NDLI: BDE-154 induces mitochondrial permeability transition and impairs mitochondrial bioenergetics.

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BDE-154 induces mitochondrial permeability transition and impairs mitochondrial bioenergetics.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Pereira, Lílian Cristina Miranda, Luiz Felippe Cabral de Souza, Alecsandra Oliveira Dorta, Daniel Junqueira
Description	Country affiliation: Brazil Author Affiliation: Pereira LC ( a Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Departamento de Análises Clínicas , Toxicológicas e Bromatológicas, Universidade de São Paulo , Ribeirão Preto , São Paulo , Brasil.)
Abstract	Brominated flame retardants are used in various consumer goods to make these materials difficult to burn. Polybrominated diphenyl ethers (PBDE), which are representative of this class of retardants, consist of two benzene rings linked by an oxygen atom, and contain between 1 and 10 bromine atoms in their chemical structure, with the possibility of up to 209 different congeners. Among these congeners, BDE-154 (hexa-BDE) is persistent in the environment and easy to detect in the biota, but no apparent information regarding the mechanism underlying action and toxicity is available. Mitochondria, as the main energy-producing organelles, play an important role in the maintenance of various cellular functions. Therefore, mitochondria were used in the present study as an experimental model to determine the effects of BDE-154 congener at concentrations ranging from 0.1 µM to 50 µM. Our results demonstrated that BDE-154 interacts with the mitochondrial membrane, preferably by inserting into the hydrophobic core of the mitochondrial membrane, which partially inhibits respiration, dissipates Δψ, and permeabilizes the inner mitochondrial membrane to deplete ATP. These effects are more pronounced at concentrations equal to or higher than 10 µM. Results also showed that BDE-154 did not induce reactive oxygen species (ROS) accumulation within the mitochondria, indicating the absence of oxidative stress. Therefore, BDE-154 impairs mitochondrial bioenergetics and permeabilizes the mitochondrial membrane, potentially leading to cell death but not via mechanisms involving oxidative stress.
File Format	HTM / HTML
ISSN	15287394
Issue Number	1-3
Volume Number	77
e-ISSN	10872620
Journal	Journal of Toxicology and Environmental Health, Part A
Language	English
Publisher	Taylor & Francis
Publisher Date	2014-01-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Environmental Health Discipline Toxicology Cell Membrane Permeability Drug Effects Environmental Pollutants Toxicity Mitochondria Mitochondrial Membranes Polybrominated Biphenyls Adenosine Triphosphate Metabolism Animals Biological Markers Cell Respiration Dose-response Relationship, Drug In Vitro Techniques Male Oxidative Stress Rats Rats, Wistar Reactive Oxygen Species Evaluation Studies Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Toxicology

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BDE-154 induces mitochondrial permeability transition and impairs mitochondrial bioenergetics.