Implication of mitochondrial dysfunction and cell death in cold preservation--warm reperfusion-induced hepatocyte injury.

Cold ischemia--warm reperfusion (CI/WR) injury of liver transplantation involves hepatocyte cell death, the nature and underlying mechanisms of which remain unclear. Isolated hepatocytes and isolated perfused livers were used to determine the prevalence of necrosis and apoptosis as well as mitochondrial dysfunction. In isolated cells, propidium iodide and Hoechst 33342 staining showed a cold-storage, time-dependent increase in necrosis, whereas apoptosis was minimal even after 48 h of hypothermia.

Resveratrol protects against cold ischemia-warm reoxygenation-induced damages to mitochondria and cells in rat liver.

Ischemia-reperfusion is a critical event in the development of primary graft dysfunctions after liver transplantations. Ischemia-reperfusion causes cell injuries which are related to the successive cold preservation-warm reperfusion (CPWR) periods required by the graft. Recent evidences suggest that oxidative stress plays an important role in the development of these injuries and that mitochondrial dysfunctions are involved.

Role of the permeability transition pore in cytochrome C release from mitochondria during ischemia-reperfusion in rat liver.

Ischemia and reperfusion cause mitochondrial dysfunctions that initiate the mitochondrial apoptosis pathway. They involve the release of cytochrome C and the activation of the caspase cascade but the mechanism(s) leading to cytochrome C release is(are) poorly understood. The aim of this study was to analyse the relation between cytochrome C release and the opening of the permeability transition pore (PTP) during in situ liver ischemia and reperfusion.

Protection by cyclosporin A of mitochondrial and cellular functions during a cold preservation-warm reperfusion of rat liver.

Liver transplantation is an effective therapeutic option for end-stage liver disease, but initial poor graft function still occurs, often related to cold preservation-warm reperfusion (CPWR) conditions. Damages to mitochondria could be implicated in hepatocyte cell death since opening of the permeability transition pore (PTP) can lead to necrosis and apoptosis. The purpose of this study was to test the hypothesis that inhibition of mitochondrial permeability transition by cyclosporin A could improve rat liver mitochondrial and hepatocellular parameters after 24-h cold preservation followed by a warm reperfusion in Krebs-Henseleit Buffer.

Development of an internal control for the detection of the African swine fever virus by PCR.

For the detection of African swine fever virus (ASFV) by polymerase chain reaction (PCR) in clinical samples, an internal control was constructed to identify false negative results in each reaction. The internal control was designed in such a way that the same primer pair was used to amplify the internal control and the target DNA which were differentiated by size. The lower detection limit was reached at about 30 internal control DNA copies and about 50 genomic ASFV DNA copies.