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Titolo:
Ethylazinphos interaction with membrane lipid organization induces increase of proton permeability and impairment of mitochondrial bioenergetic functions
Autore:
Videira, RA; Antunes-Madeira, MC; Madeira, VMC;
Indirizzi:
Univ Coimbra, Dept Zool, Ctr Neurociencias & Biol Celular, P-3004517 Coimbra, Portugal Univ Coimbra Coimbra Portugal P-3004517 lar, P-3004517 Coimbra, Portugal Inst Super Politecn Viseu, Escola Super Tecnol, Dept Ambiente, P-3500 Viseu, Portugal Inst Super Politecn Viseu Viseu Portugal P-3500 , P-3500 Viseu, Portugal
Titolo Testata:
TOXICOLOGY AND APPLIED PHARMACOLOGY
fascicolo: 3, volume: 175, anno: 2001,
pagine: 209 - 216
SICI:
0041-008X(20010915)175:3<209:EIWMLO>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
ORGANO-PHOSPHORUS INSECTICIDES; TOXICITY; MECHANISMS; BILAYERS; FLUIDITY; VESICLES; MODEL; STATE; MOUSE; ACETYLCHOLINESTERASE;
Keywords:
ethylazinphos; membrane organization; proton permeability; mitochondrial respiration; transmembrane potential; oxidative phosphorylation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
57
Recensione:
Indirizzi per estratti:
Indirizzo: Madeira, VMC Univ Coimbra, Dept Zool, Ctr Neurociencias & Biol Celular, P-3004517 Coimbra, Portugal Univ Coimbra Coimbra Portugal P-3004517 7 Coimbra, Portugal
Citazione:
R.A. Videira et al., "Ethylazinphos interaction with membrane lipid organization induces increase of proton permeability and impairment of mitochondrial bioenergetic functions", TOX APPL PH, 175(3), 2001, pp. 209-216

Abstract

Ethylazinphos increases the passive proton permeability of lipid bilayers reconstituted with dipalmitoylphosphatidylcholine (DPPC) and mitochondrial lipids. A sharp increase of proton permeability is detected at insecticide/lipid molar ratios identical to those inducing phase separation in the plane of DPPC bilayers, as revealed by differential scanning calorimetry (I)SQ. Ethylazinphos progressively depresses the transmembrane potential (AW) of mitochondria supported by piruvate/malate, succinate, or ascorbate/TMPD. Additionally, a decreased depolarization induced by ADP depends on ethylazinphos concentration, reflecting a phosphorylation depression. This loss of phosphorylation is a consequence of a decreased AV. A decreased respiratory control ratio is also observed, since ethylazinphos stimulates state 4 respiration and inhibits ADP-stimulated respiration (state 3). Ethylazinphos concentrations up to 100 nmol/mg mitochondrial protein increase the rate of state 4 together with a decrease in Delta Psi, without significant perturbation of state 3 and carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP)-uncoupled respiration. For increased insecticide concentrations, the state3 and FCCP-uncoupled respiration are inhibited to approximately the same extent. The perturbations are more pronounced when the energization is supported by pyruvate/malate and less effective when succinate is used as substrate. The present data, in association with previous DSC studies, indicate that ethylazinphos, at concentrations up to 100 nmol/mg mitochondrial protein, interacts with the lipid bilayer of mitochondrial membrane, changing thelipid organization and increasing the proton permeability of the inner membrane. The increased proton permeability explains the decreased oxidative phosphorylation coupling. Resulting disturbed ATP synthesis may significantly underlie the mechanisms of ethylazinphos toxicity, since most of cell energy in eukaryotes is provided by mitochondria. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 08/07/20 alle ore 07:54:01