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      Metales interesantes de la familia III A: contaminación, toxicocinética y genotoxicidad del galio, indio y talio Translated title: Interesting metals of family III A: Pollution, toxicokinetic and genotoxicity of gallium, indium, and thallium

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          Abstract

          RESUMEN El galio (Ga), indio (In) y talio (Tl) son tres metales pertenecientes a la familia 13 (IIIA) de la tabla periódica de los elementos químicos y por sus múltiples aplicaciones industriales, tecnológicas, agrícolas y médicas, se ha propiciado el incremento de su presencia en el ambiente y en los ecosistemas. Sin embargo, ninguno tiene funciones biológicas reconocidas. La presente revisión se realizó con la finalidad de compilar la información disponible sobre la contaminación, exposición humana, toxicocinética y genotoxicidad del Ga, In y Tl en estado de oxidación +3. El Ga3+, In3+ y Tl3+ tienen propiedades particulares que influyen en su mecanismo de acción, tal como la composición química, la solubilidad y el tamaño de la partícula; las cuales a su vez participan en los procesos de inducción de toxicidad. Varios de sus efectos están asociados con la ruta de exposición, su absorción y entrada a la célula, la capacidad de desbalancear la homeostasis oxidante-antioxidante, alterar las funciones moleculares y generar toxicidad celular. Asimismo, la capacidad de generar daño a las biomoléculas, entre ellas el ADN. En general, los estudios realizados sobre el Ga3+, In3+ y Tl3+ demuestran su capacidad de inducir varios efectos adversos que pueden repercutir en la salud humana.

          Translated abstract

          ABSTRACT Gallium (Ga), indium (In) and thallium (Tl) are three metals belonging to the group 13 (IIIA) of the periodic table of chemical elements and due to their many industrial, technological, agricultural, and medical applications, their presence has been increased in the environment and ecosystems. However, none of them have any recognized biological functions. The present review was carried out with the purpose of compiling the available information on contamination, human exposure, toxicokinetic and genotoxicity associated with Ga, In and Tl in their +3 oxidation state (in mammalian). Ga3+, In3+ and Tl3+ have particular properties that influence their mechanism of action, such as chemical composition, solubility and particle size; which in turn influence their associated toxicity. Several of their effects are associated with the exposure route, their absorption and entry into the cell, the ability to unbalance oxidant-antioxidant homeostasis, alter molecular functions and generate cell toxicity, as well as the ability to generate damage to biomolecules, including DNA. In general, the studies carried out on Ga3+, In3+ and Tl3+ show that they can induce several adverse effects that can have an impact on human health.

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          Activation of apoptosis signalling pathways by reactive oxygen species.

          Reactive oxygen species (ROS) are short-lived and highly reactive molecules. The generation of ROS in cells exists in equilibrium with a variety of antioxidant defences. At low to modest doses, ROS are considered to be essential for regulation of normal physiological functions involved in development such as cell cycle progression and proliferation, differentiation, migration and cell death. ROS also play an important role in the immune system, maintenance of the redox balance and have been implicated in activation of various cellular signalling pathways. Excess cellular levels of ROS cause damage to proteins, nucleic acids, lipids, membranes and organelles, which can lead to activation of cell death processes such as apoptosis. Apoptosis is a highly regulated process that is essential for the development and survival of multicellular organisms. These organisms often need to discard cells that are superfluous or potentially harmful, having accumulated mutations or become infected by pathogens. Apoptosis features a characteristic set of morphological and biochemical features whereby cells undergo a cascade of self-destruction. Thus, proper regulation of apoptosis is essential for maintaining normal cellular homeostasis. ROS play a central role in cell signalling as well as in regulation of the main pathways of apoptosis mediated by mitochondria, death receptors and the endoplasmic reticulum (ER). This review focuses on current understanding of the role of ROS in each of these three main pathways of apoptosis. The role of ROS in the complex interplay and crosstalk between these different signalling pathways remains to be further unravelled during the coming years.
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            Gallium disrupts bacterial iron metabolism and has therapeutic effects in mice and humans with lung infections

            The lack of new antibiotics is among the most critical challenges facing medicine. The problem is particularly acute for Gram-negative bacteria. An unconventional antibiotic strategy is to target bacterial nutrition and metabolism. The metal gallium can disrupt bacterial iron metabolism because it substitutes for iron when taken up by bacteria. We investigated the antibiotic activity of gallium ex vivo, in a mouse model of airway infection, and in a phase 1 clinical trial in individuals with cystic fibrosis (CF) and chronic Pseudomonas aeruginosa airway infections. Our results show that micromolar concentrations of gallium inhibited P. aeruginosa growth in sputum samples from patients with CF. Ex vivo experiments indicated that gallium inhibited key iron-dependent bacterial enzymes and increased bacterial sensitivity to oxidants. Furthermore, gallium resistance developed slowly, its activity was synergistic with certain antibiotics, and gallium did not diminish the antibacterial activity of host macrophages. Systemic gallium treatment showed antibiotic activity in murine lung infections. In addition, systemic gallium treatment improved lung function in people with CF and chronic P. aeruginosa lung infection in a preliminary phase 1 clinical trial. These findings raise the possibility that human infections could be treated by targeting iron metabolism or other nutritional vulnerabilities of bacterial pathogens.
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              Cytotoxicity evaluation of 43 metal salts using murine fibroblasts and osteoblastic cells.

              Metallic biomaterials are generally used for replacement of structural components of the human body such as bones, joints, and tooth roots. When they are implanted inside a body, metallic biomaterials may corrode and/or wear, releasing metal ions and debris which may have toxic effects on tissues and organs. Since it is important for biomaterials to have no toxicity against a living body, a systematic and quantitative evaluation of the cytotoxicity of metallic elements is required for the development of new metallic biomaterials with superior biocompatibility. In this study, the cytotoxicity of 43 metal salts were evaluated by the colony formation method using two kinds of cultured cells. The effects of the difference in valence numbers of metallic elements in the salts on cytotoxicity were examined. The cytotoxicity of the salts of metallic elements' oxo acids was also investigated. As a result, the intensity of metal salts' cytotoxicity tends to be quite similar between MC3T3-E1 and L929 (the correlation coefficient of metal salts' IC50s is 0.82). The intensity of metal salts' cytotoxicity depends on the kinds of metallic elements, their chemical states, and concentrations. The IC50 of the highest toxic salt is 1.36 x 10(-6) mol L-1, which differs four orders of magnitude from the IC50 of the lowest toxic salt. K2Cr2O7, CdCl2, VCl3, AgNO3, HgCl2, SbCl3, BeSO4, and InCl3 are high toxic salts in which IC50s are smaller then 10(-5) mol L-1 for both or either of the cell lines. HgCl, Tl(NO3)3, GaCl3, CuCl2, MnCl2, CoCl2, ZnCl2, NiCl2, SnCl2, IrCl4, TlNO3, CuCl, RhCl3, Pb(NO3)2, Cr(NO3)3 and Bi(NO3)3 are relatively high toxic salts in which IC50s are smaller than 10(-4) mol L-1 for both or either cell lines.
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                Author and article information

                Journal
                rica
                Revista internacional de contaminación ambiental
                Rev. Int. Contam. Ambient
                Universidad Nacional Autónoma de México, Centro de Ciencias de la Atmósfera (Ciudad de México, Ciudad de México, Mexico )
                0188-4999
                2023
                : 39
                : 54784
                Affiliations
                [2] Ciudad de México orgnameUniversidad Nacional Autónoma de México orgdiv1Posgrado en Ciencias Biológicas Mexico
                [1] Ciudad de México orgnameUniversidad Nacional Autónoma de México orgdiv1Facultad de Estudios Superiores Zaragoza Mexico
                Article
                S0188-49992023000100201 S0188-4999(23)03900000201
                10.20937/rica.54784
                bb8b1f73-1da6-498f-9016-693aa11f5f3e

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

                History
                : 01 November 2022
                : 01 March 2022
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 195, Pages: 0
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                SciELO Mexico

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                mechanisms of action,metal toxicity,human exposure,exposure limits,cytotoxicity,mutagenicity,toxicidad de metales,exposición humana,límites de exposición,citotoxicidad,mutagenicidad,mecanismos de acción

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