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      Excess Zinc Supply Reduces Cadmium Uptake and Mitigates Cadmium Toxicity Effects on Chloroplast Structure, Oxidative Stress, and Photosystem II Photochemical Efficiency in Salvia sclarea Plants

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      Toxics
      MDPI AG

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          Abstract

          Salvia sclarea L. is a Cd2+ tolerant medicinal herb with antifungal and antimicrobial properties cultivated for its pharmacological properties. However, accumulation of high Cd2+ content in its tissues increases the adverse health effects of Cd2+ in humans. Therefore, there is a serious demand to lower human Cd2+ intake. The purpose of our study was to evaluate the mitigative role of excess Zn2+ supply to Cd2+ uptake/translocation and toxicity in clary sage. Salvia plants were treated with excess Cd2+ (100 μM CdSO4) alone, and in combination with Zn2+ (900 μM ZnSO4), in modified Hoagland nutrient solution. The results demonstrate that S. sclarea plants exposed to Cd2+ toxicity accumulated a significant amount of Cd2+ in their tissues, with higher concentrations in roots than in leaves. Cadmium exposure enhanced total Zn2+ uptake but also decreased its translocation to leaves. The accumulated Cd2+ led to a substantial decrease in photosystem II (PSII) photochemistry and disrupted the chloroplast ultrastructure, which coincided with an increased lipid peroxidation. Zinc application decreased Cd2+ uptake and translocation to leaves, while it mitigated oxidative stress, restoring chloroplast ultrastructure. Excess Zn2+ ameliorated the adverse effects of Cd2+ on PSII photochemistry, increasing the fraction of energy used for photochemistry (ΦPSII) and restoring PSII redox state and maximum PSII efficiency (Fv/Fm), while decreasing excess excitation energy at PSII (EXC). We conclude that excess Zn2+ application eliminated the adverse effects of Cd2+ toxicity, reducing Cd2+ uptake and translocation and restoring chloroplast ultrastructure and PSII photochemical efficiency. Thus, excess Zn2+ application can be used as an important method for low Cd2+-accumulating crops, limiting Cd2+ entry into the food chain.

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          Reactive oxygen species and antioxidant machinery in abiotic stress tolerance in crop plants.

          Various abiotic stresses lead to the overproduction of reactive oxygen species (ROS) in plants which are highly reactive and toxic and cause damage to proteins, lipids, carbohydrates and DNA which ultimately results in oxidative stress. The ROS comprises both free radical (O(2)(-), superoxide radicals; OH, hydroxyl radical; HO(2), perhydroxy radical and RO, alkoxy radicals) and non-radical (molecular) forms (H(2)O(2), hydrogen peroxide and (1)O(2), singlet oxygen). In chloroplasts, photosystem I and II (PSI and PSII) are the major sites for the production of (1)O(2) and O(2)(-). In mitochondria, complex I, ubiquinone and complex III of electron transport chain (ETC) are the major sites for the generation of O(2)(-). The antioxidant defense machinery protects plants against oxidative stress damages. Plants possess very efficient enzymatic (superoxide dismutase, SOD; catalase, CAT; ascorbate peroxidase, APX; glutathione reductase, GR; monodehydroascorbate reductase, MDHAR; dehydroascorbate reductase, DHAR; glutathione peroxidase, GPX; guaicol peroxidase, GOPX and glutathione-S- transferase, GST) and non-enzymatic (ascorbic acid, ASH; glutathione, GSH; phenolic compounds, alkaloids, non-protein amino acids and α-tocopherols) antioxidant defense systems which work in concert to control the cascades of uncontrolled oxidation and protect plant cells from oxidative damage by scavenging of ROS. ROS also influence the expression of a number of genes and therefore control the many processes like growth, cell cycle, programmed cell death (PCD), abiotic stress responses, pathogen defense, systemic signaling and development. In this review, we describe the biochemistry of ROS and their production sites, and ROS scavenging antioxidant defense machinery. Copyright © 2010 Elsevier Masson SAS. All rights reserved.
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            Reactive oxygen species: metabolism, oxidative stress, and signal transduction.

            Several reactive oxygen species (ROS) are continuously produced in plants as byproducts of aerobic metabolism. Depending on the nature of the ROS species, some are highly toxic and rapidly detoxified by various cellular enzymatic and nonenzymatic mechanisms. Whereas plants are surfeited with mechanisms to combat increased ROS levels during abiotic stress conditions, in other circumstances plants appear to purposefully generate ROS as signaling molecules to control various processes including pathogen defense, programmed cell death, and stomatal behavior. This review describes the mechanisms of ROS generation and removal in plants during development and under biotic and abiotic stress conditions. New insights into the complexity and roles that ROS play in plants have come from genetic analyses of ROS detoxifying and signaling mutants. Considering recent ROS-induced genome-wide expression analyses, the possible functions and mechanisms for ROS sensing and signaling in plants are compared with those in animals and yeast.
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              ROS Are Good.

              Reactive oxygen species (ROS) are thought to play a dual role in plant biology. They are required for many important signaling reactions, but are also toxic byproducts of aerobic metabolism. Recent studies revealed that ROS are necessary for the progression of several basic biological processes including cellular proliferation and differentiation. Moreover, cell death-that was previously thought to be the outcome of ROS directly killing cells by oxidation, in other words via oxidative stress-is now considered to be the result of ROS triggering a physiological or programmed pathway for cell death. This Opinion focuses on the possibility that ROS are beneficial to plants, supporting cellular proliferation, physiological function, and viability, and that maintaining a basal level of ROS in cells is essential for life.
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                Author and article information

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                Journal
                TOXIC8
                Toxics
                Toxics
                MDPI AG
                2305-6304
                January 2022
                January 12 2022
                : 10
                : 1
                : 36
                Article
                10.3390/toxics10010036
                35051078
                0cf09d63-db4d-4492-abbc-41b37cfb7b33
                © 2022

                https://creativecommons.org/licenses/by/4.0/

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