Protective effect of desferrioxamine during canine liver transplantation: significance of peritransplant liver biopsy

Park, Kyong; Chung, Kwansoo; Sung, Sun Hee; Kim, B.R; Kim, Y.S

doi:10.1016/s0041-1345(02)03971-4

Cited by 15 publications

(13 citation statements)

References 10 publications

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“…In animal models, increased iron deposition is associated with increased lipid peroxidation and collagen type 1 deposition [6]. This pattern of iron deposition, occurring mainly in the periportal hepatocytes in rats, closely approximates that of hereditary hemochromatosis seen in humans [131, 136]. …”

Section: Redox In Pathologic Hepatocytesmentioning

confidence: 83%

“…Other antioxidant agents that have been shown to have beneficial effects in liver ischemia reperfusion injury include coenzyme Q/pentoxyfylline [139], idebenone [151], lipoic acid [117], desferrioxamine [131], trimetaxidine [163], quercetin [158], cyanidin [164], plant extracts [164, 182], bucillamine [2], SOD derivatives [121], CAT derivatives [178], allopurinol [71], and aminoguanidine [78]. (Table 3) Allopurinol at high [71], but not low doses [70], have shown some beneficial effects in preventing liver damage, but again, the results are preliminary, with more systematic in depth evaluation needed.…”

Section: Implication For Future Interventionsmentioning

confidence: 99%

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Nitric Oxide and Redox Regulation in the Liver: Part II. Redox Biology in Pathologic Hepatocytes and Implications for Intervention

Diesen¹,

Kuo²

2011

Journal of Surgical Research

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Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are created in normal hepatocytes and are critical for normal physiological processes including oxidative respiration, growth, regeneration, apoptosis, and microsomal defense. When the levels of oxidation products exceed the capacity of normal antioxidant systems, oxidative stress occurs. This type of stress, in the form of ROS and RNS, can be damaging to all liver cells, including hepatocytes, Kupffer cells, stellate cells, and endothelial cells, through induction of inflammation, ischemia, fibrosis, necrosis, apoptosis, or through malignant transformation by damaging lipids, proteins, and/or DNA. In part I of this review, we will discuss basic redox biology in the liver, including a review of ROS, RNS, and antioxidants, with a focus on nitric oxide as a common source of RNS. We will then review the evidence for oxidative stress as a mechanism of liver injury in hepatitis (alcoholic, viral, nonalcoholic). In part II of this review, we will review oxidative stress in common pathophysiological conditions including ischemia/reperfusion injury, fibrosis, hepatocellular carcinoma, iron overload, Wilson's disease, sepsis and acetaminophen overdose. Finally, biomarkers, proteomic, and antioxidant therapies will be discussed as areas for future therapeutic interventions.

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Section: Redox In Pathologic Hepatocytesmentioning

confidence: 83%

Section: Implication For Future Interventionsmentioning

confidence: 99%

Nitric Oxide and Redox Regulation in the Liver: Part II. Redox Biology in Pathologic Hepatocytes and Implications for Intervention

Diesen¹,

Kuo²

2011

Journal of Surgical Research

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“…It has been observed that when administered during reperfusion most of these compounds exerted considerable protection against IR-induced injury. Desferrioxamine, a strong and rather specific iron chelator that is often used in clinical settings, has been extensively studied in such models and repeatedly found to be protective against IRinduced injury [168][169][170][171]. However, it should be noted that desferrioxamine, due to its hydrophilicity and its relatively high molecular weight (about 500 Da) is not able to penetrate through plasma membranes by passive diffusion.…”

Section: Redox-active Iron In Hepatic Ir Injurymentioning

confidence: 99%

Oxidative Stress in Hepatic Ischemia-Reperfusion Injury: The Role of Antioxidants and Iron Chelating Compounds

Galaris¹,

Barbouti²,

Korantzopoulos

2006

CPD

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Ischemia-reperfusion (IR) injury is a multifactorial process triggered when the liver or other organs are transiently subjected to reduced blood supply followed by reperfusion. It has been shown that "reactive oxygen species" (ROS) are generated during ischemia and reperfusion and may represent pivotal mediators of the ensuing pathological complications. In some cases, however, moderate production of ROS may exert protective effects, a phenomenon presumably related to "ischemic preconditioning". This review will focus mainly on: a) describing the sources and the biochemical mechanisms of ROS generation during ischemia and reperfusion, b) discussing current developments in understanding the biochemical pathways by which ROS may induce toxic or protective effects, c) critically evaluating the results of previous attempts to counteract the toxic effects of ROS by using a variety of antioxidant and transition metalchelating agents, and d) if feasible, proposing potential new pharmaceutical agents aimed at ameliorating ROS-inducing deleterious effects during reperfusion. It is concluded that ROS are generated from different sources, at different periods during IR, and may act by a variety of not well understood biochemical mechanisms which ultimately lead to cell damage and tissue failure.

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“…Studies have shown that desferrioxamine (DFX), a potent iron chelator, improves experimental liver failure and liver transplantation by attenuating oxidative stress [9,10]. Interestingly, the antioxidant effects of iron chelation were also proven beneficial in models of lung injury [11,12].…”

mentioning

confidence: 99%

Desferrioxamine attenuates minor lung injury following surgical acute liver failure

Kostopanagiotou

Kalimeris²,

Arkadopoulos³

et al. 2008

Eur Respir J

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Acute liver failure (ALF) can be complicated by lung dysfunction. The aim of this study was to test the hypothesis that inhibition of oxidative stress through iron chelation with desferrioxamine (DFX) attenuates pulmonary injury caused by ALF.14 adult female domestic pigs were subjected to surgical devascularisation of the liver and were randomised to a study group (DFX group, n57), which received post-operative intravenous infusion of DFX (14.5 mg?kg ?h -1 until completion of 24 h), and a control group (n57). Post-operative lung damage was evaluated by histological and bronchoalveolar lavage fluid (BALF) analysis. DFX resulted in reduced BALF protein levels and tissue phospholipase (PL)A 2 activity. Plasma malondialdehyde and BALF nitrate and nitrite concentrations were lower, while catalase activity in the lung was higher after DFX treatment. PLA 2 , platelet-activating factor acetylhydrolase and total cell counts in BALF did not differ between groups. Histological examination revealed reduced alveolar collapse, pneumonocyte necrosis and total lung injury in the DFX-treated animals.DFX reduced systemic and pulmonary oxidative stress during ALF. The limited activity of PLA 2 and the attenuation of pneumonocyte necrosis could represent beneficial mechanisms by which DFX improves alveolar-capillary membrane permeability and prevents alveolar space collapse.

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Protective effect of desferrioxamine during canine liver transplantation: significance of peritransplant liver biopsy

Cited by 15 publications

References 10 publications

Nitric Oxide and Redox Regulation in the Liver: Part II. Redox Biology in Pathologic Hepatocytes and Implications for Intervention

Nitric Oxide and Redox Regulation in the Liver: Part II. Redox Biology in Pathologic Hepatocytes and Implications for Intervention

Oxidative Stress in Hepatic Ischemia-Reperfusion Injury: The Role of Antioxidants and Iron Chelating Compounds

Desferrioxamine attenuates minor lung injury following surgical acute liver failure

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