Ischemia-Reperfusion Injury: Processes in Pathogenetic Networks: A Review

Groot, Herbert de; Rauen, Ursula

doi:10.1016/j.transproceed.2006.12.012

Cited by 234 publications

(184 citation statements)

References 13 publications

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“…In the ischemic period, various modifications occur at the cellular level, which promote cell injury. A decline in oxidative phosphorylation leads to ATP depletion and loss of calcium homeostasis [48].…”

Section: Ischemia/reperfusion Liver Injury and Free Radicalsmentioning

confidence: 99%

Role of free radicals in liver diseases

2009

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Reactive oxygen and nitrogen species (ROS and RNS) are produced by metabolism of normal cells. However, in liver diseases, redox is increased thereby damaging the hepatic tissue; the capability of ethanol to increase both ROS/RNS and peroxidation of lipids, DNA, and proteins was demonstrated in a variety of systems, cells, and species, including humans. ROS/RNS can activate hepatic stellate cells, which are characterized by the enhanced production of extracellular matrix and accelerated proliferation. Cross-talk between parenchymal and nonparenchymal cells is one of the most important events in liver injury and fibrogenesis; ROS play an important role in fibrogenesis throughout increasing platelet-derived growth factor. Most hepatocellular carcinomas occur in cirrhotic livers, and the common mechanism for hepatocarcinogenesis is chronic inflammation associated with severe oxidative stress; other risk factors are dietary aflatoxin B 1 consumption, cigarette smoking, and heavy drinking. Ischemia-reperfusion injury affects directly on hepatocyte viability, particularly during transplantation and hepatic surgery; ischemia activates Kupffer cells which are the main source of ROS during the reperfusion period. The toxic action mechanism of paracetamol is focused on metabolic activation of the drug, depletion of glutathione, and covalent binding of the reactive metabolite N-acetyl-pbenzoquinone imine to cellular proteins as the main cause of hepatic cell death; intracellular steps critical for cell death include mitochondrial dysfunction and, importantly, the formation of ROS and peroxynitrite. Infection with hepatitis C is associated with increased levels of ROS/RNS and decreased antioxidant levels. As a consequence, antioxidants have been proposed as an adjunct therapy for various liver diseases.

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Section: Ischemia/reperfusion Liver Injury and Free Radicalsmentioning

confidence: 99%

Role of free radicals in liver diseases

2009

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“…1,2 Ischemiareperfusion injury is a complex phenomenon involving not only intracellular processes but also an injurious inflammatory response that are interconnected. 3 While the pathogenesis of ischemia-reperfusion is not completely understood, there is considerable evidence implicating the decreased mitochondrial ATP generation, loss of selective permeability of cell membranes, impairment of cellular ion homeostasis (rise of intracellular sodium and calcium) with activation of hydrolases and accumulation of reactive oxygen species (ROS) leading to cell injury or death. [3][4][5] ROS formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks, all potentially damaging to normal cellular function.…”

Section: Introductionmentioning

confidence: 99%

“…3 While the pathogenesis of ischemia-reperfusion is not completely understood, there is considerable evidence implicating the decreased mitochondrial ATP generation, loss of selective permeability of cell membranes, impairment of cellular ion homeostasis (rise of intracellular sodium and calcium) with activation of hydrolases and accumulation of reactive oxygen species (ROS) leading to cell injury or death. [3][4][5] ROS formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks, all potentially damaging to normal cellular function. 3,4 Lipid peroxidation is an autocatalytic mechanism leading to oxidative destruction of cellular membranes, and their destruction can lead to the production of toxic reactive aldehydic metabolites and cell death.…”

Section: Introductionmentioning

confidence: 99%

“…[3][4][5] ROS formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks, all potentially damaging to normal cellular function. 3,4 Lipid peroxidation is an autocatalytic mechanism leading to oxidative destruction of cellular membranes, and their destruction can lead to the production of toxic reactive aldehydic metabolites and cell death. [5][6][7][8] A range of drugs and methods have been tested with the intention to block the pathways of cell injury at different levels and to thereby enhance viability of the kidney challenged by ischemia/ reperfusion stress with variable results, such as: heat shock (interferes with the L-arginine-nitric oxide pathway), 9 antioxidants, 10,11 dipyridamole (increases endogenous adenosine), 12,13 nicotine (inhibit cholinergic antiinflammatory pathway), 14 calcium channel blockers or antagonists, [15][16][17][18] chlorpromazine, 19,20 etc.…”

Section: Introductionmentioning

confidence: 99%

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Renal ischemia and reperfusion injury: influence of chorpromazine on renal function and lipid peroxidation

et al. 2008

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Purpose: To evaluate the influence of chlorpromazine (CPZ) on renal function and lipid peroxidation in a rat model of kidney ischemia/reperfusion injury. Methods: Forty eight Wistar rats underwent a laparotomy for hilar clamping of left kidney with a bulldog clamp for 60 minutes followed by organ reperfusion and contralateral nephrectomy. Of these, 26 received 3mg/kg of CPZ intravenously 15 minutes before renal ischemia (G-E) while the remaining 22 were used as ischemic control group (G-C). Eleven rats of G-E and 8 of G-C were followed for blood urea nitrogen and creatinine determinations before renal ischemia and at 1 st , 4 th and 7 th postoperative days. Samplings of left renal tissue were obtained at 5 minutes (5 rats from each group) and 24 hours (9 G-C and 10 of G-E) of reperfusion for malondialdehy (MDA) content determination. Controls of renal MDA content were determined in kidneys harvested from 6 additional normal rats. Results: Acute renal failure occurred in all animals but levels of BUN and creatinine were significantly lower in G-E (p<0.001). MDA content rose strikingly at 5 minutes of reperfusion in both groups (p>0.05) and returned near to normal levels 24 hours later. Conclusion: CPZ conferred partial protection of renal function to kidneys submitted to ischemia/reperfusion injury that seems to be not dependent on inhibition of lipid peroxidation. Key words:Renal Ischemia/Reperfusion. Lipid Peroxidation. Malondialdehyde. Chlorpromazine. Free Radicals. RESUMOObjetivo: avaliar a influência da clorpromazina (CPZ) na função renal e na peroxidação lipídica num modelo de lesão de isquemia/reperfusão renal em ratos. Métodos: 48 ratos Wistar foram submetidos à laparotomia para clampamento da artéria renal esquerda durante 60 minutos, seguido da reperfusão e nefrectomia contralateral. Destes animais, 26 receberam 3 mg/ kg de CPZ intravenosa 15 minutos antes da isquemia renal (G-E), sendo os 22 animais restantes utilizados como grupo controle isquêmico (G-C). Em 11 ratos do G-E e 8 do G-C foi feita a dosagem de uréia e creatinina sérica antes da isquemia renal e no 1º, 4º e 7º dia pós-operatório. Amostras de tecido do rim esquerdo foram obtidas aos 5 minutos (5 ratos de cada grupo) e 24 horas após reperfusão (9 G-C e 10 G-E) para dosagem de malondialdeído (MDA). Valores controle para níveis de MDA foram obtidos em rins retirados de 6 ratos normais. Resultados: insuficiência renal aguda ocorreu em todos os animais mas os níveis séricos de uréia e creatinina foram significativamente menores no G-E (p<0,001). Os níveis de MDA apresentaram elevação acentuada na avaliação aos 5 minutos de reperfusão em ambos os grupos (p<0,05), retornando a valores próximos aos normais na avaliação com 24 horas. Conclusão: a CPZ conferiu proteção parcial da função renal aos rins submetidos à lesão de isquemia e reperfusão, aparentemente independente da inibição da peroxidação lipídica.

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“…This process is markedly slower if organs are kept between 4 and 0°C (De Groot and Rauen, 2007). Upon reperfusion of the organ, an inflammatory response is triggered by cell debris and/or altered tissue matrix as a result of anoxic cell injury; this may also be triggered by cold-induced iron ion-dependent apoptosis (e.g., endothelial cells, renal tubular cells, hepatocytes).…”

Section: Methodologies Used For Extracorporeal Perfusion Of Large Animentioning

confidence: 99%

Extracorporeal perfusion of isolated organs of large animals – Bridging the gap between in vitro and in vivo studies

Daniel¹

2018

ALTEX

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Ischemia-Reperfusion Injury: Processes in Pathogenetic Networks: A Review

Cited by 234 publications

References 13 publications

Role of free radicals in liver diseases

Role of free radicals in liver diseases

Renal ischemia and reperfusion injury: influence of chorpromazine on renal function and lipid peroxidation

Extracorporeal perfusion of isolated organs of large animals – Bridging the gap between in vitro and in vivo studies

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