Role of the Mitochondrial Membrane Permeability Transition (MPT) in Rotenone-Induced Apoptosis in Liver Cells
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چکیده
منابع مشابه
Role of the mitochondrial membrane permeability transition (MPT) in rotenone-induced apoptosis in liver cells.
Rotenone inhibits spontaneously and chemically induced hepatic tumorigenesis in rodents through the induction of apoptosis. However, the mechanism for the induction of apoptosis by rotenone has not been defined. Mitochondrial dysfunction, in particular the induction of the mitochondrial membrane permeability transition (MPT), has been implicated in the cascade of events involved in the inductio...
متن کاملRotenone inhibits the mitochondrial permeability transition-induced cell death in U937 and KB cells.
The permeability transition pore (PTP) is a mitochondrial inner membrane Ca(2+)-sensitive channel that plays a key role in different models of cell death. Because functional links between the PTP and the respiratory chain complex I have been reported, we have investigated the effects of rotenone on PTP regulation in U937 and KB cells. We show that rotenone was more potent than cyclosporin A at ...
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Objective: Extracts of Anchomanes difformis (AD) are used in folkloric medicine to treat several diseases and infections. However, their roles in mitochondrial permeability transition pore opening are not known. Material and Methods: The viability of mitochondria isolated from Wistar rat liver used in this experiment, was assessed by monitoring their swel...
متن کاملRole of the mitochondrial permeability transition pore in apoptosis.
Mitochondrial permeability transition (PT) involves the formation of proteaceous, regulated pores, probably by apposition of inner and outer mitochondrial membrane proteins which cooperate to form the mitochondrial megachannel (= mitochondrial PT pore). PT has important metabolic consequences, namely the collapse of the mitochondrial transmembrane potential, uncoupling of the respiratory chain,...
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ژورنال
عنوان ژورنال: Toxicological Sciences
سال: 2000
ISSN: 1096-0929
DOI: 10.1093/toxsci/53.2.340