Abstract

Heavy metal (HM) toxicity is one of the major abiotic stresses leading to hazardous effects in plants. A common consequence of HM toxicity is the excessive accumulation of reactive oxygen species (ROS) and methylglyoxal (MG), both of which can cause peroxidation of lipids, oxidation of protein, inactivation of enzymes, DNA damage and/or interact with other vital constituents of plant cells. Higher plants have evolved a sophisticated antioxidant defense system and a glyoxalase system to scavenge ROS and MG. In addition, HMs that enter the cell may be sequestered by amino acids, organic acids, glutathione (GSH), or by specific metal-binding ligands. Being a central molecule of both the antioxidant defense system and the glyoxalase system, GSH is involved in both direct and indirect control of ROS and MG and their reaction products in plant cells, thus protecting the plant from HM-induced oxidative damage. Recent plant molecular studies have shown that GSH by itself and its metabolizing enzymes—notably glutathioneS-transferase, glutathione peroxidase, dehydroascorbate reductase, glutathione reductase, glyoxalase I and glyoxalase II—act additively and coordinately for efficient protection against ROS- and MG-induced damage in addition to detoxification, complexation, chelation and compartmentation of HMs. The aim of this review is to integrate a recent understanding of physiological and biochemical mechanisms of HM-induced plant stress response and tolerance based on the findings of current plant molecular biology research.

Highlights

  • The molecular and physiological basis of crop plant interactions with the environment has attracted considerable interest in recent years

  • Molecular and cellular adaptation of plant cells in response to Heavy metal (HM) stress appears to be necessary to improve plant HM tolerance that reduces the chance of entering HM into the food chain

  • A wealth of recent studies demonstrated that plants protect themselves from HM toxicity, besides other mechanisms, through an elevated level of nonenzymatic and enzymatic components of antioxidant and glyoxalase defense systems [2, 3, 8, 11, 13, 17, 19, 31]

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Summary

Introduction

The molecular and physiological basis of crop plant interactions with the environment has attracted considerable interest in recent years. A complete understanding of the molecular mechanisms and genetic basis of phytoremediation is an important aspect of developing plants as agents for phytoremediating contaminated sites Depending on their oxidation states, HMs can be highly reactive, resulting in toxicity of plant cells in many ways. At the cellular and molecular level, HM toxicity results in alterations of different plant physiological processes, including inactivation and denaturation of enzymes, proteins, blocking of functional groups of metabolically important molecules, displacement/substitution of essential metal ions from biomolecules and functional cellular units, conformational modifications and disruption of membrane integrity [5, 6], which is attributed to altered plant metabolism, inhibition of photosynthesis, respiration, and alerted activities of several key enzymes [2, 3, 7,8,9,10,11,12,13]. Special emphasis will be given to ROS and MG metabolism in HMstressed plants in relation to GSH and its related enzymes, proteins, and genes and their consequence in HM-induced ROS and MG detoxification based on the findings of current plant molecular biology research

Mode of Action of Toxic HMs in Plant Cells
Heavy Metal Stress and Plant Responses
Molecular Mechanisms of Heavy Metal Tolerance in Plants
Restriction of Uptake and Transport of HMs
Complexation and Compartmentation of HMs within the
Reactive Oxygen Species Production in Plant Cells
O2 Protein kinase cascades
O2 CAT H2O
ROS and MG Scavenging and Detoxification Systems in Plants
Plant Metal Tolerance and Involvement of Antioxidative and Glyoxalase Systems
O2 GPX
10. Proteomic Changes in Response to HM Stress in relation to GSH Metabolism
13. Transgenic Plants and Heavy Metal Tolerance with reference to Glutathione
Findings
14. Conclusion and Future Perspective
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