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Assessment of mitochondrial and cellular changes induced by representatives of major classes of poly-brominated biphenyls (PBDEs)

Abstract

The brominated flame retardants are used widely in a variety of consumer goods to increase their fire resistance and/or to high temperatures in case of fire, thereby increasing the chances of escape and reducing the severity of burns. To this end the polybrominated diphenyl ethers (PBDEs) represent the most used class in light of their efficiency in controlling the spread of flame and low cost. These compounds are among the newly emerging environmental contaminants known to have a lack of toxicological data, mainly related to the harmful effects and exposure biomarkers, in addition to the potential damage to the environment, which is a recent concern of the scientific community. The probable contamination by these compounds of the sources of water brings the concrete possibility of shortages of fresh water in the near future, making essential studies that provide data for the elaboration of laws that adequately protect this natural resource. In Brazil, was recently published in the Resolution 396 of the National Environmental Council (CONAMA), which legislates on the reserves of groundwater. While this legislation is broad, does not include any of the emerging contaminants, which can contaminate both surface water in the underground reservoirs. Because mitochondria is recognized as the main cellular energy-producing organelle, in addition to its key role in the maintenance of many cellular functions, the mitochondria is a great tool for the study of activities of toxic substances such as the brominated flame retardants. Thus, this project aims to provide data to the scientific community and especially the legislative authorities of the country on the harmful effects of PBDEs using tests with isolated mitochondria and in cellular systems in order to assess the need for inclusion of these compounds in the resolution of the National Council on the Environment on groundwater. With the resources requested here, the Laboratory of Toxicology and Biochemical Toxicology will be set up at the Department of Chemistry FFCLRP / USP. For the development of this project, collaborations with professors from this and other departments (Campus USP Ribeirão Preto) will be made. The project also proposes the formation of human resources in the area of toxicology, by the selection of students to the masters and basic scientific research initiation programs, to carry out the analysis. (AU)

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Scientific publications (9)
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
PAZIN, MURILO; PEREIRA, LILIAN CRISTINA; DORTA, DANIEL JUNQUEIRA. Toxicity of brominated flame retardants, BDE-47 and BDE-99 stems from impaired mitochondrial bioenergetics. TOXICOLOGY MECHANISMS AND METHODS, v. 25, n. 1, p. 34-41, . (09/06912-6, 12/04542-0)
PEREIRA, LILIAN CRISTINA; CABRAL MIRANDA, LUIZ FELIPPE; DE SOUZA, ALECSANDRA OLIVEIRA; DORTA, DANIEL JUNQUEIRA. BDE-154 INDUCES MITOCHONDRIAL PERMEABILITY TRANSITION AND IMPAIRS MITOCHONDRIAL BIOENERGETICS. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES, v. 77, n. 1-3, SI, p. 24-36, . (09/06912-6, 10/02661-6)
PEREIRA, LILIAN CRISTINA; DE SOUZA, ALECSANDRA OLIVEIRA; DORTA, DANIEL JUNQUEIRA. Polybrominated Diphenyl Ether Congener (BDE-100) Induces Mitochondrial Impairment. BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY, v. 112, n. 6, p. 418-424, . (09/06912-6, 10/02661-6)
PAZIN, MURILO; PEREIRA, LILIAN CRISTINA; DORTA, DANIEL JUNQUEIRA. Toxicity of brominated flame retardants, BDE-47 and BDE-99 stems from impaired mitochondrial bioenergetics. TOXICOLOGY MECHANISMS AND METHODS, v. 25, n. 1, p. 8-pg., . (09/06912-6, 12/04542-0)
PEREIRA, LILIAN C.; SOUZA, ALECSANDRA O.; TASSO, MARIA J.; OLIVEIRA, ALANA M. C.; DUARTE, FILIPE V.; PALMEIRA, CARLOS M.; DORTA, DANIEL J.. Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES, v. 80, n. 19-21, SI, p. 1129-1144, . (12/13123-0, 09/06912-6, 10/02661-6)
PEREIRA, LILIAN CRISTINA; CABRAL MIRANDA, LUIZ FELIPE; FRANCO-BERNARDES, MARIANA FURIO; TASSO, MARIA JULIA; DUARTE, FILIPE VALENTE; INACIO VARELA, ANA TERESA; ROLO, ANABELA PINTO; MARQUES PALMEIRA, CARLOS MANUEL; DORTA, DANIEL JUNQUEIRA. Mitochondrial damage and apoptosis: Key features in BDE-153-induced hepatotoxicity. Chemico-Biological Interactions, v. 291, p. 192-201, . (09/06912-6, 10/02661-6)
SOUZA, A. O.; PEREIRA, L. C.; OLIVEIRA, D. P.; DORTA, D. J.. BDE-99 congener induces cell death by apoptosis of human hepatoblastoma cell line-HepG2. TOXICOLOGY IN VITRO, v. 27, n. 2, p. 580-587, . (09/06912-6)
PEREIRA, LILIAN C.; SOUZA, ALECSANDRA O.; TASSO, MARIA J.; OLIVEIRA, ALANA M. C.; DUARTE, FILIPE V.; PALMEIRA, CARLOS M.; DORTA, DANIEL J.. Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES, v. 80, n. 19-21, p. 16-pg., . (12/13123-0, 09/06912-6, 10/02661-6)
PEREIRA, LILIAN CRISTINA; CABRAL MIRANDA, LUIZ FELIPPE; DE SOUZA, ALECSANDRA OLIVEIRA; DORTA, DANIEL JUNQUEIRA. BDE-154 INDUCES MITOCHONDRIAL PERMEABILITY TRANSITION AND IMPAIRS MITOCHONDRIAL BIOENERGETICS. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES, v. 77, n. 1-3, p. 13-pg., . (09/06912-6, 10/02661-6)