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Giuseppe Petrosillo

Researcher at National Research Council

Publications -  60
Citations -  7154

Giuseppe Petrosillo is an academic researcher from National Research Council. The author has contributed to research in topics: Cardiolipin & Mitochondrion. The author has an hindex of 41, co-authored 56 publications receiving 6416 citations. Previous affiliations of Giuseppe Petrosillo include University of Bari & University of Texas at San Antonio.

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Decrease in Mitochondrial Complex I Activity in Ischemic/Reperfused Rat Heart. Involvement of Reactive Oxygen Species and Cardiolipin

TL;DR: It is proposed that the defect in complex I activity in ischemic/reperfused rat heart could be ascribed to a ROS-induced cardiolipin damage, which may provide an explanation for some of the factors responsible for myocardial reperfusion injury.
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Functional role of cardiolipin in mitochondrial bioenergetics.

TL;DR: The current understanding of the functional role that cardiolipin plays in several reactions and processes involved in mitochondrial bioenergetics, including the respiratory chain complexes and substrate carrier proteins is discussed.
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Role of reactive oxygen species and cardiolipin in the release of cytochrome c from mitochondria

TL;DR: It is suggested that mitochondrial‐induced ROS production promotes cytochrome c release from mitochondria by a two‐steps process, consisting of the dissociation of this protein from cardiolipin, followed by permeabilization of the outer membrane, probably by interaction with VDAC.
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Melatonin, cardiolipin and mitochondrial bioenergetics in health and disease.

TL;DR: The role of melatonin in preventing mitochondrial dysfunction and disease is discussed and recently, melatonin was reported to protect the mitochondria from oxidative damage by preventing cardiolipin oxidation and this may explain the beneficial effect of this molecule in mitochondrial physiopathology.
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Reactive oxygen species affect mitochondrial electron transport complex I activity through oxidative cardiolipin damage.

TL;DR: It is demonstrated that ROS affect the mitochondrial complex I activity via oxidative damage of cardiolipin which is required for the functioning of this multisubunit enzyme complex.