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Heavy Metal Toxicity: Oxidative Stress Parameters and DNA Repair

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Metal Toxicity in Plants: Perception, Signaling and Remediation

Abstract

Plant growth and productivity are adversely affected by frequent exposure to various abiotic and biotic stress factors, such as heavy metals. Heavy metals are elements with a relatively high density and are toxic or poisonous. Different molecular mechanisms for heavy metal toxicity have been described, and, among these, the production of reactive oxygen species (ROS) deserves special attention. ROS are highly reactive atoms or molecules naturally produced in plants and predominantly formed in the electron transport chain of cellular respiration (chloroplasts) and in photoreactivation. Oxidative attack on DNA generates both altered bases and damaged sugar residues that undergo fragmentation and lead to strand breaks. DNA damage caused by exposure to ROS is one of the primary causes of DNA decay in most organisms. The irreversible DNA damage can interfere with plant development and affect crop productivity. To protect the cells, a complex network of proteins is activated for damage control and repair that includes both antioxidant enzymes removing ROS and DNA repair proteins. The DNA repair response includes different pathways, such as mismatch repair (MMR), base excision repair (BER), nucleotide excision repair (NER), nonhomologous end joining (NHEJ), and homologous recombination (HR). Recent advances in the study of DNA repair in higher plants show that they use similar mechanisms to those present in other eukaryotes to remove and/or tolerate oxidized bases and other oxidative DNA lesions. The aim of this chapter is to review the latest data regarding the induction of oxidative stress by heavy metals in higher plants, introducing some basic concepts and seeking a relationship with DNA damage repair mechanisms.

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Abbreviations

Ag:

Silver

AP:

Site apurinic and/or apyrimidinic site

APX:

Ascorbate peroxidase

As:

Arsenic

BER:

Base excision repair

CAT:

Catalase

Cd:

Cadmium

Co:

Cobalt

Cr:

Chromium

Cu:

Copper

Cu/Zn-SOD:

Cooper/zinc superoxide dismutase

Cys:

Cysteine

DMAV :

Dimethylarsinic acid

DMDSe:

Dimethyl diselenide

DMSe:

Dimethyl selenide

DSB:

Double strand breaks

Fe:

Iron

Fe-SOD:

Iron superoxide dismutase

gEC:

γ-Glutamylcystein

gECS:

γ-Glutamylcystein synthetase

GGR:

Global genome repair

GPX:

Glutathione peroxidase

GSH:

Glutathione

H2O2 :

Hydrogen peroxide

Hg:

Mercury

HR:

Homologous recombination

LMWT:

Low-molecular-weight thiols

MMR:

Mismatch repair

Mn:

Manganese

Mn-SOD:

Manganese superoxide dismutase

Mo:

Molybdenum

NER:

Nucleotide excision repair

NHEJ:

Nonhomologous end joining

Ni:

Nickel

O •−2 :

Superoxide radicals

OH• :

Hydroxyl radicals

Pb:

Lead

PC:

Phytochelatins

RAPD:

Random amplification of polymorphic DNA

SCE:

Sister chromatid exchanges

SOD:

Superoxide dismutase

TCR:

Transcription-coupled repair

Zn:

Zinc

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Authors and Affiliations

  1. Department of Basic Health Sciences, Federal University of Health Sciences of Porto Alegre, Porto Alegre, RS, Brazil

    Dinara Jaqueline Moura, Valéria Flores Péres & Jenifer Saffi

  2. Department of Chemistry, Federal University of Rio Grande do Sul, Porto Alegre, RS, Brazil

    Rosangela Assis Jacques

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  1. Dinara Jaqueline Moura
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  2. Valéria Flores Péres
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  3. Rosangela Assis Jacques
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  4. Jenifer Saffi
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Correspondence to Jenifer Saffi .

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  1. CSIC, Bioquímica, Estación Experimental Del Zaidín, Apartado 419, Granada, E-18008, Spain

    Dharmendra K. Gupta

  2. CSIC, Bioquímica, Estación Experimental Del Zaidín, Apartado 419, Granada, E-18080, Spain

    Luisa M. Sandalio

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Moura, D.J., Péres, V.F., Jacques, R.A., Saffi, J. (2012). Heavy Metal Toxicity: Oxidative Stress Parameters and DNA Repair. In: Gupta, D., Sandalio, L. (eds) Metal Toxicity in Plants: Perception, Signaling and Remediation. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-22081-4_9

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