In this paper new evidence is given to support the hypothesis that the triehtyllead compound (TEL) is an uncoupler of the oxidative phosphorylation. By means of an Arrhenius plot, it has been demonstrated that the transport kinetic of the TEL compound in mitochondria behaves in a manner which is similar to that obtained using classical uncouplers. The break point at 170C observed in the Arrhenius plot is interpreted as due to a phase change in the lipidic bilayer, since the TEL compound, like uncouplers and mobile carriers, is sensitive to the phospholipidic phase change. Therefore, we can confirm our previous hypothesis that, as TEL is an uncoupler it, like uncouplers, crosses the biological membranes by means of an electrophoretic mechanism. An understanding of this behaviour is essential to explain the neurotoxicity of TEL compound.
Triethyllead: new evidences supporting the uncoupling mechanism in rat liver mitochondria
MANENTE, Sabrina;GALLO, Michele;BRAGADIN, Marcantonio
2005-01-01
Abstract
In this paper new evidence is given to support the hypothesis that the triehtyllead compound (TEL) is an uncoupler of the oxidative phosphorylation. By means of an Arrhenius plot, it has been demonstrated that the transport kinetic of the TEL compound in mitochondria behaves in a manner which is similar to that obtained using classical uncouplers. The break point at 170C observed in the Arrhenius plot is interpreted as due to a phase change in the lipidic bilayer, since the TEL compound, like uncouplers and mobile carriers, is sensitive to the phospholipidic phase change. Therefore, we can confirm our previous hypothesis that, as TEL is an uncoupler it, like uncouplers, crosses the biological membranes by means of an electrophoretic mechanism. An understanding of this behaviour is essential to explain the neurotoxicity of TEL compound.
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