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Current Scenario of Pb Toxicity in Plants: Unraveling Plethora of Physiological Responses

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Reviews of Environmental Contamination and Toxicology Volume 249

Abstract

Lead (Pb) is an extremely toxic metal for all living forms including plants. It enters plants through roots from soil or soil solution. It is considered as one of the most eminent examples of anthropogenic environmental pollutant added in environment through mining and smelting of lead ores, coal burning, waste from battery industries, leaded paints, metal plating, and automobile exhaust. Uptake of Pb in plants is a nonselective process and is driven by H+/ATPases. Translocation of Pb metal ions occurs by apoplastic movement resulting in deposition of metal ions in the endodermis and is further transported by symplastic movement. Plants exposed to high concentration of Pb show toxic symptoms due to the overproduction of reactive oxygen species (ROS) through Fenton-Haber-Weiss reaction. ROS include superoxide anion, hydroxyl radical, and hydrogen peroxide, which reach to macro- and micro-cellular levels in the plant cells and cause oxidative damage. Plant growth and plethora of biochemical and physiological attributes including plant growth, water status, photosynthetic efficiency, antioxidative defense system, phenolic compounds, metal chelators, osmolytes, and redox status are adversely influenced by Pb toxicity. Plants respond to toxic levels of Pb in varied ways such as restricted uptake of metal, chelation of metal ions to the root endodermis, enhancement in activity of antioxidative defense, alteration in metal transporters expression, and involvement of plant growth regulators.

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Abbreviations

AAS:

Atomic absorption spectrophotometer

ABA:

Abscisic acid

ABC:

ATP-binding cassettes

Ag:

Silver

APOX:

Ascorbate peroxidase

As:

Arsenic

ATSDR:

Agency for Toxic Substances and Disease Registry

Au:

Gold

Ca:

Calcium

CAA:

Clean Air Act

CAT:

Catalase

Chl a:

Chlorophyll a

Chl b:

Chlorophyll b

CO2 :

Carbon dioxide

Cu:

Copper

Cu/Zn-SOD:

Copper/zinc superoxide dismutase

DHAR:

Dehydroascorbate reductase

EDTA:

Ethylene diamine tetraacetic acid

ETC:

Electron transport chain

Fe:

Iron

GB:

Glycine betaine

GPOX:

Glutathione peroxidase

GR:

Glutathione reductase

GSH:

Glutathione

GSSG:

Glutathione disulfide

GST:

Glutathione-S-transferase

H2O2 :

Hydrogen peroxide

Hg:

Mercury

HO. :

Hydroxyl radical

ICP-MS:

Inductively coupled plasma-mass spectrometry

ICP-AES:

Inductively coupled plasma atomic emission spectrometry

K:

Potassium

MCs:

Metallothionins

MDA:

Malondialdehyde

MDHAR:

Monodehydroascorbate reductase

Mg:

Magnesium

Mn:

Manganese

Mn/Zn-SOD:

Manganese/zinc superoxide dismutase

Na:

Sodium

Ni:

Nickel

\( {\mathrm{NO}}_3^{-} \) :

Nitrate

1O2 :

Singlet oxygen radical

O2− :

Superoxide anion radical

P:

Phosphorus

Pb:

Lead

PCS:

Phytochelatin synthetase

PCs:

Phytochelatins

PGRs:

Plant growth regulators

\( {\mathrm{PO}}_4^{-} \) :

Phosphate

POD:

Guaiacol peroxidase

ROS:

Reactive oxygen species

SDWA:

Safe Drinking Water Act

SOD:

Superoxide dismutase

TBARs:

Thiobarbituric acid

TF:

Transfer factor

TSCA:

Toxic Substances Control Act

WHO:

World Health Organization

Zn:

Zinc

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Acknowledgment

Financial help for carrying out above work was given by the University Grant Commission, Government of India, GOI (Maulana Azad National Fellowship), and DST-FIST, of GOI, is also duly acknowledged.

Contribution of Authors

Sukhmeen Kaur Kohli, Renu Bhardwaj, and Saroj Arora designed the layout of the review article. Neha Handa, Shagun Bali, Kanika Khanna, and Anket Sharma helped in writing of the different sections of the manuscript. Renu Bhardwaj, Sukhmeen Kaur Kohli, and Kanika Khanna revised the manuscript to present form.

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Kohli, S.K. et al. (2019). Current Scenario of Pb Toxicity in Plants: Unraveling Plethora of Physiological Responses. In: de Voogt, P. (eds) Reviews of Environmental Contamination and Toxicology Volume 249. Reviews of Environmental Contamination and Toxicology, vol 249. Springer, Cham. https://doi.org/10.1007/398_2019_25

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