Effects of Arsenic toxicity on germination, Seedling growth and Peroxidase activity in Cicer...

131 International Journal of Agriculture and Food Science 2012, 2(4): 131-137

ISSN 2249-8516

Original Article

Effects of Arsenic toxicity on germination, Seedling growth and Peroxidase

activity in Cicer arietinum

Sayan Bhattacharya1*

, Navonil De Sarkar2, Priya Banerjee

1, Shamayita Banerjee

1, Sohini Mukherjee

1, Dhrubajyoti

Chattopadhyay3 and Aniruddha Mukhopadhyay

1.

1. Department of Environmental Science, University of Calcutta, 51/2 Hazra Road, Kolkata- 700019, India. 2.

Human Genetics Unit, Indian Statistical Institute, 203, B.T. Road, Kolkata-700108, India. 3. Department of Biotechnology, University of Calcutta, 35, Ballygunge Circular Road. Kolkata-700019, India.

* Corresponding Author: Sayan Bhattacharya.

E-mail: [email protected]

Telephone: +91-9830950351.

Received 21 October 2012; accepted 09 November 2012

Abstract

Arsenic is toxic to most plants in high concentration. It interferes with metabolic processes and inhibits plant growth and

development through arsenic induced phytotoxicity. The objective of this study was to investigate the in vitro effects of

arsenic on germination and change in peroxidase activity in chickpea (Cicer arietinum) seeds and seedlings. The

germination of chickpea seeds were studied in presence of both arsenic tri-oxide and sodium arsenate solutions (200 ppb,

400 ppb, 600 ppb and 800 ppb). In order to assess the oxidative stress, Guiacol peroxidase (GPX) activity was also

estimated in different parts of the seedlings. The germination of the seeds decreased significantly with the increase in

concentrations of both As (III) and As (V) salts. However, peroxidase activity in the seeds and seedlings increased

significantly with time in response to arsenic stress. Interestingly, maximum increase in enzyme activity was observed in

seeds, followed by shoots and roots. The experiment indicates that arsenic toxicity may has the potential to affect both the quantity and quality of chickpea seed production in arsenic contaminated areas.

© 2012 Universal Research Publications. All rights reserved

Key Words: Arsenic, toxicity, germination, Peroxidase.

1. Introduction: Arsenic is a metalloid (atomic no. 33) of great

environmental concern because of its extravagant toxicity

and wide abundance [1]. Arsenic is a potent endocrine

disruptor and can alter hormone mediated cell signaling

process at extremely low concentration [2]. It ranks 20th in

abundance in the earth’s crust, 14th in the seawater and 12th

in the human body [3]. Arsenic naturally occurs in over 200 different mineral forms, of which around 60% are

arsenates, 20% are sulfides and sulfosalts and the rest 20%

are arsenides, arsenites, oxides, silicates and elemental

arsenic [4]. The source of arsenic is mainly geological, but

anthropological activities like mining, burning of fossil

fuels and uses of pesticides also cause arsenic

contamination [5]. Arsenic contamination in groundwater

has been reported in Bangladesh, India, China, Taiwan,

Vietnam, USA, Argentina, Chile and Mexico. In many of

these places the concentration has exceeded the permissible

limit of 50 ppb recommended by EPA and WHO [6].

The Bengal basin is regarded to be the most acutely arsenic

affected geological province in the world [7]. Groundwater

is regularly used for agricultural and household purposes in

these areas. The use of arsenic contaminated groundwater

for irrigation purpose in crop fields elevates arsenic

concentration in surface soil and in the plants grown in

those areas [8]. Soil arsenic levels are very much related

with local well water arsenic concentration, which suggests that the source of soil contamination is the irrigation water

(Bhattacharya et al. 2009). The absorption of arsenic by

plants is influenced by the concentration of arsenic in the

soil.

The arsenic concentrations in the edible parts of a plant

depend on the availability of the soil arsenic and the

accumulation and translocation ability of a plant [9]. The

arsenic detoxification in plants involves arsenic

mobilization from roots to aerial parts of the plant

(translocation). This movement is controlled by the external

arsenic concentration [10].

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International Journal of Agricultural and Food Science

Universal Research Publications. All rights reserved

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The arsenic concentrations in the edible parts of a plant

depend on the availability of the soil arsenic and the

accumulation and translocation ability of a plant [9]. In

general, plants uptake and metabolize As(V) through the

phosphate transport channels [11]. Because of their

chemical similarity, arsenic competes with phosphate for root uptake and interferes with metabolic process like ATP

synthesis and oxidative phosphorylation [11]. Arsenate is

taken up by phosphate transporter in plants grown on

aerobic soils. Plants generally have a low efficiency of

arsenic translocation from roots to shoots, may be due to

the formation of complexes of arsenite, less toxic organic

compounds and thiol compounds and subsequent

sequestration in the root vacuoles, or because of the strong

efflux of arsenite to the external medium [12].

At a higher concentration, arsenic is toxic to most plants. It

interferes with metabolic processes and inhibits plant

growth and development through arsenic induced phytotoxicity [13]. When plants are exposed to excess

arsenic either in soil or in solution culture, they exhibit

toxicity symptoms such as inhibition of seed germination

[14]; decrease in plant height [13,15]; decrease in tillering

[16,17]; reduction in root growth [14]; decrease in shoot

growth [18]; lower fruit and grain yield [15,16] and

sometimes, leads to death [13,19]. However, visible

injuries and significant changes in growth inhibition and

poor yield become apparent only after the plants are

exposed to relatively high levels of pollutants or after a

certain growth period. Seed is one of the vital components of the world’s diet.

Cereal grains comprise 90% of all cultivated seeds and can

contribute up to half of the global per capita energy intake.

Seed biology is one of the most extensively researched

areas in plant physiology. The seed, containing the embryo

as the new plant in miniature, is structurally and

physiologically equipped for its role as a dispersal unit and

is well provided with food reserves to sustain the growing

seedling until it establishes itself as a self-sufficient,

autotrophic organism. In comparison, seed germination

frequency and the early seedling growth are more sensitive

to metal toxicity than the mature plants because some of the plants’ defense mechanisms have not yet developed and

hence effects at early stages of plant development can be

very useful for toxicity assessment [20]. Seed germination

is the first physiological process affected by metals as

reported in previous studies [21].

Heavy metals including arsenic have been reported to

stimulate the formation of free radicals and reactive oxygen

species leading to oxidative stress [22,23]. Interestingly,

some recent reports have provided experimental evidences

that arsenic-induced generation of free radicals can cause

cell damage and death through activation of oxidative sensitive signaling pathways [24]. Requejo and Tena [25]

proved that the induction of oxidative stress is the main

process underlying arsenic toxicity in plants. Plants respond

to oxidative stress by increasing the production of

antioxidant enzymes, e.g. peroxidase (POD). The

overexpression in peroxidase (POD) activity was correlated

with increasing arsenic stress in plants [26]. According to

the studies, arsenic accumulated in the plant tissue

stimulates peroxidase synthesis during the early phases of

plant development, long before the visible changes take

place.

Chickpea (Cicer arietinum) seeds are widely cultivated in

Bengal and are a major food source in the region. The

cultivation of chickpea seeds is an important controlling factor in Indian agricultural economy. The objective of this

study was to investigate the in vitro effects of trivalent and

pentavalent arsenic on germination in chickpea seeds

(Cicer arietinum) and seedlings. As arsenic is reported to

cause oxidative stress in plant systems, the enzyme

peroxidase was selected for study as this enzyme is a very

important biomarker in stress response [25,26].

2. Materials and methods:

2.1. Germination assay:

Prior to germination, the chickpea seeds were surface-

sterilized in 3% H2O2 and then rinsed with distilled water.

Seed germination was tested on moist filter papers. Pieces of filter papers were placed on petri plates and then

moistened with 10 ml aqueous solutions of arsenic trioxide

and sodium arsenate of 200 ppb, 400 ppb, 600 ppb and 800

ppb concentrations. The concentrations of arsenic were

selected according to the levels of contamination found in

different zones of Bengal Delta in a previous study, ranging

from 230 ppb. to 730 ppb [27]. The arsenic solutions were

freshly prepared by dissolving sodium arsenate in

deionized water and adjusting their pH to 5.8 with 2mM

Mes-Tris buffer [20]. Controls were maintained by

moistening the filter papers with 10 ml deionized water. Thirty seeds were placed in each plate, covered by lid, and

incubated at 27oC. Geminated seeds were studied after 120

hours (5 days). Seeds were considered germinated when

both the plumule and radicle were extended from their

junction. Each treatment was replicated three times. The

fresh masses of the shoots and roots were taken (after 120

hours) and shoot height was measured from culms base to

the tip of the longest leaf and root length was measured

from the root-shoot junction to the tip of the longest root.

The root and shoot lengths of all the seeds under of each set

were measured and mean values were calculated

accordingly.

2.2. Peroxidase assay:

Shoots, roots and seeds were separated carefully by cutting

the junctions and were rinsed thoroughly with distilled

water to remove the arsenic solutions on the surfaces of the

plant parts. For determination of peroxidase activity, 0.5

gm. of roots, shoots and seeds were homogenized in 0.5 ml.

of respective extraction buffer in a pre-chilled mortar and

pestle. The homogenate was filtered and centrifuged at

22,000g for 20 mins. At 4oC. Peroxidase (POD) activity

was determined with guaiacol by spectrophotometry [28].

In the presence of H2O2, POD catalyzes the transformation of guaiacol to tetraguaiacol. This reaction can be recorded

at 470 nm. The reaction mixture contained 100mM

phosphate buffer (pH 6.0), 33mM guaiacol and 0.3mM

H2O2. Enzyme activity was measured in spectrophotometer

in 470 nm. wavelength in every 10 second interval. Six

readings were taken for each sample. The enzyme activities

were calculated by converting the readings in OD/min./gm.

fresh tissue.


Fig. 1a: Change of the percentage of germination in

chickpea seeds treated with sodium arsenate.

Fig. 1b: Change of the percentage of germination in

chickpea seeds treated with arsenic trioxide.

3. Results and discussion:

3.1. Effects on germination:

The results showed that arsenic was highly toxic to germination of chickpea seeds. The percentage of

germination decreased with the increase in arsenic

concentrations in the solutions (Figure 1a,1b). No shoot

formation was observed in 800 ppb concentrations of

sodium arsenate and arsenic trioxide, and the root lengths

were negligibly small in this concentration (Figure 2a, 2b

and Figure 3a, 3b). Additionally, most of the roots turned

black, probably due to arsenic toxicity in this concentration.

More reduction in germination percentage with arsenite

than with arsenate was observed, probably because of

higher toxicity of trivalent arsenic than pentavalent form

[20]. The effect of arsenic trioxide on the changes in root length was more profound than sodium arsenate in the

experimental plates. The effect of arsenic trioxide on the

shoot lengths of germinating chickpea seeds was also more

prominant than sodium arsenate stress. In 800ippb.

concentration, there was no shoot formed in the

germinating seeds in response to both sodium arsenate and

arsenic trioxide solutions.

Fig. 2a: Changes in root lengths of chickpea seeds treated

with sodium arsenate.

Fig. 2b: Changes in root lengths of chickpea seeds treated

with arsenic trioxide.

Fig. 3a: Changes in shoot lengths of chickpea seeds treated

with sodium arsenate.

Fig. 3b: Changes in shoot lengths of chickpea seeds treated

with arsenic trioxide.

In case of shoot development, the rate of decease in shoot

length was also higher in presence of arsenic trioxide,

which supported the previous findings (Kabata-Pendias and

Pendias 1984; Hartley-Whitaker et al. 2001; Sneller et al.

2000). Abedin and Meharg (2002) also reported that

germination and early seedling growth of rice can also decrease significantly with increasing concentrations of

arsenic; the growth of the whole plant was constrained, and

the plant biomass decreased finally. Our study also showed

similar trend in case of chickpea seedlings.

3.2. Effects on Peroxidase activity:

In response to arsenic stress in the seedlings, peroxidase

activity in the roots (Figure 4a, 4b), shoots (Figure 5a,

Figure 5b) and seeds (Figure 6a, Figure 6b) increased

significantly with time in response to arsenic stress.

Maximum enzyme activity was observed in roots (ranged


Fig. 4a: Changes in peroxidase expressions in chickpea

roots treated with sodium arsenate.

Fig. 4b: Changes in peroxidase expressions in chickpea

roots treated with arsenic trioxide.

Fig. 5a: Changes in peroxidase expressions in chickpea

shoots treated with sodium arsenate.

Fig. 5b: Changes in peroxidase expressions in chickpea

shoots treated with arsenic trioxide.

Fig. 6a: Changes in peroxidase expressions in germinated

chickpea seeds treated with sodium arsenate.

Fig. 6b: Changes in peroxidase expressions in germinated chickpea seeds treated with arsenic trioxide.

between 41.09 ± 0.919 to 120.07 ± 0.996 OD/min./gm.

fresh tissue in response to sodium arsenate and 41.09 ±

0.919 to 75.13 ± 0.229 OD / min. / gm. Fresh tissue in

response to arsenic trioxide), followed by seeds (ranged

between 3.97 ± 0.079 to 74.59 ± 0.549 OD/min./gm. fresh

tissue in response to sodium arsenate and 3.97 ± 0.079 to

37.55 ± 0.482 OD/ min./gm. fresh tissue in response to

arsenic trioxide) and shoots (ranged between 18.29 ± 1.389

to 46.47 ± 0.768 OD/min./gm. fresh tissue in response to sodium arsenate and 18.29 ± 1.389 to 58.1 ± 0.954

OD/min./gm. fresh tissue in response to arsenic trioxide).

Interestingly, changes in peroxidase expressions with

respect to control were maximum in the seeds (expressions

increased 18.8 times and 9.45 times in 800 ppb sodium

arsenate and arsenic trioxide respectively with respect to

the control), followed by shoots (expressions increased

2.54 times and 3.18 times in 800 ppb sodium arsenate and

arsenic trioxide respectively with respect to the control) and

roots (expressions increased 2.92 times and 1.83 times in

800 ppb sodium arsenate and arsenic trioxide respectively

with respect to the control). Perhaps, the seeds were in direct contact with the arsenic solutions, which is the

possible reason of increased enzyme activity in that part.

Furthermore, it is the seed which got maximum exposure of

stress right from the beginning of the experiment as the

germinating part i.e. shoots and roots appeared in later

stages. But there is no reason found that can explain the

comparatively higher overexpression of peroxidase in

shoots than roots. But, irrespective of shoots, roots

or stems, peroxidase activity increased throughout with the


Table: Peroxidase activity on different parts of plant following different level category of arsenic stress.

peroxidase of root treated with sodium arsenate

OD / min / g tissue OD / min / g tissue

OD / min / g tissue mean SD

control 41 40.23 42.06 41.09667 0.918822 200 ppb 41.1 39.67 42.59 41.12 1.460103

400 ppb 56.8 55.68 57.61 56.69667 0.969141

600 ppb 58.4 57.7 59.08 58.39333 0.690024

800 ppb 120.2 119.02 121 120.0733 0.996059

peroxidase of root treated with arsenic trioxide

control 41 40.23 42.06 41.09667 0.918822

200 ppb 50 50.12 49.67 49.93 0.233024

400 ppb 59.32 60.4 61.16 60.29333 0.924626

600 ppb 66.6 66.14 65.98 66.24 0.32187

800 ppb 75.2 74.87 75.31 75.12667 0.228983

peroxidase of shoot treated with sodium arsenate control 18.06 17.03 19.78 18.29 1.389352

200 ppb 3.6 2.7 4.2 3.5 0.754983

400 ppb 32.6 31.6 33.67 32.62333 1.035197

600 ppb 46.8 45.6 47.03 46.47667 0.767876

800 ppb 0 0 0 0 0

peroxidase of shoot treated with arsenic trioxide

control 18.06 17.03 19.78 18.29 1.389352

200 ppb 26.4 25.3 27.01 26.23667 0.866622

400 ppb 52 51.68 53.71 52.46333 1.091436

600 ppb 58.2 57.1 59 58.1 0.953939

800 ppb 0 0 0 0 0

peroxidase of seed treated with sodium arsenate

control 4 3.88 4.03 3.97 0.079373

200 ppb 23.6 24.01 23 23.53667 0.50797 400 ppb 48.8 47.95 49.02 48.59 0.565066

600 ppb 57.6 56.84 58.01 57.48333 0.593661

800 ppb 74.8 73.97 75.01 74.59333 0.549939

peroxidase of seed treated with arsenic trioxide

control 4 3.88 4.03 3.97 0.079373

200 ppb 12.4 11.93 13.02 12.45 0.546717

400 ppb 16.6 15.73 17.42 16.58333 0.845123

600 ppb 22 21.86 22.67 22.17667 0.432936

800 ppb 37.6 38.01 37.05 37.55333 0.481698

increase in arsenic concentrations. Interestingly, sodium

arsenate had more pronounced effect on the peroxidase

overexpressions than arsenic trioxide in the root and seed

parts, whereas arsenic trioxide has executed more toxicity than sodium arsenate in the shoot parts. Different molecular

mechanisms may be responsible for such differences in

enzyme expressions, which can be explored in details in

future researches.

The up-regulation of peroxidase enzyme activities found in

the seeds in response to arsenic stress indicated that excess

arsenic can generate oxidative stress. According to our

experimental results, it is also clear that peroxidase can be

considered as an effective indicator for arsenic stress in

germinating seeds.

4. Conclusions: The overall study indicated that arsenic is capable of

inducing stress on Chickpea seed (Cicer arietinum)

germination. Many different vegetative response endpoints

such as germination percentage, root length, shoot length;

root biomass, shoot biomass and total biomass are used to

indicate metal resistance to plants [14,29]. In our study,

germination of chickpea seeds was found to be affected

considerably with arsenic species and their concentrations. Reduction of both root and shoot length is a typical of

response to toxic metals [30]. Reduced root length growth

in response to arsenic exposure has been reported by a

number of investigators [31,32]. Reduction of root length

growth with increasing concentration of arsenic is due to

the fact that plant roots were the first point of contact for

these toxic arsenic species in the nutrient media.

Reductions in Chickpea seed shoot lengths with increasing

arsenic concentration suggest that gram shoot length can

also be used as a good indicator for arsenic toxicity.

However, the effects of arsenic in seed germination depend on the plant species, as different species give different

responses in presence of arsenic. We cannot make a

generalized conclusion, as there are significant variations

among the varieties in tolerance to arsenite and arsenate.


Our experiments also represent much simpler conditions

than plants experience under field conditions. Furthermore,

most of the added arsenic will be adsorbed on soil particle

surfaces, leaving a relatively lower concentration in the soil

solution [33,34]. Soil factors can significantly influence

solubility, mobility and toxicity of arsenic in soil in natural field conditions, and the effects may differ from artificial

lab conditions [33,35].

The seeds of metal tolerant plants and hyperaccumulators

may have a substantially higher threshold for toxicity than

non-tolerant ones. However, knowledge of the effects of

metals on seeds is only starting to emerge, in particular on

the mechanisms of damage. Moreover, it is largely

unknown where metals are deposited in developing seeds

and which levels are toxic to the embryo as compared to

the endosperm or cotyledons. More research is needed to

understand how seed longevity is affected by metals, both

in soil seed banks and in seed banks used for agricultural or conservation purposes. Importantly, for a more

comprehensive understanding of the effects of metals on

seed viability and dormancy, the signaling networks need

to be explored including the interaction of ROS, RNS and

seed hormones with metals.

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Source of support: Nil; Conflict of interest: None declared

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