MiP2005: Session 9

 

Role of mitochondrial dysfunction in mechanism of reversible metabolic depression of over-wintering lamprey liver during pre-spawning migration.

Larisa V Emelyanova, MV Savina, EA Belyaeva

Lab. Comp. Biochem. of Inorganic Ions, Sechenov Inst. Evolutionary Physiol. Biochem., Russian Academy of Sciences, Thorez pr. 44, 194223, St.-Petersburg, Russia. – evlara@mail.ru

    We have conducted an investigation with the aim to clarify mechanism(s) of metabolic depression observed in poikilothermic animals during over-wintering period. In this study we have elucidated the role of mitochondria in reversible metabolic depression of hepatocytes of Baltic lamprey (Lampetra fluviatilis L.) taking place in the last year of its life cycle. It is known that in autumn the lamprey migrates from the Gulf of Finland to the Neva River (North-Western Russia) and switches off the exogenous feeding during all period of pre-spawning migration. Using isolated mitochondria as a model, we have revealed clear-cut seasonal variations of the main bioenergetical parameters of the lamprey liver. These changes indicate that the metabolic depression observed during the last winter of the lamprey’s life cycle is mediated by prolonged reversible mitochondrial dysfunction. The dysfunction is found to manifest itself in: (1) the very low activity of mitochondrial respiratory chain, especially of its complex I, (2) low oxidative phosphorylation, (3) decreased content of mitochondrial adenine nucleotides, (4) high level of reduced pyridine nucleotides, and (5) leaky mitochondrial membranes. The sharp activation of oxidation and phosphorylation in the lamprey liver mitochondria followed by spawning and death of the animal is observed in spring. The possible causes of the phenomenon and its difference from that taking place under oxidative stress are discussed. An amazing analogy between some molecular mechanisms underlying the metabolic depression in lamprey liver cells and those in cells of patients suffering from mitochondrial encephalomyopathies, neurogenerative diseases, sepsis, poisoning, and cancerogenesis is revealed [1-3].

1.    Luft R (1995) The development of mitochondrial medicine. Biochim. Biophys Acta. 1271: 1-6.

2.    Gellerich FN, Trumbeckaite S, Mueller T, Deschauer M, Chen Y, Gizatullina Z, Zeiz S (2004) Mol. Cell. Biochem. 256/257: 391-405.

3.    Greenamyre JT, Sherer TB, Betarbet R, Panov AV (2001) Complex I and Parkinson's disease. IUBMB Life. 52: 135-141.


to topPrint page

 
 

© Mitochondrial Physiology • Webdesign: Mag. Christian Schönherr