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337 results on '"Roselló-Catafau, J."'

25. Polyethylene glycols: An effective strategy for limiting liver ischemia reperfusion injury

Author

#NODATA#, Pasut, G., Panisello, A., Folch-Puy, E., Lopez, A., Castro-Benítez, C., Calvo, Marta M, Carbonell, T., García-Gil, A., Adam, R., Roselló-Catafau, J., #NODATA#, Pasut, G., Panisello, A., Folch-Puy, E., Lopez, A., Castro-Benítez, C., Calvo, Marta M, Carbonell, T., García-Gil, A., Adam, R., and Roselló-Catafau, J.

Abstract

Liver ischemia-reperfusion injury (IRI) is an inherent feature of liver surgery and liver transplantation in which damage to a hypoxic organ (ischemia) is exacerbated following the return of oxygen delivery (reperfusion). IRI is a major cause of primary non-function after transplantation and may lead to graft rejection, regardless of immunological considerations. The immediate response involves the disruption of cellular mitochondrial oxidative phosphorylation and the accumulation of metabolic intermediates during the ischemic period, and oxidative stress during blood flow restoration. Moreover, a complex cascade of inflammatory mediators is generated during reperfusion, contributing to the extension of the damage and finally to organ failure. A variety of pharmacological interventions (antioxidants, anti-cytokines, etc.) have been proposed to alleviate graft injury but their usefulness is limited by the local and specific action of the drugs and by their potential undesirable toxic effects. Polyethylene glycols (PEGs), which are non-toxic water-soluble compounds approved by the FDA, have been widely used as a vehicle or a base in food, cosmetics and pharmaceuticals, and also as adjuvants for ameliorating drug pharmacokinetics. Some PEGs are also currently used as additives in organ preservation solutions prior to transplantation in order to limit the damage associated with cold ischemia reperfusion. More recently, the administration of PEGs of different molecular weights by intravenous injection has emerged as a new therapeutic tool to protect liver grafts from IRI. In this review, we summarize the current knowledge concerning the use of PEGs as a useful target for limiting liver IRI.

Published
2016

26. Trimetazidine and liver preservation against ischaemia-reperfusion injury

Author

Mosbah, I. B., Abdennebi, H. B., mohamed amine zaouali, Padrissa-Altes, S., Peralta, C., and Roselló-Catafau, J.

Abstract

Trimetazidine is an anti-ischaemic drug used for angina pectoris treatment. Recently, it has been shown that trimetazidine protects against hepatic ischaemia reperfusion injury. Several hypotheses have been proposed to explain the exact hepatoprotective mechanisms but they still remain unclear. This review assesses the possible mechanisms responsible for the increase of the liver's tolerance against ischaemia-reperfusion injury with special emphasis on: (1) the prevention of oxidative stress and protection of mitochondrial function; (2) the generation of vasoactive mediators such as nitric oxide and endothelins; and finally (3) the preservation of liver energy metabolism. Copyright © 2007 Termedia & Banach., This work was supported by the Ministerio de Educación y Ciencia (project grant SAF 2005-00385), Ministerio de Sanidad y Consumo (project grant PIO60021) and Ministerio de Asuntos Exteriores y de Cooperación Internacional/Agencia Española De Cooperación Internacional.

Published
2007

27. Modification of oxidative stress in response to intestinal preconditioning

Author

Sola, A., Georgina Hotter, Prats, N., Xaus, C., Gelpi, E., and Roselló-Catafau, J.

Abstract

Previous studies have demonstrated that intestinal preconditioning protects the organ from ischemia reperfusion damage. Xanthine oxidase mediating free radical generation contributes to the development of injury associated to ischemia reperfusion. Thus, any process able to modulate the oxygen free radical generation system could attenuate the injury. Also, it is known that nitric oxide is implicated in the preconditioning response. The aim of this work is to determine: (1) the effect of intestinal preconditioning on the xanthine oxidase system, (2) the relevance of this system in the development of injury, and (3) its relationship with nitric oxide. For this purpose, we have determined the activity of the xanthine dehydrogenase/xanthine oxidase system, the levels of its substrate (xanthine), and end-product (uric acid) and oxidant stress status in rat small intestine subjected to ischemic preconditioning. The effects of nitric oxide inhibition have also been evaluated. Results show that the percentage of xanthine dehydrogenase to xanthine oxidase conversion, xanthine, uric acid concentration, lipoperoxides, and reduced glutathione were significantly reduced in preconditioned rats irrespectively of nitric oxide inhibition. In summary, this work shows that oxidative stress in intestinal preconditioning is reduced as consequence of the diminished conversion of xanthine dehydrogenase to xanthine oxidase, and also as a consequence of the reduced availability of xanthine.

Published
2000

28. Free radicals generated by xanthine oxidase mediate pancreatitis- associated organ failure

Author

Emma Folch Puy, Gelpí, E., Roselló-Catafau, J., and Closa, D.

Subjects
Pancreatitis, Neutrophil, Xanthine oxidase, Xanthine, Glutathione
Abstract

In the present study we evaluate the possibility that xanthine oxidase released by damaged pancreas could act as a source of oxidative damage in systemic tissues during the early stages of acute pancreatitis. This was accomplished by evaluating the effects of xanthine oxidase inhibition with oxypurinol infused into the portal vein. Under these conditions, we inhibited the enzyme before it reached the liver and other distant organs, without inducing changes in the severity of pancreatic damage. Results indicate that pancreatitis parallels increases in xanthine oxidase activity in plasma. Superoxide radicals generated by this enzyme appears to be involved in the decrease of reduced glutathione levels in the plasma and liver. In addition, xanthine oxidase inhibition prevents the infiltration of neutrophils into the lungs. We conclude that oxygen free radicals generated by xanthine and xanthine oxidase released to the bloodstream are involved in the systemic organ failure associated with acute pancreatitis., This work was supported by grant WHO-FISS 96/1815

Published
1998

38. H2O2 and PARS mediate lung P-selectin upregulation in acute pancreatitis

Author

Folch, E., Salas, A., Prats, N., Panés, J., Piqué, J.M., Gelpí, E., Roselló-Catafau, J., Closa, D., Folch, E., Salas, A., Prats, N., Panés, J., Piqué, J.M., Gelpí, E., Roselló-Catafau, J., and Closa, D.

Abstract

P-selectin and circulating xanthine oxidase are involved in the process of neutrophil infiltration into the lung associated with acute pancreatitis. This study investigated the mediators that trigger the upregulation of P-selectin in this process. Pancreatitis was induced in rats by intraductal administration of 5% sodium taurocholate. P-selectin expression was measured using radiolabeled antibodies. Neutrophil infiltration and PAF levels were also evaluated. The role of superoxide radical, H2O2, or the enzyme poly (ADP-ribose) synthetase (PARS) on these processes was determined in groups of animals treated with the corresponding inhibitors. Pancreatitis was associated with an increase in P-selectin expression in the lung. Inhibition of PARS or H2O2 abrogated P-selectin upregulation, PAF generation, and neutrophil recruitment. Superoxide dismutation prevented neutrophil recruitment and PAF generation, but had no effect on P-selectin expression. We conclude that during acute pancreatitis, upregulation of P-selectin in the pulmonary endothelium is triggered by H2O2 and PARS activity. Copyright (C) 2000 Elsevier Science Inc.

Published
2000

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