In situ demonstration of improvement of liver mitochondria function by melatonin after cold ischemia

Isabel Freitas, Vittorio Bertone, Catia Guarnaschelli, Andrea Ferrigno, Eleonora Boncompagni, Vittoria Rizzo, Russel J. Reiter, Sergio Barni, Mariapia Vairetti

Research output: Contribution to journalArticle

Abstract

In a previous investigation, reperfusion with a melatonin-containing medium was demonstrated to enhance bile production and tissue ATP levels in rat livers, cold-preserved with University of Wisconsin (UW) or Celsior solutions, with respect to melatonin-free reperfusion; lipid peroxidation products in the perfusate were not influenced by the indole. This was ascribed to an increased efficiency of the hepatocyte mitochondria induced by melatonin. Reactive oxygen species (ROS) normally leak from the electron transfer chain in mitochondria and excessive ROS production is presumed to mediate ischemia-reperfusion (I/R) damage. A histochemical reaction was used to demonstrate ROS on the same model. Compared to the lobular zonation of ROS in control livers, the stained area of cold-preserved livers reperfused without melatonin was restricted to a narrow portal region, in keeping with the much lower ATP content. When reperfusion was performed with melatonin, the liver morphology was improved and the ROS reaction in hepatocytes more intense, though not reaching the control liver pattern. Sinusoidal cells were poorly-stained in both cases. In conclusion, with this different approach, melatonin was confirmed to improve mitochondrial performance and to discriminate parenchymal from sinusoidal cell behavior. Our observations confirm that melatonin mitigates I/R injury and support its potential in liver transplantation.

Original languageEnglish
Pages (from-to)229-238
Number of pages10
JournalIn Vivo
Volume20
Issue number2
Publication statusPublished - Mar 2006

Fingerprint

Cold Ischemia
Mitochondria
Liver Mitochondrion
Melatonin
Liver
Demonstrations
Reactive Oxygen Species
Reperfusion
Reperfusion Injury
Hepatocytes
Adenosine Triphosphate
Bile
Liver Transplantation
Lipid Peroxidation
Rats
Ischemia
Electrons
Tissue
Lipids

Keywords

  • Cold storage
  • Ischemia-reperfusion
  • Liver transplantation
  • Melatonin
  • Mitochondria
  • Reactive oxygen species

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Freitas, I., Bertone, V., Guarnaschelli, C., Ferrigno, A., Boncompagni, E., Rizzo, V., ... Vairetti, M. (2006). In situ demonstration of improvement of liver mitochondria function by melatonin after cold ischemia. In Vivo, 20(2), 229-238.

In situ demonstration of improvement of liver mitochondria function by melatonin after cold ischemia. / Freitas, Isabel; Bertone, Vittorio; Guarnaschelli, Catia; Ferrigno, Andrea; Boncompagni, Eleonora; Rizzo, Vittoria; Reiter, Russel J.; Barni, Sergio; Vairetti, Mariapia.

In: In Vivo, Vol. 20, No. 2, 03.2006, p. 229-238.

Research output: Contribution to journalArticle

Freitas, I, Bertone, V, Guarnaschelli, C, Ferrigno, A, Boncompagni, E, Rizzo, V, Reiter, RJ, Barni, S & Vairetti, M 2006, 'In situ demonstration of improvement of liver mitochondria function by melatonin after cold ischemia', In Vivo, vol. 20, no. 2, pp. 229-238.
Freitas I, Bertone V, Guarnaschelli C, Ferrigno A, Boncompagni E, Rizzo V et al. In situ demonstration of improvement of liver mitochondria function by melatonin after cold ischemia. In Vivo. 2006 Mar;20(2):229-238.
Freitas, Isabel ; Bertone, Vittorio ; Guarnaschelli, Catia ; Ferrigno, Andrea ; Boncompagni, Eleonora ; Rizzo, Vittoria ; Reiter, Russel J. ; Barni, Sergio ; Vairetti, Mariapia. / In situ demonstration of improvement of liver mitochondria function by melatonin after cold ischemia. In: In Vivo. 2006 ; Vol. 20, No. 2. pp. 229-238.
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