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      • Record: found
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      Protective Effects of Plathymenia reticulata and Connarus favosus Aqueous Extracts against Cadmium- and Mercury-Induced Toxicities

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          Abstract

          The extracts of Plathymenia reticulata and Connarus favosus are widely used in the folk medicine. The potential protective effects of these extracts have been evaluated against cadmium in the yeast Saccharomyces cerevisiae, and against mercurial contamination in zebrafish Danio rerio. In yeast, both extracts efficiently protected the Δ ycf1 mutant strain exposed to cadmium chloride restoring the growth, the expression of stress-response genes and decreasing the level of oxidative stress. In zebrafish, the supplementation of methylmercury-contaminated diet with both plant extracts similarly protected fish through the suppression of the methylmercury-induced lipid peroxidation, decrease of acetylcholinesterase activity, and restoring the expression levels of stress-response genes. This study particularly demonstrates the protective potential of both aqueous extracts against methylmercury, and could represent an interesting alternative for the Amazonian fish-eating communities to cope with the impact of chronic exposure to contaminated diets.

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          Environmental Mercury and Its Toxic Effects

          Kevin Rice, Ernest Walker, Miaozong Wu … (2014)
          Mercury exists naturally and as a man-made contaminant. The release of processed mercury can lead to a progressive increase in the amount of atmospheric mercury, which enters the atmospheric-soil-water distribution cycles where it can remain in circulation for years. Mercury poisoning is the result of exposure to mercury or mercury compounds resulting in various toxic effects depend on its chemical form and route of exposure. The major route of human exposure to methylmercury (MeHg) is largely through eating contaminated fish, seafood, and wildlife which have been exposed to mercury through ingestion of contaminated lower organisms. MeHg toxicity is associated with nervous system damage in adults and impaired neurological development in infants and children. Ingested mercury may undergo bioaccumulation leading to progressive increases in body burdens. This review addresses the systemic pathophysiology of individual organ systems associated with mercury poisoning. Mercury has profound cellular, cardiovascular, hematological, pulmonary, renal, immunological, neurological, endocrine, reproductive, and embryonic toxicological effects.
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            Mechanisms of methylmercury-induced neurotoxicity: evidence from experimental studies.

            Marcelo Farina, João B T Rocha, Michael Aschner (2011)
            Neurological disorders are common, costly, and can cause enduring disability. Although mostly unknown, a few environmental toxicants are recognized causes of neurological disorders and subclinical brain dysfunction. One of the best known neurotoxins is methylmercury (MeHg), a ubiquitous environmental toxicant that leads to long-lasting neurological and developmental deficits in animals and humans. In the aquatic environment, MeHg is accumulated in fish, which represent a major source of human exposure. Although several episodes of MeHg poisoning have contributed to the understanding of the clinical symptoms and histological changes elicited by this neurotoxicant in humans, experimental studies have been pivotal in elucidating the molecular mechanisms that mediate MeHg-induced neurotoxicity. The objective of this mini-review is to summarize data from experimental studies on molecular mechanisms of MeHg-induced neurotoxicity. While the full picture has yet to be unmasked, in vitro approaches based on cultured cells, isolated mitochondria and tissue slices, as well as in vivo studies based mainly on the use of rodents, point to impairment in intracellular calcium homeostasis, alteration of glutamate homeostasis and oxidative stress as important events in MeHg-induced neurotoxicity. The potential relationship among these events is discussed, with particular emphasis on the neurotoxic cycle triggered by MeHg-induced excitotoxicity and oxidative stress. The particular sensitivity of the developing brain to MeHg toxicity, the critical role of selenoproteins and the potential protective role of selenocompounds are also discussed. These concepts provide the biochemical bases to the understanding of MeHg neurotoxicity, contributing to the discovery of endogenous and exogenous molecules that counteract such toxicity and provide efficacious means for ablating this vicious cycle. Copyright © 2011 Elsevier Inc. All rights reserved.
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              A new pathway for vacuolar cadmium sequestration in Saccharomyces cerevisiae: YCF1-catalyzed transport of bis(glutathionato)cadmium.

              Z Li, D Thiele, R G Zhen … (1997)
              The yeast cadmium factor (YCF1) gene encodes an MgATP-energized glutathione S-conjugate transporter responsible for the vacuolar sequestration of organic compounds after their S-conjugation with glutathione. However, while YCF1 was originally isolated according to its ability to confer resistance to cadmium salts, neither its mode of interaction with Cd2+ nor the relationship between this process and organic glutathione-conjugate transport are known. Here we show through direct comparisons between vacuolar membrane vesicles purified from Saccharomyces cerevisiae strain DTY167, harboring a deletion of the YCF1 gene, and the isogenic wild-type strain DTY165 that YCF1 mediates the MgATP-energized vacuolar accumulation of Cd-glutathione complexes. The substrate requirements, kinetics and Cd2+/glutathione stoichiometry of cadmium uptake and the molecular weight of the transport-active complex demonstrate that YCF1 selectively catalyzes the transport of bis(glutathionato)cadmium (Cd x +GS2). On the basis of these results--the Cd2+ hypersensitivity of DTY167, versus DTY165, cells, the inducibility of YCF1-mediated transport, and the rapidity and spontaneity of Cd-GS2 formation--this new pathway is concluded to contribute substantially to Cd2+ detoxification.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Toxicol Res
                Journal ID (iso-abbrev): Toxicol Res
                Journal ID (publisher-id): Toxicological Research
                Title: Toxicological Research
                Publisher: Korean Society of Toxicology
                ISSN (Print): 1976-8257
                ISSN (Electronic): 2234-2753
                Publication date (Print): January 2019
                Publication date (Electronic): 15 January 2018
                Volume: 35
                Issue: 1
                Pages: 25-35
                Affiliations
                [1 ]University of Bordeaux, CNRS, UMR 5805, EPOC, Arcachon Marine Station, 33120 Arcachon, France
                [3 ]Federal University of Western Pará - UFOPA, PPGRNA, LABBEX, Tapajós Campus, Rua Vera Paz s/n, Bairro Salé, CEP, 68040-050, Caranazal, 88040-060 Santarém, Pará, Brazil
                Author notes
                Correspondence to: Jean-Paul Bourdineaud, University of Bordeaux, CNRS, UMR MFP 5234, European Institute of Chemistry and Biology, 2 rue Robert Escarpit, 33607 Pessac, France, E-mail: jean-paul.bourdineaud@ 123456u-bordeaux.fr
                [2]

                Present address: University of Bordeaux, CNRS, UMR5095 CNRS, Institute for Cellular Biochemistry and Genetics, 1 rue Camille Saint Saëns, CS 61390, 33077 Bordeaux cedex, France

                [4]

                Present address: University of Bordeaux, CNRS, UMR MFP 5234, European Institute of Chemistry and Biology, 2 rue Robert Escarpit, 33607 Pessac, France

                Article
                Publisher ID: tr-34-025
                DOI: 10.5487/TR.2019.35.1.025
                PMC ID: 6354948
                PubMed ID: 30766655
                SO-VID: a31c5683-b253-4f03-b3cd-653656592c24
                Copyright © Copyright © 2019 The Korean Society Of Toxicology
                License:

                This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 16 May 2018
                Date revision received : 21 June 2018
                Date accepted : 20 July 2018
                Categories
                Subject: Original Article

                Keywords: plant extract,methylmercury,cadmium,saccharomyces cerevisiae,danio rerio,oxidative stress
                Data availability:
                Keywords: plant extract, methylmercury, cadmium, saccharomyces cerevisiae, danio rerio, oxidative stress

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