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Possible involvement of the adenine nucleotide translocase in the activation of the permeability transition pore induced by cadmium.
TLDR
It was found that cadmium bound mainly to proteins of molecular weight between 30 and 50 kDa, and the 30 kDa protein was identified as the adenine nucleotide translocase by labelling experiments with eosin 5-maleimide and experiments of reconstitution. Expand
On the Role of the Respiratory Complex I on Membrane Permeability Transition
TLDR
It is proposed that the mechanism for pore opening, in addition to the oxidative stress, involves the uncoupling effect of fatty acids providing activation of phospholipase A2, lipid peroxidation, and the oxidation of membrane thiols. Expand
Changes in specific lipids regulate BAX‐induced mitochondrial permeability transition
TLDR
Investigation of the relevance of the main components of membrane microdomains in activation of the mitochondrial permeability transition pore by recombinant BAX suggests that enriched cholesterol and ganglioside domains in the mitochondrial membranes may determine BAX interaction with the mPTP. Expand
Post-conditioning Preserves Glycolytic ATP During Early Reperfusion: A survival Mechanism for the Reperfused Heart
TLDR
It is concluded that in the post-conditioned heart, a functional compartmentation of anaerobic energy metabolism, at early reperfusion, plays a significant role in cardiac protection against reperfusions damage. Expand
Proinflammatory Cytokines Are Soluble Mediators Linked with Ventricular Arrhythmias and Contractile Dysfunction in a Rat Model of Metabolic Syndrome
TLDR
This study highlights the possible role of serum proinflammatory mediators in the development of arrhythmic events during MS as spontaneous Ca2+ releases provide a substrate for ventricular arrhythmias. Expand
The permeability transition pore as a pathway for the release of mitochondrial DNA.
TLDR
It was observed that mtDNA was hydrolyzed after the oxidative stress, and it is proposed that some of the fragments were released from the matrix, in such a way that approximately 12% of the total mtDNA remained in the mitochondria. Expand
Impaired oxidative metabolism and calcium mishandling underlie cardiac dysfunction in a rat model of post-acute isoproterenol-induced cardiomyopathy.
TLDR
It is suggested that post-ISO-OV mitochondrial dysfunction may underlie decreased cardiac contractility, mainly by depletion of ATP needed for myofilaments and Ca(2+) transport by SERCA, while exacerbated oxidative stress may enhance diastolic RyR2 activity. Expand
The flavonoid quercetin induces changes in mitochondrial permeability by inhibiting adenine nucleotide translocase
TLDR
Quercetin-induced permeability transition pore opening was inhibited by 0.5 µM cyclosporin A, but, interestingly, the release of cytochrome c was not inhibited by the immunosuppressor, as quercet in was found to disrupt the outer membrane. Expand
Mitochondrial DNA fragments released through the permeability transition pore correspond to specific gene size.
TLDR
It is shown that after induction of mitochondrial damage by oxidative stress, in the presence of calcium, matrix DNA content decreased to 42+/-6%. Expand
Myocardial protective effect of octylguanidine against the damage induced by ischemia reperfusion in rat heart
TLDR
The histological images showed that myocardium fibers from treated rats were in good shape and retained their striae, also there was absence of edema, and the accumulation of 201Tl in hearts from these rats indicated that the tissue did not suffer disruption or impairment in membrane functions. Expand
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