Weihua Chen

Bio: Weihua Chen is an academic researcher from University of Western Australia. The author has contributed to research in topics: Arsenite & Arsenate. The author has an hindex of 3, co-authored 3 publications receiving 539 citations.

Arsenic toxicity: The effects on plant metabolism

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

Disruption of ptLPD1 or ptLPD2, Genes That Encode Isoforms of the Plastidial Lipoamide Dehydrogenase, Confers Arsenate Hypersensitivity in Arabidopsis

Abstract: Arsenic is a ubiquitous environmental poison that inhibits root elongation and seed germination to a variable extent depending on the plant species. To understand the molecular mechanisms of arsenic resistance, a genetic screen was developed to isolate arsenate overly sensitive (aos) mutants from an activation-tagged Arabidopsis (Arabidopsis thaliana) population. Three aos mutants were isolated, and the phenotype of each was demonstrated to be due to an identical disruption of plastidial LIPOAMIDE DEHYDROGENASE1 (ptLPD1), a gene that encodes one of the two E3 isoforms found in the plastidial pyruvate dehydrogenase complex. In the presence of arsenate, ptlpd1-1 plants exhibited reduced root and shoot growth and enhanced anthocyanin accumulation compared with wild-type plants. The ptlpd1-1 plants accumulated the same amount of arsenic as wild-type plants, indicating that the aos phenotype was not due to increased arsenate in the tissues but to an increase in the innate sensitivity to the poison. Interestingly, a ptlpd1-4 knockdown allele produced a partial aos phenotype. Two loss-of-function alleles of ptLPD2 in Arabidopsis also caused elevated arsenate sensitivity, but the sensitivity was less pronounced than for the ptlpd1 mutants. Moreover, both the ptlpd1 and ptlpd2 mutants were more sensitive to arsenite than wild-type plants, and the LPD activity in isolated chloroplasts from wild-type plants was sensitive to arsenite but not arsenate. These findings show that the ptLPD isoforms are critical in vivo determinants of arsenite-mediated arsenic sensitivity in Arabidopsis and possible strategic targets for increasing arsenic tolerance.

The metabolic acclimation of Arabidopsis thaliana to arsenate is sensitized by the loss of mitochondrial LIPOAMIDE DEHYDROGENASE2, a key enzyme in oxidative metabolism.

Abstract: Mitochondrial lipoamide dehydrogenase is essential for the activity of four mitochondrial enzyme complexes central to oxidative metabolism. The reduction in protein amount and enzyme activity caused by disruption of mitochondrial LIPOAMIDE DEHYDROGENASE2 enhanced the arsenic sensitivity of Arabidopsis thaliana. Both arsenate and arsenite inhibited root elongation, decreased seedling size and increased anthocyanin production more profoundly in knockout mutants than in wild-type seedlings. Arsenate also stimulated lateral root formation in the mutants. The activity of lipoamide dehydrogenase in isolated mitochondria was sensitive to arsenite, but not arsenate, indicating that arsenite could be the mediator of the observed phenotypes. Steady-state metabolite abundances were only mildly affected by mutation of mitochondrial LIPOAMIDE DEHYDROGENASE2. In contrast, arsenate induced the remodelling of metabolite pools associated with oxidative metabolism in wild-type seedlings, an effect that was enhanced in the mutant, especially around the enzyme complexes containing mitochondrial lipoamide dehydrogenase. These results indicate that mitochondrial lipoamide dehydrogenase is an important protein for determining the sensitivity of oxidative metabolism to arsenate in Arabidopsis.

A New Strategy for Heavy Metal Polluted Environments: A Review of Microbial Biosorbents

Abstract: Persistent heavy metal pollution poses a major threat to all life forms in the environment due to its toxic effects. These metals are very reactive at low concentrations and can accumulate in the food web, causing severe public health concerns. Remediation using conventional physical and chemical methods is uneconomical and generates large volumes of chemical waste. Bioremediation of hazardous metals has received considerable and growing interest over the years. The use of microbial biosorbents is eco-friendly and cost effective; hence, it is an efficient alternative for the remediation of heavy metal contaminated environments. Microbes have various mechanisms of metal sequestration that hold greater metal biosorption capacities. The goal of microbial biosorption is to remove and/or recover metals and metalloids from solutions, using living or dead biomass and their components. This review discusses the sources of toxic heavy metals and describes the groups of microorganisms with biosorbent potential for heavy metal removal.

Arsenic toxicity: The effects on plant metabolism

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

The relative impact of toxic heavy metals (THMs) (arsenic (As), cadmium (Cd), chromium (Cr)(VI), mercury (Hg), and lead (Pb)) on the total environment: an overview.

Abstract: Certain five heavy metals viz. arsenic (As), cadmium (Cd), chromium (Cr)(VI), mercury (Hg), and lead (Pb) are non-threshold toxins and can exert toxic effects at very low concentrations. These heavy metals are known as most problematic heavy metals and as toxic heavy metals (THMs). Several industrial activities and some natural processes are responsible for their high contamination in the environment. In recent years, high concentrations of heavy metals in different natural systems including atmosphere, pedosphere, hydrosphere, and biosphere have become a global issue. These THMs have severe deteriorating effects on various microorganisms, plants, and animals. Human exposure to the THMs may evoke serious health injuries and impairments in the body, and even certain extremities can cause death. In all these perspectives, this review provides a comprehensive account of the relative impact of the THMs As, Cd, Cr(VI), Hg, and Pb on our total environment.

Arsenic uptake, toxicity, detoxification, and speciation in plants : physiological, biochemical, and molecular aspects

Abstract: Environmental contamination with arsenic (As) is a global environmental, agricultural and health issue due to the highly toxic and carcinogenic nature of As. Exposure of plants to As, even at very low concentration, can cause many morphological, physiological, and biochemical changes. The recent research on As in the soil-plant system indicates that As toxicity to plants varies with its speciation in plants (e.g., arsenite, As(III); arsenate, As(V)), with the type of plant species, and with other soil factors controlling As accumulation in plants. Various plant species have different mechanisms of As(III) or As(V) uptake, toxicity, and detoxification. This review briefly describes the sources and global extent of As contamination and As speciation in soil. We discuss different mechanisms responsible for As(III) and As(V) uptake, toxicity, and detoxification in plants, at physiological, biochemical, and molecular levels. This review highlights the importance of the As-induced generation of reactive oxygen species (ROS), as well as their damaging impacts on plants at biochemical, genetic, and molecular levels. The role of different enzymatic (superoxide dismutase, catalase, glutathione reductase, and ascorbate peroxidase) and non-enzymatic (salicylic acid, proline, phytochelatins, glutathione, nitric oxide, and phosphorous) substances under As(III/V) stress have been delineated via conceptual models showing As translocation and toxicity pathways in plant species. Significantly, this review addresses the current, albeit partially understood, emerging aspects on (i) As-induced physiological, biochemical, and genotoxic mechanisms and responses in plants and (ii) the roles of different molecules in modulation of As-induced toxicities in plants. We also provide insight on some important research gaps that need to be filled to advance our scientific understanding in this area of research on As in soil-plant systems.