Effects of Hypothermia on the Function, Membrane Integrity, and Cytoskeletal Structure of Hepatocytes

Stefanovich, Peter; Ezzell, Robert M.; Sheehan, Sean J.; Tompkins, Ronald G.; Yarmush, Martin L.; Toner, Mehmet

doi:10.1006/cryo.1995.1039

Cited by 94 publications

(57 citation statements)

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“…A cascade of damaging events may follow including: activation and leakage of lysosomal and lipoprotein hydrolases, 35,36 activation of calcium-dependent phospholipases 37,38 and the release of free fatty acids, 39 activation of the apoptotic cascade [40][41][42][43][44] and disruption of the cytoskeletal matrix. [45][46][47] Along with the generation of free radicals, the oxidative stressors attendant to hypothermia may result in the onset of apoptosis or gene regulated cell death. 11,12,20,[48][49][50][51] …”

Section: A Long Cold Journeymentioning

confidence: 99%

Cryopreservation

Baust¹,

2009

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Section: A Long Cold Journeymentioning

confidence: 99%

Cryopreservation

Baust¹,

2009

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“…Several mechanisms of hypothermic injury have been proposed, including the loss of ionic homeothese points corresponds to an activation energy of stasis (31,46), the uncoupling of cellular metabolism decreasing temperature. A swelling mechanism could, however, contribute to cell killing below 10°C because (21), lipid phase transitions in membranes (13,26), depolymerization of the cytoskeleton (49,56), and oxidative k increases with decreasing temperature in this range. However, it is unlikely that cell swelling contributes to stress (8,39).…”

Section: Introductionmentioning

confidence: 99%

Endothelial Cell Preservation at 10°C Minimizes Catalytic Iron, Oxidative Stress, and Cold-Induced Injury

Zieger

Gupta

2006

Cell Transplant

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There is growing evidence that oxidative stress plays an important role in mediating the injury induced by hypothermia during the preservation of cells and tissues for clinical or research use. In cardiovascular allografts, endothelial cell loss or injury may lead to impaired control of vascular permeability and tone, thrombosis, and inflammation. We hypothesized that hypothermia-induced damage to the endothelium is linked to increases in intracellular catalytic iron pools and oxidative stress. In this study, bovine aortic endothelial cells and cell culture methods were used to model the response of the endothelium of cardiovascular tissues to hypothermia. Confluent cells were stored at 0°C to 25°C and cell damage was measured by lipid peroxidation (LPO) and lactate dehydrogenase release. Varying the bleomycin-detectible iron (BDI) in cells modulated cold-induced LPO and cell injury. In untreated cells, injury was highest at 0°C and a minimum at 10°C. A similar temperature-dependent trend was found in BDI levels and cell plating efficiencies. Arrhenius plots of cell killing and iron accumulation rates showed biphasic temperature dependence, with minima at 10°C and matching activation energies above and below 10°C. These findings imply that the mechanisms underlying the hypothermic increase in catalytic iron, oxidative stress, and cell killing are the same and that preservation of the endothelium may be optimized at temperatures above those routinely used.

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“…PEG, and particularly PEG 20M, has been found to improve tissue and organ preservation. The addition of PEG to the cooling solution preserved actin filament and microtubule morphology in hepatocytes during cold treatment at 4°C for up to 24 h (Stefanovich et al, 1995). The mode of action includes the prevention of osmotic swelling and formation of malondialdehyde (Mack et al, 1991;Ganote et al, 1997;Hauet et al, 2001).…”

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confidence: 99%

Polyethylene Glycol Reduces Early and Long-Term Cold Ischemia-Reperfusion and Renal Medulla Injury

Fauré¹,

Hauet²,

Han³

et al. 2002

J Pharmacol Exp Ther

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Ischemia-reperfusion injury (IRI) after transplantation is a major cause of delayed graft function, which has a negative impact on early and late graft function and improve acute rejection. We have previously shown that polyethylene glycol (PEG) and particularly PEG 20M has a protective effect against cold ischemia and reperfusion injury in an isolated perfused pig and rat kidney model. We extended those observations to investigate the role of PEG using different doses (30g or 50g/l) added (ICPEG30 or ICPEG50) or not (IC) to a simplified preservation solution to reduce IRI after prolonged cold storage (48-h) of pig kidneys when compared with Euro-Collins and University of Wisconsin solutions. The study of renal function and medulla injury was performed with biochemical methods and proton NMR spectroscopy. Histological and inflammatory cell studies were performed after reperfusion (30 -40 min) and on days 7 and 14 and weeks 4, 8, and 12. Peripheral-type benzodiazepine receptor (PBR), a mitochondrial protein involved in cholesterol homeostasis, was also studied. The results demonstrated that ICPEG30 improved renal function and reduced medulla injury. ICPEG30 also improved tubular function and strongly protect mitochondrial integrity. Post-IRI inflammation was strongly reduced in this group, particularly lymphocytes TCD4 ϩ , PBR expression was influenced by IRI in the early period and during the development of chronic dysfunction. This study clearly shows that PEG has a beneficial effect in renal preservation and suggests a role of PBR as a marker IRI and repair processes.

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Effects of Hypothermia on the Function, Membrane Integrity, and Cytoskeletal Structure of Hepatocytes

Cited by 94 publications

References 0 publications

Cryopreservation

Cryopreservation

Endothelial Cell Preservation at 10°C Minimizes Catalytic Iron, Oxidative Stress, and Cold-Induced Injury

Polyethylene Glycol Reduces Early and Long-Term Cold Ischemia-Reperfusion and Renal Medulla Injury

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