Trends in Food Science & Technology 21 (2010) 502e509

Review

Impact of salicylic
acid on post-harvest
physiology of
horticultural crops
Mohammadreza Asgharia,* and
Morteza Soleimani Aghdamb
a

Department of Horticulture, Faculty of Agriculture,

Urmia University, Nazloo street, Urmia, Iran (Tel.:
D98 914 343 3494; fax: D98 441 297 2360; e-mails:
m.asghari@urmia.ac.ir; mhamadreza@yahoo.com)
b
Iranian Young Researchers Club, Islamic Azad
University, Ahar Branch, Ahar, Iran
Salicylic acid (SA), an endogenous plant growth regulator, has
been found to generate a wide range of metabolic and physiological responses in plants thereby affecting their growth and
development. SA as a natural and safe phenolic compound exhibits a high potential in controlling post-harvest losses of horticultural crops. In the present review, we have focused on
various intrinsic biosynthetic pathways and effects of exogenous salicylic acid on post-harvest decay and disease resistance, oxidative stress, fruit ripening, ethylene biosynthesis
and action, fruit firmness, respiration, antioxidant systems
and nutritional quality have also been discussed.

Introduction
Salicylic acid (SA) and methyl salicylate (MeSA) are
endogenous signal molecules, playing pivotal roles in regulating stress responses and plant developmental processes
including heat production or thermogenesis, photosynthesis, stomatal conductance, transpiration, ion uptake and
transport, disease resistance, seed germination, sex polarization, crop yield and glycolysis (Klessig & Malamy,
1994). Recently, SA has received a particular attention because it is a key signal molecule for expression of multiple
modes of plant stress resistance. Although the focus has
* Corresponding author.
0924-2244/$ - see front matter 2010 Elsevier Ltd. All rights reserved.
doi:10.1016/j.tifs.2010.07.009

been mainly on the roles of SA on biotic stresses, several

studies also support major roles of salicylates in modulation
of the plant response to several abiotic stresses, such as UV
light, drought, salinity, chilling stress and heat shock (Ding
& Wang, 2003; Ding, Wang, Gross, & Smith, 2001).
Salicylates delay the ripening of fruits, probably through inhibition of ethylene biosynthesis or action, and maintain
post-harvest quality (Srivastava & Dwivedi, 2000). Some
of the results reported by several authors regarding the effects of SA on quality aspects of different harvested horticultural crops have been summarized in Table 1.
Postharvest decay control in horticultural crops
Plants continuously remain exposed to the challenging
threats of a variety of pathogenic attacks. For many years
synthetic fungicides were used to control post-harvest decay but, the public concerns about fungicide residues in
fresh horticultural crops and the harmful effects of chemicals on human health and environment have recently caused
scientists to search for new alternatives to chemical fungicides (Babalar, Asghari, Talaei, & Khosroshahi, 2007). Recent studies have shown that SA can be introduced as
a potent alternative to chemicals (Table 1). Malamy, Carr,
and Klessig (1990) showed that large amount of SA accumulates in the leaves of tobacco mosaic virus (TMV) resistant tobacco variety Nicotiana tabaccum cv. Xanthi upon
inoculation with TMV. Further, SA or acetyl salicylic
acid (ASA), a synthetic analogue of SA, when applied exogenously induced the expression of PR (pathogenesis related) genes and also conferred resistance against various
pathogens (Malamy & Klessig, 1992). Exogenous application of SA at nontoxic concentrations to susceptible fruits
and vegetables could enhance resistance to pathogens and
control post-harvest decay (Asghari, Hajitagilo, &
JaliliMarandi, 2009; Asghari, Hajitagilo, & Shirzad, 2007;
Babalar et al., 2007). SA in a concentration dependent manner from 1 to 2 mmol L
1 effectively reduced fungal decay
in Selva strawberry fruit (Babalar et al., 2007).
MeSA triggers disease resistance and mediates the expression of defense related genes in neighboring plants and
in healthy tissue of infected plants (Shulaev, Silverman, &
Raskin, 1997). In Hayward kiwifruit post-harvest decay
was significantly affected by MeSA vapor at the end of storage period. Decay incidence in fruit treated with 32 ml L
1
was 6.3% whereas it was 34.2% in control fruits (Aghdam,
Mostofi, Motallebiazar, Ghasemneghad, & Fattahi

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503

Table 1. Summary of some effects of SA on some harvested horticultural crops reported by different authors
Author(s)

Reported results

Commodity

Babalar et al. (2007)

Sayyari, Babalar, Kalantari,
Serrano, and Valero (2009)
Zhang et al. (2003)

Marketability retention, decrease in ethylene production & fungal decay

Inhibition of PAL activity, retention of vitamin C content reduction of CI & EL

Strawberry
Pomegranate

Inhibition of ACS, ACO & LOX activity, suppression of ethylene & superoxide free radical
production, increase in total SA content,
Decrease in fruit softening, pulp/peel ratio,reducing sugar content, invertase activity &
respiration rate, inhibition of cellulase, PG, xylanase, CAT & POX activity
Increase in firmness, APX, GR activity, AsA/DHAsA & GSH/GSSG ratios, decrease in CI, DI
induction of HSP101 & HSP73 genes
Increase in b-1, 3-glucanase, PAL & POD activity, induction of disease resistance, direct
antifungal activity
Increase in transcript levels of AOX, CI protection
Development of red color, regulation of ACS genes expression
Accumulation of HSPs, CI reduction
Acceleration of H2O2 accumulation, increase in SOD, GR, APX & DHAR activity & ASA/
DHASA & GSH/GSSG ratios, decrease in lipid peroxidation & MDA
Decreased ethylene, LOX activity, MDA content, DI, softening & respiration rates, TSS &
activated the SOD, POD, CAT&APX enzymes
Inhibition of ethylene production, ripening & decay control
Expression of AOX, CI resistance
Decay control, increase in CAT, GPX, b-1, 3-glucanase& chitinase
Increase in GPX, APX, CAT, SOD & GR activity, induction of resistance to CI

Kiwifruit

Kiwifruit
Tomato
Sweet cherry
Watermelon

Enhanced the biological efficacy of antagonist C. laurentii

Decay, Ripening& weight loss reduction

Apple
Strawberry

Inhibition of PAL, CAT & POD decrease in superoxide free radical production & CI
Induction of resistance to diseases, increase in POD, PAL, GR, Chitinase & b-1,
3-glucanase, decrease in CAT & APX
Delayed discoloration, maintained edible quality, activity of PPO, POD & PAL

Loquat
Pear

Srivastava and Dwivedi (2000)

Wang, Chen, Kong, Li, and
Archbold (2006)
Yao and Tian (2005)
Fung et al. (2004)
Ding and Wang (2003)
Ding et al. (2001)
Hung, Liu, Lu, and Xia (2007)
Mo et al. (2008)
Aghdam et al., (2009)
Fung et al. (2006)
Xu and Tian (2008)
Jing-Hua, Yuan, Yan-Man,
Xiao-Hua, and Zhang (2008)
Yu and Zheng (2006)
Shafiee, Taghavi, and Babalar
(2010)
Cao, Zeng, and Jiang (2006)
Cai et al. (2006)
Peng and Jiang (2006)

Banana
Peach
Sweet cherry
Sweet pepper
Tomato
Tomato
Orange
Apple

Fresh-cut
Chestnut

DI decay index, GR glutathione reductase, GSSG oxidized glutathione, GSH reduced glutathione, DHAR dehydroascorbate reductase, AsA ascorbate, DHAsA dehydroascorbate, MDA Malondialdehyde.

Moghaddam, 2009). Dipping of pear fruit in 1 mmol L
1 SA

solution effectively controlled fruit decay during 5 months of
cold storage (Asghari et al., 2007). Treatment of strawberry
plants at vegetative stage and fruit development stage followed by post-harvest treatment of fruits with 1 and
2 mmol L
1 effectively controlled the total decay and increased fruit shelf life (Babalar et al., 2007). Postharvest
treatment of table grapes with SA before coating with chitosan significantly enhanced the efficacy of coating and decreased fruit total decay (Asghari et al., 2009). Some
researches indicate that SA also exhibits direct antifungal effects against pathogens. Lu and Chen (2005) have demonstrated the inhibitory action of SA on botrytis rot in lily
leaves. Foliar application of Asilbenzolar-S-Methyl (a synthetic analogue of SA) has led to protection of post-harvest
Rock melons and Hami melons from diseases (Huang,
Deverall, Tang, Wang, & Wu, 2000). 2 mmol L
1 SA showed
direct fungal toxicity on Monilinia fructicola and significantly inhibited the mycelial growth and spore germination
of the pathogen in vitro (Yao & Tian, 2005).
SA also effectively enhances the biocontrol efficacy of
antagonist yeasts. According to the results of Qin, Tian,

Xu, and Wan (2003), 0.5 mmol L
1 SA significantly reduced the incidence of blue mould (P. expansum) and alternaria rot (A. alternata) in sweet cherry without any surface
injury. Adding SA significantly improved the activity of
R. glutinis against both pathogens.
Plants protect themselves against the pathogen attacks
by activating some kinds of defense mechanisms such as local acquired resistance (LAR) and systemic acquired resistance (SAR) (Vlot, Dempsey, & Klessig, 2009). As seen in
Fig. 1, salicylates are a major component in the signal
transduction pathways of plants playing an important role
in disease resistance (Park, Kaimoyo, Kumar, Mosher, &
Klessig, 2007). Once plant defense responses are activated
at the site of infection (LAR), a systemic defense response
is often triggered in distal plant parts to protect these undamaged tissues against subsequent invasion by the pathogen. This long-lasting and broad-spectrum induced disease
resistance is referred to as SAR and is characterized by the
coordinate activation of a specific set of PR-genes, many of
which encode for proteins with antimicrobial activity
(Durrant & Dong, 2004; Van Loon, Rep, & Pieterse,
2006). The onset of SAR is associated with increased levels

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rate of superoxide radical (O2
) generation in SA-treated

fruits were higher than that in controls after 8 days of treatment. According to the findings of Tian et al. (2007) the
balance between superoxide dismutase (SOD), POD and
catalase (CAT) activities in cells is crucial for determining
the steady-state level of O2
and H2O2. SA interaction
with the above mentioned enzymes leads to high levels of
H2O2 accumulating in cells, which induces fruit resistance
against pathogens via activating protective enzymes and
PR-proteins (Klessig & Malamy, 1994; Malamy &
Klessig, 1992;). It has been demonstrated that, SA inhibits
the H2O2-scavenging activity of cytosolic ascorbate peroxidase (APX), and H2O2 levels concomitantly rise upon SA
treatment of tobacco leaves (Fig. 1). Thus, SA may also
facilitate H2O2 accumulation during the oxidative burst
(OB) induced by infection with the virulent pathogens.
The increased ROS associated with the OB may contribute
to resistance via several mechanisms, including directly
killing the invading pathogen and/or activating cell wall
crosslinking and lignification, thereby strengthening the
cell wall and helping confine the pathogen to the infection
site (Dempsey, Shah, & Klessig, 1999)

Fig. 1. SA decreases the expression of ascorbate peroxidase (APX) &

catalase (CAT) genes leading to substantial increase in H2O2 which
is crucial for the activation of local acquired resistance (LAR) &
systemic acquired resistance (SAR).

of SA, locally at the site of infection and often also systemically in distant tissues (Klessig & Malamy, 1994; Malamy
& Klessig, 1992; Tsuda, Sato, Glazebrook, Cohen, &
Katagiri, 2008). Park et al., (2007) demonstrated that
MeSA acts as a crucial long distance SAR signal in tobacco. SA can induce the accumulation of hydrogen peroxide (H2O2) levels in plant tissues which acts as a signal
activating the SAR (Fig. 1) (Klessig & Malamy, 1994;
Tian, Qin, Li, Wang, & Meng, 2007). Mutant and transgenic plants that are impaired in SA signaling are incapable
of developing SAR and dont show PR gene activation
upon pathogen infection, which indicates that SA is a necessary intermediate in the SAR signaling pathway (Durrant &
Dong, 2004; Pieterse, Leon-Reyes, Van der Ent, & Van
Wees, 2009). The SA induced defense responses are probably involved in the expression of a range of defense genes,
especially those encoding PR-proteins such as chitinase,
b-1, 3-glucanase and peroxidase (POD) (Meena,
Marimuthu, & Velazhahan, 2001). According to Zeng,
Cao, and Jiang (2006), in a study on mangoes after
4 days of treatment the activity of b-1, 3-glucanase in
SA-treated fruits were over higher than in controls. They
found that the level of hydrogen peroxide (H2O2) and the

SA prevents post-harvest oxidative stress and alleviates chilling injury during cold storage
Plant defense system against oxidative stress consists of
two lines; The first line of defense is termed ROS avoidance
genes includes alternative oxidase (AOX) and the second is
termed as ROS scavenging genes includes SOD, CAT, the
ascorbate/glutathione cycle, the glutathione peroxidase system and thioredoxin system (Fig. 2) (Buchanan, Gruissem,
& Jones, 2000, p 1343). SA has been shown to induce expression of AOX and increase the antioxidant capacity of
the cells (Table 1, Fig. 2). For example, SA stimulates
the synthesis of antioxidant enzymes and induces the activity of PPO, PAL and b-1, 3-glucanase in sweet cherries
(Fig. 3) (Qin et al., 2003). Yao and Tian (2005) reported
that pre-harvest treatment of sweet cherries with SA has induced b-1, 3-glucanase, PAL and POD activities during the
short time storage period and the activity of these enzymes
in SA-treated cherries stored at 25  C was higher than in
fruits stored at 0  C. SA, in a concentration dependent manner from 0 to 2 mmol L
1, enhanced the strawberry fruit
total antioxidant capacity (TAC). 2 mmol L
1 was the
most effective concentration while SA at 4 mmol L
1
caused a slight increase in fruit TAC. Consequent application of SA at three stages of vegetative growth, fruit development and post-harvest stage was the most effective
strategy in improving fruit TAC (Asghari, & Babalar,
2009). Postharvest treatment of sweet cherry fruits with
SA significantly inhibited CAT activity, but stimulated the
activity of SOD and POD. After inoculation with P. expansum, CAT activity decreased and SOD activity increased in
SA-treated fruits. SA treatment also changed the expression
of POD isozymes, indicating that SA directly or indirectly
activates antioxidant enzymes (Tian et al., 2007).

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505

Fig. 2. Antioxidant systems in plants.

Chilling injury (CI) is a type of damage caused by low

temperature as a result of oxidative burst. Although there
are many methods to reduce CI in various horticultural
crops, SA and MeSA treatments are inexpensive, easy to
set up and applicable to various horticultural crops (Ding
et al., 2001). Increase in AOX transcript levels using SA
and MeSA before cold treatment reduced incidence of CI
in freshly green bell peppers (Fung, Wang, Smith, Gross,
& Tian, 2004). In response to abiotic stresses, all living organisms synthesis new proteins, for example, plants respond to high temperatures with the synthesis of a group
of proteins known as heat shock proteins (HSPs) (Fig. 3).
Often the accumulation of HSPs not only confers protection
against the stress that causes their biosynthesis but also
against any other subsequent stress situation (Tian et al.,
2007). Treatments with SA and MeSA prior to low-temperature storage induce HSPs biosynthesis and, at the same
time, CI tolerance in tomatoes and peaches (Ding et al.,
2001). Accumulation of the HSPs in chilling-sensitive horticultural products with SA and MeSA treatments would

allow their storage at low temperatures without CI development. On the other hand lipid peroxidation is one of the adverse effects of CI on plant cells leading to
malondialdehyde (MDA) accumulation. It has been reported that MDA accumulation is prevented after SA treatment (Table 1 & Fig. 3)
SA delays fruit ripening
Impact of SA on fruit softening
Fruit ripening and senescence are accompanied by
changes in several quality aspects such as softening, decrease in total acidity and increase in sugar contents, color
development, aroma production and etc. (Wills,
McGlasson, Graham, & Joyce, 1998). Softening of fruits
is a main and critical quality change. MeSA, in a concentration dependent manner from 0 to 32 ml L
1, maintained
firmness of kiwifruit during storage (Aghdam et al.,
2009). Srivastava and Dwivedi (2000) reported that in
bananas treated with SA fruit softening markedly
decreased. Zhang, Chen, Zhang, and Ferguson (2003)

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Fig. 3. Induction of chilling resistance in plants by SA.

reported a positive correlation between fruit free SA content and firmness in kiwifruit during ripening. Retention
of fruit firmness as the result of SA treatment has been reported in several crops (Table 1). It has been demonstrated
that SA decreases ethylene production and inhibits cell wall
and membrane degrading enzymes such as polygalacturonase (PG), lipoxygenase (LOX), cellulase and pectinemethylesterase (PME) leading to decreasing the fruit
softening rate (Srivastava & Dwivedi, 2000; Zhang et al.,
2003).
Effect on TSS and sugars
TSS and soluble sugars may increase during fruit ripening due to the action of sucrose-phosphate synthase (SPS),
a key enzyme in sucrose biosynthesis (Hubbard, Pharr, &
Huber, 1991). This enzyme is activated by ethylene and
the ripening process itself during storage (Langenkamper,
McHale, Gardner, & MacRae, 1998). Recently, an increase
in sucrose-phosphate synthase and invertase activities and
a decrease in sucrose synthase activity have been reported
during ripening of some fruits (Cordenunsi & Lajolo,
1995). Treatment of kiwifruits with MeSA of 32 ml L
1
maintained a lower TSS content than the control fruits at
the end of cold storage (Aghdam et al., 2009). The authors
proposed that MeSA reduced ethylene production may results to decreased SPS enzyme activity leading to decrease
in sucrose synthesis.
The ripening of banana fruit is accompanied by increase
in pulp to peel ratio. Rise in pulp to peel ratio during fruit
ripening may be due to change in sugar concentration in the
two tissues. A rapid increase in sugar contents in the pulp

than those in the peel leads to a change in osmotic pressure,

as a result of which water is withdrawn from the peel and
hence pulp to peel ratio increases accordingly. According
to the findings of Srivastava and Dwivedi (2000), SA treatment, in a concentration dependent manner, reduces this increase in pulp to peel ratio, leading to a delay in banana
fruit ripening. The result showed that the invertase activity
is concomitant with decrease in nonreducing sugar content.
The level of reducing sugars is increased and nonreducing
sugars is decreased during ripening and senescence. This
accumulation of reducing sugars may be due to increased
breakdown of starch during ripening as reported by
Beaudry, Ray, Clanton, and Stanley (1989). SA treatment
resulted in decreased levels of invertase and reducing sugar
contents while an opposite effect on nonreducing sugar
content, suggesting that SA delays banana fruit ripening.
On the other hand cell walls contain large amounts of
polysaccharides, mainly pectins and cellulose, and are digested due to the activity of the cell wall degrading enzymes
leading to a significant increase in TSS content. Then any factor preventing these enzymes will prevent from a dramatic increase in TSS content. As seen in Table 1 and Fig. 4, SA
effectively protects cell walls by decreasing the expression
of degrading enzymes and as a consequence prevents from
dramatic increase in TSS content of the cells.
Inhibition of ethylene biosynthesis
Ethylene plays a key role in fruit ripening and senescence. This hormone triggers the induction of cell wall hydrolyzing enzymes leading to increase in respiration rate,
fruit softening and senescence (Wills et al., 1998). SA

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507

Fig. 4. Schematic overview of mechanisms by which SA delays fruit ripening and extends storage life.

effectively decreases ethylene production in several horticultural crops (Table 1). It has been shown that MeSA treatment significantly decreases ethylene production in
kiwifruits (Aghdam et al., 2009). Both SA and ASA have
been shown to inhibit ethylene production in cultured
pear cells, mung bean hypocotyls, apple and pear fruit tissue discs, carrot cell suspension cultures and some fruits
(Babalar et al., 2007; Romani, Hess, & Leslie, 1989).
Srivastava and Dwivedi (2000) reported that SA has delayed the ripening of banana fruit, probably through inhibition of ethylene biosynthesis or action. SA decreases
ethylene production by decreasing ACS and ACO production and activity. Zhang et al., (2003) reported that postharvest treatment of kiwifruit with ASA resulted in a lower
ACO and ACS activity and decreased ethylene production
during the early stages of fruit ripening.
Effect on LOX activity
There is evidence for a positive correlation between
LOX activity, free radicals production and ethylene biosynthesis in fruit tissue (Marcelle, 1991). SA inhibited woundinduced transcription and also activity of ACS in tomato
and decreased LOX activity in disks of kiwifruit leading
to the consequent reduction in the production of free radicals and ethylene biosynthesis (Zhang et al., 2003). Ding
and Wang (2003) showed that ripening process in mature
green tomatoes was enhanced by 0.1 mmol L
1 MeSA
and by 0.01 mmol L
1 during breaker stage. But in fruit
at turning stage even 0.01 mmol L
1 SA inhibited the ripening process. 0.5 mmol L
1 SA prevented red color

development and increased ethylene production and respiration rate in all maturity stages.
Effect on cell respiration
SA has been reported to effectively reduce the respiration rate in several fruits (Table 1). SA as a signal triggers
the induction of cyanide resistance respiration in plant cells
by affecting the AOX enzyme activity (Raskin, Turner, &
Melander, 1989). In horticultural crops, SA affects AOX
activity leading to decrease in the harmful effects of different post-harvest oxidative stresses such as chilling injury,
prevents fermentation, and maintains low respiration rates
and decreases fruit ripening and senescence rates. Respiration of harvested crops is highly dependent to ethylene production and activity and any factor increasing the
production and activity of ethylene leads to increases in respiration and consequently increases the senescence rate. Effect of SA in decreasing the respiration rate is mainly due
to its negative effects on ACC, ACO, PG, PME, cellulase
and antioxidant enzymes leading to decrease in ethylene
production and action (Fig. 4).
Conclusion
SA, as a natural and safe phenolic compound, exhibits
a high potential in controlling post-harvest losses of horticultural crops. Decrease in ethylene production and action, induction of disease resistance, prevention of oxidative
stresses, induction of crop tolerance to chilling injury, decrease in respiration rate, decrease in ripening and senescence rate, prevention of cell wall degrading enzymes and

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maintaining crop firmness are of main results obtained following SA treatment. The application of SA and especially
pre-harvest, for inducing the defense resistance systems
against post-harvest diseases may be a useful and promising
measure for controlling post-harvest decay on a commercial
scale. Since it effectively enhances the effects of other postharvest treatments, such as heat treatments and biocontrol
agents, use of SA in combination with other post-harvest
treatments may give better results in controlling post-harvest
losses. SA can be used as an appropriate alternative to chemicals in post-harvest technology of horticultural crops to assure food safety. Since SA, like any other post-harvest
treatment, may have different effects on different crops at
different circumstances, it is necessary to determine the
best and safe concentration for each crop cultivar.

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