Difference between revisions of "Cecatto 2020 Mitochondrion"
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{{Labeling | {{Labeling | ||
|area=Respiration, Pharmacology;toxicology | |area=Respiration, Pharmacology;toxicology | ||
|diseases=Other | |diseases=Inherited, Other | ||
|injuries=Permeability transition | |injuries=Permeability transition | ||
|organism=Rat | |organism=Rat | ||
|tissues=Liver | |tissues=Liver, Other cell lines | ||
|preparations=Permeabilized cells, Isolated mitochondria | |preparations=Permeabilized cells, Isolated mitochondria | ||
|topics=Calcium, mt-Membrane potential, Fatty acid | |||
|couplingstates=LEAK, OXPHOS, ET | |couplingstates=LEAK, OXPHOS, ET | ||
|pathways=N, S | |pathways=N, S |
Revision as of 11:08, 3 March 2020
Cecatto C, Amaral AU, Wajner A, Wajner SM, Castilho RF, Wajner M (2019) Disturbance of mitochondrial functions associated with permeability transition pore opening induced by cis-5-tetradecenoic and myristic acids in liver of adolescent rats. Mitochondrion 50:1-13. |
Cecatto C, Amaral AU, Wajner A, Wajner SM, Castilho RF, Wajner M (2019) Mitochondrion
Abstract: Patients affected by very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency commonly present liver dysfunction whose pathogenesis is poorly known. We demonstrate here that major metabolites accumulating in this disorder, namely cis-5-tetradecenoic acid (Cis-5) and myristic acid (Myr), markedly impair mitochondrial respiration, decreasing ATP production in liver mitochondrial preparations from adolescent rats. Other parameters of mitochondrial homeostasis such as membrane potential (ΞΞ¨m) and Ca2+retention capacity were strongly compromised by these fatty acids, involving induction of mitochondrial permeability transition. The present data indicate that disruption of mitochondrial bioenergetics and Ca2+homeostasis may contribute to the liver dysfunction of VLCAD deficient patients.
Copyright Β© 2019 Elsevier B.V. and Mitochondria Research Society. All rights reserved. β’ Keywords: Cis-5-tetradecenoic acid, Liver mitochondria, Mitochondrial homeostasis, Mitochondrial permeability transition, Myristic acid, VLCAD deficiency β’ Bioblast editor: Plangger M β’ O2k-Network Lab: BR Porto Alegre Souza DOG
Labels: MiParea: Respiration, Pharmacology;toxicology
Pathology: Inherited, Other
Stress:Permeability transition
Organism: Rat
Tissue;cell: Liver, Other cell lines
Preparation: Permeabilized cells, Isolated mitochondria
Regulation: Calcium, mt-Membrane potential, Fatty acid Coupling state: LEAK, OXPHOS, ET Pathway: N, S HRR: Oxygraph-2k
Labels, 2019-11