aas_physiology.pdf

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Review

Impact of salicylic

acid on post-harvest

physiology of

horticultural crops

Mohammadreza Asgharia,*andMorteza Soleimani Aghdamb

aDepartment of Horticulture, Faculty of Agriculture,Urmia University, Nazloo street, Urmia, Iran (Tel.:

D98 914 343 3494; fax: D98 441 297 2360; e-mails:[email protected];[email protected])

bIranian Young Researchers Club, Islamic AzadUniversity, Ahar Branch, Ahar, Iran

Salicylic acid (SA), an endogenous plant growth regulator, hasbeen found to generate a wide range of metabolic and physi-

ological responses in plants thereby affecting their growth and

development. SA as a natural and safe phenolic compound ex-

hibits a high potential in controlling post-harvest losses of hor-

ticultural crops. In the present review, we have focused on

various intrinsic biosynthetic pathways and effects of exoge-

nous salicylic acid on post-harvest decay and disease resis-

tance, oxidative stress, fruit ripening, ethylene biosynthesis

and action, fruit firmness, respiration, antioxidant systems

and nutritional quality have also been discussed.

IntroductionSalicylic acid (SA) and methyl salicylate (MeSA) are

endogenous signal molecules, playing pivotal roles in reg-

ulating stress responses and plant developmental processes

including heat production or thermogenesis, photosynthe-

sis, stomatal conductance, transpiration, ion uptake and

transport, disease resistance, seed germination, sex polari-

zation, crop yield and glycolysis (Klessig & Malamy,

1994). Recently, SA has received a particular attention be-

cause it is a key signal molecule for expression of multiple

modes of plant stress resistance. Although the focus has

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 in-

hibition of ethylene biosynthesis or action, and maintain

post-harvest quality (Srivastava & Dwivedi, 2000). Someof the results reported by several authors regarding the ef-

fects of SA on quality aspects of different harvested horti-

cultural crops have been summarized inTable 1.

Postharvest decay control in horticultural cropsPlants continuously remain exposed to the challenging

threats of a variety of pathogenic attacks. For many years

synthetic fungicides were used to control post-harvest de-

cay but, the public concerns about fungicide residues in

fresh horticultural crops and the harmful effects of chemi-

cals on human health and environment have recently caused

scientists to search for new alternatives to chemical fungi-

cides (Babalar, Asghari, Talaei, & Khosroshahi, 2007). Re-cent 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 accu-

mulates in the leaves of tobacco mosaic virus (TMV) resis-

tant tobacco variety Nicotiana tabaccum cv. Xanthi upon

inoculation with TMV. Further, SA or acetyl salicylic

acid (ASA), a synthetic analogue of SA, when applied ex-

ogenously induced the expression of PR (pathogenesis re-

lated) genes and also conferred resistance against various

pathogens (Malamy & Klessig, 1992). Exogenous applica-

tion of SA at nontoxic concentrations to susceptible fruits

and vegetables could enhance resistance to pathogens andcontrol post-harvest decay (Asghari, Hajitagilo, &

JaliliMarandi, 2009; Asghari, Hajitagilo, & Shirzad, 2007;

Babalaret al., 2007). SA in a concentration dependent man-

ner from 1 to 2 mmol L1 effectively reduced fungal decay

in Selva strawberry fruit (Babalar et al., 2007).

MeSA triggers disease resistance and mediates the ex-

pression 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 stor-

age period. Decay incidence in fruit treated with 32 ml L1

was 6.3% whereas it was 34.2% in control fruits (Aghdam,

Mostofi, Motallebiazar, Ghasemneghad, & Fattahi* Corresponding author.

0924-2244/$ - see front matter 2010 Elsevier Ltd. All rights reserved.doi:10.1016/j.tifs.2010.07.009

Trends in Food Science & Technology 21 (2010) 502e509
mailto:[email protected]:[email protected]://dx.doi.org/10.1016/j.tifs.2010.07.009http://dx.doi.org/10.1016/j.tifs.2010.07.009http://dx.doi.org/10.1016/j.tifs.2010.07.009mailto:[email protected]:[email protected]://dx.doi.org/10.1016/j.tifs.2010.07.009http://dx.doi.org/10.1016/j.tifs.2010.07.009http://dx.doi.org/10.1016/j.tifs.2010.07.009


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Moghaddam, 2009). Dipping of pear fruit in 1 mmol L1 SA

solution effectively controlled fruit decay during 5 months of

cold storage (Asghariet al., 2007). Treatment of strawberry

plants at vegetative stage and fruit development stage fol-

lowed by post-harvest treatment of fruits with 1 and

2 mmol L1 effectively controlled the total decay and in-

creased fruit shelf life (Babalar et al., 2007). Postharvest

treatment of table grapes with SA before coating with chito-

san significantly enhanced the efficacy of coating and de-creased fruit total decay (Asghari et al., 2009). Some

researches indicate that SA also exhibits direct antifungal ef-

fects against pathogens.Lu and Chen (2005)have demon-

strated the inhibitory action of SA on botrytis rot in lily

leaves. Foliar application of Asilbenzolar-S-Methyl (a syn-

thetic analogue of SA) has led to protection of post-harvest

Rock melons and Hami melons from diseases (Huang,

Deverall,Tang, Wang, & Wu, 2000).2mmolL1 SA showed

direct fungal toxicity on Monilinia fructicola and signifi-

cantly inhibited the mycelial growth and spore germination

of the pathogenin 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 L1 SA significantly re-

duced the incidence of blue mould (P. expansum) and alter-

naria 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 lo-

cal acquired resistance (LAR) and systemic acquired resis-

tance (SAR) (Vlot, Dempsey, & Klessig, 2009). As seen inFig. 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 un-

damaged tissues against subsequent invasion by the patho-

gen. 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 ofPR-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

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) Marketability retention, decrease in ethylene production & fungal decay StrawberrySayyari, Babalar, Kalantari,Serrano, and Valero (2009)

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

Zhang et al. (2003) Inhibition of ACS, ACO & LOX activity, suppression of ethylene & superoxide free radicalproduction, increase in total SA content,

Kiwifruit

Srivastava and Dwivedi (2000) Decrease in fruit softening, pulp/peel ratio,reducing sugar content, invertase activity &respiration rate, inhibition of cellulase, PG, xylanase, CAT & POX activity

Banana

Wang, Chen, Kong, Li, andArchbold (2006)

Increase in firmness, APX, GR activity, AsA/DHAsA & GSH/GSSG ratios, decrease in CI, DIinduction of HSP101 & HSP73 genes

Peach

Yao and Tian (2005) Increase in b-1, 3-glucanase, PAL & POD activity, induction of disease resistance, directantifungal activity

Sweet cherry

Fung et al. (2004) Increase in transcript levels of AOX, CI protection Sweet pepperDing and Wang (2003) Development of red color, regulation of ACS genes expression TomatoDing et al. (2001) Accumulation of HSPs, CI reduction TomatoHung, Liu, Lu, and Xia (2007) Acceleration of H2O2accumulation, increase in SOD, GR, APX & DHAR activity & ASA/

DHASA & GSH/GSSG ratios, decrease in lipid peroxidation & MDAOrange

Moet al. (2008) Decreased ethylene, LOX activity, MDA content, DI, softening & respiration rates, TSS &activated the SOD, POD, CAT&APX enzymes

Apple

Aghdam et al., (2009) Inhibition of ethylene production, ripening & decay control KiwifruitFung et al. (2006) Expression of AOX, CI resistance TomatoXu and Tian (2008) Decay control, increase in CAT, GPX, b-1, 3-glucanase& chitinase Sweet cherryJing-Hua, Yuan, Yan-Man,Xiao-Hua, and Zhang (2008)

Increase in GPX, APX, CAT, SOD & GR activity, induction of resistance to CI Watermelon

Yu and Zheng (2006) Enhanced the biological efficacy of antagonistC. laurentii AppleShafiee, Taghavi, and Babalar(2010)

Decay, Ripening& weight loss reduction Strawberry

Cao, Zeng, and Jiang (2006) Inhibition of PAL, CAT & POD decrease in superoxide free radical production & CI LoquatCai et al. (2006) Induction of resistance to diseases, increase in POD, PAL, GR, Chitinase & b-1,

3-glucanase, decrease in CAT & APXPear

Peng and Jiang (2006) Delayed discoloration, maintained edible quality, activity of PPO, POD & PAL Fresh-cutChestnut

DI decay index, GR glutathione reductase, GSSG oxidized glutathione, GSH reduced glutathione, DHAR dehydroascorbate reduc-

tase, AsA ascorbate, DHAsA dehydroascorbate, MDA Malondialdehyde.

503M. Asghari, M.S. Aghdam / Trends in Food Science & Technology 21 (2010) 502e509


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of SA, locally at the site of infection and often also system-

ically 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 to-

bacco. SA can induce the accumulation of hydrogen perox-

ide (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 trans-

genic plants that are impaired in SA signaling are incapableof developing SAR and dont show PR gene activation

upon pathogen infection, which indicates that SA is a neces-

sary intermediate in the SAR signaling pathway (Durrant &

Dong, 2004; Pieterse, Leon-Reyes, Van der Ent, & Van

Wees, 2009). The SA induced defense responses are prob-

ably 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

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

fruits were higher than that in controls after 8 days of treat-

ment. 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 interactionwith 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 perox-

idase (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 directlykilling 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)

SA prevents post-harvest oxidative stress and allevi-ates 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 sys-

tem and thioredoxin system (Fig. 2)(Buchanan, Gruissem,& Jones, 2000, p 1343). SA has been shown to induce ex-

pression 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 activ-

ity 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 in-

ducedb-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 man-

ner from 0 to 2 mmol L1

, enhanced the strawberry fruittotal antioxidant capacity (TAC). 2 mmol L1 was the

most effective concentration while SA at 4 mmol L1

caused a slight increase in fruit TAC. Consequent applica-

tion of SA at three stages of vegetative growth, fruit devel-

opment 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 withP. expan-

sum, 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).

Fig. 1. SA decreases the expression of ascorbate peroxidase (APX) &catalase (CAT) genes leading to substantial increase in H2O2 whichis crucial for the activation of local acquired resistance (LAR) &

systemic acquired resistance (SAR).

504 M. Asghari, M.S. Aghdam / Trends in Food Science & Technology 21 (2010) 502e509


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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 CIin freshly green bell peppers (Fung, Wang, Smith, Gross,

& Tian, 2004). In response to abiotic stresses, all living or-

ganisms synthesis new proteins, for example, plants re-

spond 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-temper-

ature 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 hor-

ticultural products with SA and MeSA treatments would

allow their storage at low temperatures without CI develop-

ment. On the other hand lipid peroxidation is one of the ad-

verse effects of CI on plant cells leading to

malondialdehyde (MDA) accumulation. It has been re-

ported that MDA accumulation is prevented after SA treat-

ment (Table 1& Fig. 3)

SA delays fruit ripeningImpact of SA on fruit softening

Fruit ripening and senescence are accompanied by

changes in several quality aspects such as softening, de-

crease 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 concentra-

tion dependent manner from 0 to 32 ml L1, 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)

Fig. 2. Antioxidant systems in plants.



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reported a positive correlation between fruit free SA con-

tent and firmness in kiwifruit during ripening. Retention

of fruit firmness as the result of SA treatment has been re-

ported in several crops (Table 1). It has been demonstrated

that SA decreases ethylene production and inhibits cell wall

and membrane degrading enzymes such as polygalacturo-

nase (PG), lipoxygenase (LOX), cellulase and pectineme-

thylesterase (PME) leading to decreasing the fruit

softening rate (Srivastava & Dwivedi, 2000; Zhang et al.,

2003).

Effect on TSS and sugarsTSS and soluble sugars may increase during fruit ripen-

ing 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 increasein 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 L1

maintained a lower TSS content than the control fruits at

the end of cold storage (Aghdamet al., 2009). The authors

proposed that MeSA reduced ethylene production may re-

sults 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 ofSrivastava and Dwivedi (2000), SA treat-

ment, in a concentration dependent manner, reduces this in-

crease 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 di-gested due to the activity of the cell wall degrading enzymes

leading to a significant increase in TSScontent. Then anyfac-

tor preventing these enzymes will prevent from a dramatic in-

crease in TSS content. As seen in Table 1 andFig. 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 biosynthesisEthylene plays a key role in fruit ripening and senes-

cence. This hormone triggers the induction of cell wall hy-

drolyzing enzymes leading to increase in respiration rate,

fruit softening and senescence (Wills et al., 1998). SA

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



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effectively decreases ethylene production in several horti-

cultural crops (Table 1). It has been shown that MeSA treat-

ment 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 tis-

sue discs, carrot cell suspension cultures and some fruits

(Babalar et al., 2007; Romani, Hess, & Leslie, 1989).

Srivastava and Dwivedi (2000) reported that SA has de-

layed the ripening of banana fruit, probably through inhibi-

tion of ethylene biosynthesis or action. SA decreases

ethylene production by decreasing ACS and ACO produc-

tion and activity. Zhang et al., (2003) reported that post-

harvest 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 activityThere is evidence for a positive correlation between

LOX activity, free radicals production and ethylene biosyn-

thesis in fruit tissue (Marcelle, 1991). SA inhibited wound-

induced 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 radi-

cals 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 L1 MeSA

and by 0.01 mmol L1 during breaker stage. But in fruit

at turning stage even 0.01 mmol L1 SA inhibited the rip-

ening process. 0.5 mmol L1 SA prevented red color

development and increased ethylene production and respi-

ration rate in all maturity stages.

Effect on cell respiration

SA has been reported to effectively reduce the respira-tion 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 differ-

ent post-harvest oxidative stresses such as chilling injury,

prevents fermentation, and maintains low respiration rates

and decreases fruit ripening and senescence rates. Respira-

tion of harvested crops is highly dependent to ethylene pro-

duction and activity and any factor increasing the

production and activity of ethylene leads to increases in res-

piration and consequently increases the senescence rate. Ef-

fect 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).

ConclusionSA, as a natural and safe phenolic compound, exhibits

a high potential in controlling post-harvest losses of horticul-

tural crops. Decrease in ethylene production and action, in-

duction of disease resistance, prevention of oxidative

stresses, induction of crop tolerance to chilling injury, de-

crease in respiration rate, decrease in ripening and senes-

cence rate, prevention of cell wall degrading enzymes and

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



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maintaining crop firmness are of main results obtained fol-

lowing 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 post-harvest 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 chem-

icals in post-harvest technology of horticultural crops to as-

sure 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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