradation. COI1 belongs to the family of highly conserved F-box proteins, and it
recruits substrates for the E3 ubiquitin ligase SCFCOI1. The complexes that ultimately form are known
as SCF complexes.[6] These complexes bind JAZ and target it for proteasomal degradation.
However, given the large spectrum of JA molecules, not all JA derivatives activate this pathway for
signaling, and the range of those participating in this pathway is unknown.[4] Thus far, only JA-Ile has
been shown to be necessary for COI1-mediated degradation of JAZ11. JA-Ile and structurally
related derivatives can bind to COI1-JAZ complexes and promote ubiquitination and thus
degradation of the latter.[4]
This mechanistic model raises the possibility that COI1 serves as an intracellular receptor for JA
signals. Recent research has confirmed this hypothesis by demonstrating that the COI1-JAZ
complex acts as a co-receptor for JA perception. Specifically, JA-Ile binds both to a ligand-binding
pocket in COI1 and to a 20 amino-acid stretch of the conserved Jas motif in JAZ. This JAZ residue
acts as a plug for the pocket in COI1, keeping JA-Ile bound in the pocket. Additionally, co-purification
and subsequent removal of inositol pentakisphosphate (InsP5) from COI1 suggest InsP5 is a
necessary component of the co-receptor and plays a role in potentiating the co-receptor complex.[7]
Once freed from JAZ, transcription factors can activate genes needed for a specific JA response.
The best-studied transcription factors acting in this pathway belong to the MYC family of
transcription factors, which are characterized by a basic helix-loop-helix (bHLH) DNA binding motif.
These factors (of which there are three, MYC2, 3, and 4) tend to act additively. For example, a plant
that has only lost one myc becomes more susceptible to insect herbivory than a normal plant. A
plant that has lost all three will be as susceptible to damage as coi1 mutants, which are completely
unresponsive to JA and cannot mount a defense against herbivory. However, while all these MYC
molecules share functions, they vary greatly in expression patterns and transcription functions. For
instance, MYC2 has a greater effect on root growth compared to MYC3 or MYC4.[8]
Additionally, MYC2 will loop back and regulate JAZ expression levels, leading to a negative
feedback loop.[8] These transcription factors all have different impacts on JAZ levels after JA
signaling. JAZ levels in turn affect transcription factor and gene expression levels. In other words, on
top of activating different response genes, the transcription factors can vary JAZ levels to achieve
specificity in response to JA signals.
Function[edit]
Although jasmonate (JA) regulates many different processes in the plant, its role in wound response
is best understood. Following mechanical wounding or herbivory, JA biosynthesis is rapidly
activated, leading to expression of the appropriate response genes. For example, in the tomato,
wounding produces defense molecules that inhibit leaf digestion in the insect’s gut. Another indirect
result of JA signaling is the volatile emission of JA-derived compounds. MeJA on leaves can travel
airborne to nearby plants and elevate levels of transcripts related to wound response.[1] In general,
this emission can further upregulate JA synthesis and signaling and induce nearby plants to prime
their defenses in case of herbivory.
Following its role in defense, JAs have also been implicated in cell death and leaf senescence. JA
can interact with many kinases and transcription factors associated with senescence. JA can also
induce mitochondrial death by inducing the accumulation of reactive oxygen species (ROSs). These
compounds disrupt mitochondria membranes and compromise the cell by causing apoptosis, or
programmed cell death. JAs’ roles in these processes are suggestive of methods by which the plant
defends itself against biotic challenges and limits the spread of infections.[9]
JA and its derivatives have also been implicated in plant development, symbiosis, and a host of
other processes included in the list below.

By studying mutants overexpressing JA, one of the earliest discoveries made was that JA
inhibits root growth. The mechanism behind this event is still not understood, but mutants in the
COI1-dependent signaling pathway tend to show reduced inhibition, demonstrating that the
COI1 pathway is somehow necessary for inhibiting root growth.[8][10]

JA plays many roles in flower development. Mutants in JA synthesis or in JA signaling in
Arabidopsis present with male sterility, typically due to delayed development. Interestingly, the
same genes promoting male fertility in Arabidopsis promote female fertility in tomatoes.
Overexpression of 12-OH-JA can also delay flowering.[10]

JA and MeJA inhibit the germination of nondormant seeds and stimulate the germination of
dormant seeds.[11]

High levels of JA encourage the accumulation of storage proteins; genes encoding vegetative
storage proteins are JA responsive. Specifically, tuberonic acid, a JA derivative, induces the
formation of tubers.[12][13]

JAs also play a role in symbiosis between plants and microorganisms; however, its precise role
is still unclear. JA currently appears to regulate signal exchange and nodulation regulation
between legumes and rhizobium. On the other hand, elevated JA levels appear to regulate
carbohydrate partitioning and stress tolerance in mycorrhizal plants.[14]
Role in pathogenesis[edit]
Pseudomonas syringae causes bacterial speck disease in tomatoes by hijacking the plant’s
jasmonate (JA) signaling pathway. This bacteria utilizes a type III secretion system to inject a
cocktail of viral effector proteins into host cells.
One of the molecules included in this mixture is the phytotoxin coronatine (COR). JA-insensitive
plants are highly resistant to P. syringae and unresponsive to COR; additionally, applying MeJA was
sufficient to rescue virulence in COR mutant bacteria. Infected plants also expressed downstream
JA and wound response genes but repressed levels of pathogenesis-related (PR) genes. All these
data suggest COR acts through the JA pathway to invade host plants. Activation of a wound
response is hypothesized to come at the expense of pathogen defense. By activating the JA wound
response pathway, P. syringae could divert resources from its host’s immune system and infect
more effectively.[15]
Cross talk with other defense pathways[edit]
While the jasmonate (JA) pathway is critical for wound response, it is not the only signaling pathway
mediating defense in plants. To build an optimal yet efficient defense, the different defense pathways
must be capable of cross talk to fine-tune and specify responses to abiotic and biotic challenges.
One of the best studied examples of JA cross talk occurs with salicylic acid (SA). SA, a hormone,
mediates defense against pathogens by inducing both the expression of pathogenesis-related genes
and systemic acquired resistance (SAR), in which the whole plant gains resistance to a pathogen
after localized exposure to it.
Wound and pathogen response appear to be interact negatively. For example, silencing
phenylalanine ammonia lyase (PAL), an enzyme synthesizing precursors to SA, reduces SAR but
enhances herbivory resistance against insects. Similarly, overexpression of PAL enhances SAR but
reduces wound response after insect herbivory.[16] Generally, it has been found that pathogens living
in live plant cells are more sensitive to SA-induced defenses, while herbivorous insects and
pathogens that derive benefit from cell death are more susceptible to JA defenses. Thus, this tradeoff in pathways optimizes defense and saves plant resources.[17]
Cross talk also occurs between JA and other plant hormone pathways, such as those of abscisic
acid (ABA) and ethylene (ET). These interactions similarly optimize defense against pathogens and
herbivores of different lifestyles. For example, MYC2 activity can be stimulated by both JA and ABA
pathways, allowing it to integrate signals from both pathways. Other transcription factors such as
ERF1 arise as a result of JA and ET signaling. All these molecules can act in combination to activate
specific wound response genes.[17]
Finally, cross talk is not restricted for defense: JA and ET interactions are critical in development as
well, and a balance between the two compounds is necessary for proper apical hook development
in Arabidopsisseedlings. Still, further research is needed to elucidate the molecules regulating such
cross talk.[16]
A polyamine is an organic compound having two or more primary amino groups –NH
2.[citation needed]
Low-molecular-weight linear polyamines perform essential functions in all living cells. Primary
examples are putrescine, cadaverine, spermidine, and spermine. In animals, their levels are
maintained from both the diet and de novo synthesis, and their decline with age is associated with
various pathologies. Polyamine metabolism is regulated by the activity of the enzyme ornithine
decarboxylase (ODC).[1] Polyamines are found in high concentrations in the mammalian brain.[2]
This class of compounds also includes several synthetic substances that are important feedstocks
for the chemical industry, such as ethylene diamine H
2N–CH
2–CH
2–NH
2,1,3-diaminopropane
H
2N–(CH
2)
3–NH
2,
and hexamethylenediamine H
2N–(CH
2)
6–NH
2.
Certain polyamines are employed on industrial scales as co-reactants (hardeners)
withepoxy resins.
As of 2004, there had been no reports of any geminal diamine, a compound with two or more
unsubstituted –NH
2
groups on the same carbon atom. However, substituted derivatives are known, such
as tetraethylmethylenediamine, (C
2H
5)
2N–CH
2–N(C
2H
5)
2.[3]
Piperazine is an example of a cyclic polyamine. Cyclen and cyclam are examples
of macrocyclic polyamines. Polyethylene amine is a polymer based on the aziridine monomer.
Most aromatic polyamines are crystalline solids at room temperature.
Contents
[hide]





1Functions
o 1.1Biological
o 1.2Chelating agents
2Biosynthesis of linear polyamines
o 2.1Putrescine
o 2.2Cadaverine
o 2.3Spermidine and spermine
o 2.4Thermospermine
3Polyamine Analogues
4References
5External links
Functions[edit]
Biological[edit]
Though it is known that polyamines are synthesized in cells via highly regulated pathways, their
actual function is not entirely clear. As cations, they bind to DNA, and, in structure, they represent
compounds with cations that are found at regularly spaced intervals (unlike, say, Mg2+
or Ca2+
, which are point charges). They have also been found to act as promoters of programmed
ribosomal frameshifting during translation.[4]
If cellular polyamine synthesis is inhibited, cell growth is stopped or severely retarded. The provision
of exogenous polyamines restores the growth of these cells. Most eukaryotic cells have a polyamine
transportersystem on their cell membrane that facilitates the internalization of exogenous
polyamines. This system is highly active in rapidly proliferating cells and is the target of some
chemotherapeutics currently under development.[5]
Polyamines are also important modulators of a variety of ion channels, including NMDA
receptors and AMPA receptors. They block inward-rectifier potassium channels so that the currents
of the channels are inwardly rectified, thereby the cellular energy, i.e. K+
ion gradient across the cell membrane, is conserved. In addition, polyamine participate in initiating
the expression of SOS response of Colicin E7 operon and down-regulate proteins that are essential
for colicin E7 uptake, thus conferring a survival advantage on colicin-producing E. coli under stress
conditions.[6]
Polyamines can enhance the permeability of the blood–brain barrier.[7]
They are involved in modulating senescence of organs in plants and are therefore considered as
a plant hormone.[8] In addition, they are directly involved in regulation of programmed cell death [9]
Chelating agents[edit]
Ethylenediamineligand, binding to a central atom with two bonds
Polyamines are important chelating agents. tetramethylethylenediamine (TMED) is useful for
dissolving metal ions in organic solvents. Polyamines like diethylenetriamine (DETA or
dien)and triethylenetetramine (TETA or trien) and more powerful chelating agents forming tridentate
and tetradentate complexes, respectively. Macrocyclic polyamines like cyclam add cavity selectivity
to the chelate effect. The heme group in Hemoglobin is an important example of a macrocyclic
ligand containing the polyamine motif.
There are aromatic analogues of the aliphatic linear polyamines such as dipyridine, ophenanthroline and terpyridine which are also useful chelating agents.
Protonated polyamines, particularly macrocyclic ones, can bind anions. By varying the shape and
size of the cavity the protonated polyamine can be engineered to be a specific anion receptor.
Biosynthesis of linear polyamines[edit]
Putrescine[edit]
Putrescine is synthesized biologically via two different pathways, both starting from arginine.

In one pathway, arginine is converted into agmatine, with a reaction catalyzed by the
enzyme arginine decarboxylase (ADC); then agmatine is transformed into Ncarbamoylputrescine by agmatine imino hydroxylase (AIH). Finally, N-carbamoylputrescine is
converted into putrescine.[10]

In the second pathway, arginine is converted into ornithine and then ornithine is converted into
putrescine by ornithine decarboxylase (ODC).
Cadaverine[edit]
Cadaverine is synthesized from lysine in a one-step reaction with lysine decarboxylase (LDC).
Spermidine and spermine[edit]
Biosynthesis of spermidine and spermine from putrescine. Ado = 5'-adenosyl.
Spermidine is synthesized from putrescine, using an aminopropyl group from decarboxylated Sadenosyl-L-methionine (SAM). The reaction is catalyzed by spermidine synthase.
Spermine is synthesized from the reaction of spermidine with SAM in the presence of the
enzyme spermine synthase.
Thermospermine[edit]
Thermospermine is a structural isomer of spermine and a novel type of plant growth regulator. It is
produced from spermidine by the action of thermospermine synthase, which is encoded by a gene
named ACAULIS5 (ACL5).[11]
Polyamine Analogues[edit]
The critical role of polyamines in cell growth has led to the development of a number of agents that
interfere with polyamine metabolism. These agents are used in cancer therapy. Polyamine
analogues upregulatep53 in a cell leading to restriction of proliferation and apoptosis.[12] It also
decreases the expression of estrogen receptor alpha in ER positive breast cancer.[13]