Chakraborty 2016 Pancreatology

From Bioblast
Publications in the MiPMap
Chakraborty M, Hickey AJ, Petrov MS, Macdonald JR, Thompson N, Newby L, Sim D, Windsor JA, Phillips AR (2016) Mitochondrial dysfunction in peripheral blood mononuclear cells in early experimental and clinical acute pancreatitis. Pancreatology 16:739-47.

Β» PMID: 27473495 Β»O2k-brief

Chakraborty M, Hickey AJ, Petrov MS, Macdonald JR, Thompson N, Newby L, Sim D, Windsor JA, Phillips AR (2016) Pancreatology

Abstract: Mitochondrial dysfunction occurs in vital organs in experimental acute pancreatitis (AP) and may play an important role in determining severity of AP. However, obtaining vital organ biopsies to measure mitochondrial function (MtF) in patients with AP poses considerable risk of harm. Being able to measure MtF from peripheral blood will bypass this problem. Furthermore, whether mitochondrial dysfunction is detectable in peripheral blood in mild AP is unknown. Therefore, the objective was to evaluate peripheral blood MtF in experimental and clinical AP.

Mitochondrial respiration was measured using high-resolution oxygraphy in an experimental study in caerulein induced AP and in a separate study, in patients with mild AP. Superoxide, cytochrome c, mitochondrial membrane potential (ΔΨ) and adenine triphosphate (ATP) were also measured as other markers of MtF.

Even though some states of mitochondrial respiration were increased in both experimental and clinical AP, this did not lead to an increase in net ATP in patients with AP. The increased LEAK respiration in both studies was further proof of dyscoupled mitochondria. In the clinical study there were also features of mitochondrial dysfunction with increased LEAK flux control ratio, superoxide, ΔΨ and decreased cytochrome c.

There is evidence of mitochondrial dysfunction with dyscoupled mitochondria, increased superoxide and decreased cytochrome c in patients with mild acute pancreatitis. Further studies should now determine whether mitochondrial function alters with severity in AP and whether mitochondrial dysfunction responds to treatments.

Copyright Β© 2016 IAP and EPC. Published by Elsevier B.V. All rights reserved. β€’ Keywords: Adenine triphosphate, Electron transport system, Mitochondrial membrane potential, Oxidative stress, Peripheral blood mononuclear cells β€’ Bioblast editor: Kandolf G β€’ O2k-Network Lab: NZ Auckland Hickey AJ

Labels: MiParea: Respiration, Comparative MiP;environmental MiP, Patients  Pathology: Other 

Organism: Human, Rat  Tissue;cell: Blood cells  Preparation: Permeabilized cells 

Coupling state: LEAK, ROUTINE, OXPHOS, ET  Pathway: N, S, Gp, CIV, NS, ROX  HRR: Oxygraph-2k 

MitoEAGLE blood cells data, O2k-brief, PBMCs 


An Oroboros O2k was used in this publication, whereas the Anton Paar/Oroboros Oxygraph was the first-generation instrument for high-resolution respirometry, which was replaced by the O2k in 2002.



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