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Arsenic toxicity: The effects on plant metabolism

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TLDR
The two forms of inorganic arsenic, arsenate (AsV) and arsenite (AsIII), are easily taken up by the cells of the plant root Once in the cell, AsV can be readily converted to AsIII, the more toxic of the two forms AsV and AsIII both disrupt plant metabolism, but through distinct mechanisms as mentioned in this paper.
Abstract
The two forms of inorganic arsenic, arsenate (AsV) and arsenite (AsIII), are easily taken up by the cells of the plant root Once in the cell, AsV can be readily converted to AsIII, the more toxic of the two forms AsV and AsIII both disrupt plant metabolism, but through distinct mechanisms AsV is a chemical analog of phosphate that can disrupt at least some phosphate-dependent aspects of metabolism AsV can be translocated across cellular membranes by phosphate transport proteins, leading to imbalances in phosphate supply It can compete with phosphate during phosphorylation reactions, leading to the formation of AsV adducts that are often unstable and short-lived As an example, the formation and rapid autohydrolysis of AsV-ADP sets in place a futile cycle that uncouples photophosphorylation and oxidative phosphorylation, decreasing the ability of cells to produce ATP and carry out normal metabolism AsIII is a dithiol reactive compound that binds to and potentially inactivates enzymes containing closely spaced cysteine residues or dithiol co-factors Arsenic exposure generally induces the production of reactive oxygen species that can lead to the production of antioxidant metabolites and numerous enzymes involved in antioxidant defense Oxidative carbon metabolism, amino acid and protein relationships, and nitrogen and sulfur assimilation pathways are also impacted by As exposure Readjustment of several metabolic pathways, such as glutathione production, has been shown to lead to increased arsenic tolerance in plants Species- and cultivar-dependent variation in arsenic sensitivity and the remodeling of metabolite pools that occurs in response to As exposure gives hope that additional metabolic pathways associated with As tolerance will be identified

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An Overview on Emerging and Innovative Technologies for Regulating Arsenic Toxicity in Plants

TL;DR: In this article , the uptake process of As by the plants and its toxic response is discussed, which is mainly focused on different remediation approaches for the reduction of As toxicity in the plants.
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Arsenic (As) resistant bacteria with multiple plant growth-promoting traits: Potential to alleviate As toxicity and accumulation in rice.

TL;DR: In this article , the As-resistant PGPB characteristics influencing rice growth and the mechanisms by which they function to alleviate As toxicity stress in rice plants are reviewed. And future research needs about the application of As resistant PGPBs with PGP traits to mitigate As accumulation in rice plant are described.
Book ChapterDOI

Enzymatic Role in the Degradation of E-waste Pollution

TL;DR: The role of enzymes in this way is one of the most recent technology for the management of e-waste as discussed by the authors, and enzymes have wide capacity of regulating pollution, but the exact mechanisms are still unknown.
References
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Journal ArticleDOI

A review of the source, behaviour and distribution of arsenic in natural waters

TL;DR: The scale of the problem in terms of population exposed to high As concentrations is greatest in the Bengal Basin with more than 40 million people drinking water containing ‘excessive’ As as mentioned in this paper.
Journal ArticleDOI

Ascorbate and glutathione: the heart of the redox hub.

TL;DR: The discovery that there is a close relationship between ascorbate and glutathione dates from soon after the characterization of the chemical formulae of the two molecules.
Journal ArticleDOI

A fern that hyperaccumulates arsenic

TL;DR: A hardy, versatile, fast-growing plant that helps to remove arsenic from contaminated soils.
Journal ArticleDOI

Oxidative Modifications to Cellular Components in Plants

TL;DR: The fate of the modified components, the energetic costs to the cell of replacing such components, as well as strategies to minimize transfer of oxidatively damaged components to the next generation are considered.
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