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Medicina is published by MDPI from Volume 54 Issue 1 (2018). Articles in this Issue were published by another publisher in Open Access under a CC-BY (or CC-BY-NC-ND) licence. Articles are hosted by MDPI on mdpi.com as a courtesy and upon agreement with Lithuanian Medical Association, Lithuanian University of Health Sciences, and Vilnius University.
Open AccessArticle

Contribution of mitochondria to injury of hepatocytes and liver tissue by hyperthermia

1
Faculty of Natural Sciences, Vytautas Magnus University, Kaunas, Lithuania
2
Department of Surgery, Medical Academy, Lithuanian University of Health Sciences, Kaunas, Lithuania
3
Institute for Digestive Research, Medical Academy, Lithuanian University of Health Sciences, Kaunas, Lithuania
4
Institute of Biosciences, Vilnius University Life Sciences Center, Vilnius, Lithuania
*
Author to whom correspondence should be addressed.
Medicina 2017, 53(1), 40-49; https://doi.org/10.1016/j.medici.2017.01.001
Received: 7 October 2016 / Revised: 15 December 2016 / Accepted: 2 January 2017 / Published: 9 January 2017
Objective: The aim of this study was to investigate functional changes of liver mitochondria within the experimentally modeled transition zone of radiofrequency ablation and to estimate possible contribution of these changes to the energy status of liver cells and the whole tissue.Materials and methods: Experiments were carried out on mitochondria isolated from the perfused liver and isolated hepatocytes of male Wistar rats. Hyperthermia was induced by changing the temperature of perfusion medium in the range characteristic for the transition zone (38–52 °C). After 15-min perfusion, mitochondria were isolated to investigate changes in the respiration rates and the membrane potential. Adenine nucleotides extracted from isolated hepatocytes and perfused liver subjected to hyperthermic treatment were analyzed by HPLC.Results: Hyperthermic liver perfusion at 42–52 °C progressively impaired oxidative phosphorylation in isolated mitochondria. Significant inhibition of the respiratory chain components was observed after perfusion at 42 ºC, irreversible uncoupling became evident after liver perfusion at higher temperatures (46 °C and above). After perfusion at 50–52 °C energy supplying function of mitochondria was entirely compromised, and mitochondria turned to energy consumers. Hyperthermia-induced changes in mitochondrial function correlated well with changes in the energy status and viability of isolated hepatocytes, but not with the changes in the energy status of the whole liver tissue.Conclusions: In this study the pattern of the adverse changes in mitochondrial functions that are progressing with increase in liver perfusion temperature was established. Results of experiments on isolated mitochondria and isolated hepatocytes indicate that hyperthermic treatment significantly and irreversibly inhibits energy-supplying function of mitochondria under conditions similar to those existing in the radiofrequency ablation transition zone and these changes can lead to death of hepatocytes. However, it was not possible to estimate contribution of mitochondrial injury to liver tissue energy status by estimating only hyperthermia- induced changes in adenine nucleotide amounts on the whole tissue level.
Keywords: Hepatocytes; Hyperthermia; Mitochondria; Oxidative phosphorylation; Apoptosis Hepatocytes; Hyperthermia; Mitochondria; Oxidative phosphorylation; Apoptosis
MDPI and ACS Style

Žūkienė, R.; Naučienė, Z.; Šilkūnienė, G.; Vanagas, T.; Gulbinas, A.; Zimkus, A.; Mildažienė, V. Contribution of mitochondria to injury of hepatocytes and liver tissue by hyperthermia. Medicina 2017, 53, 40-49.

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