Preservation injury of the liver: mechanisms and novel therapeutic strategies

Bilzer, Manfred; Gerbes, Alexander L.

doi:10.1016/s0168-8278(00)80404-3

Cited by 168 publications

(123 citation statements)

References 94 publications

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“…Production of reactive oxygen species (ROS) and LPO occurs in clinical settings such as hepatic surgery, hemorrhagic shock, and parasitic infections (Bilzer and Gerbes 2000;Jaeschke 2000). Normal cellular metabolism involves the production of ROS (McCord 1993).…”

Section: Introductionmentioning

confidence: 99%

Biochemical assessment of oxidative status versus liver enzymes in patients with chronic fascioliasis

2014

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The aim of this study was to examine the oxidative status in Egyptian patients suffering chronic fascioliasis. The relationship between serum malondialdehyde (MDA) levels, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities was investigated in relation to the level of liver enzymes; ALT and AST compared to healthy controls. Twenty patients versus ten controls were included in the study. Among cases the MDA, CAT, AST and ALT were higher than controls, while SOD and GPX higher values were present among controls. There was a highly significant difference between cases and controls as regard MDA, CAT, SOD, GPX, and AST, and a significant difference regarding ALT. The findings of increased serum lipid peroxidation and decreased antioxidant enzymes in erythrocytes of chronic fascioliasis patients indicated the presence of persistent inflammation and oxidative stress which confirms the underlying pathogenesis and reflected the stage of infection providing a baseline data for comparison between normal and infected patients guided by the level of liver enzymes in relation to oxidative status.

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Section: Introductionmentioning

confidence: 99%

Biochemical assessment of oxidative status versus liver enzymes in patients with chronic fascioliasis

2014

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“…Low levels of ROS are vital for many cell signaling events and essential for proper cell functioning (Harabin et al 1990;Gregorevic et al 2001;Fattman et al 2003), but excessive in vivo generation of ROS can adversely affect cell functioning (Gregorevic et al 2001). The consequence of ischemic-reperfusion (I/R) during liver transplantation, hepatic resectional surgery and hemorrhagic shock appears to be an acute inflammatory response followed by dramatic cellular damage and organ dysfunction (Bilzer et al 2000). ROS, likely to afflict direct tissue damage, are destructive products generated during I/R (Bilzer et al 2000;Khandoga et al 2003).…”

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confidence: 99%

“…The consequence of ischemic-reperfusion (I/R) during liver transplantation, hepatic resectional surgery and hemorrhagic shock appears to be an acute inflammatory response followed by dramatic cellular damage and organ dysfunction (Bilzer et al 2000). ROS, likely to afflict direct tissue damage, are destructive products generated during I/R (Bilzer et al 2000;Khandoga et al 2003). Superoxide (O 2 -) produced from a oneelectron reduction of oxygen can be modified to H 2 O 2 , undergoing either spontaneous or enzymecatalyzed dismutation.…”

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confidence: 99%

The Effects of Hyperbaric Oxygen Treatment on Oxidant and Antioxidants Levels during Liver Regeneration in Rats

Özden

Uzun

Bohloli

et al. 2004

Tohoku J. Exp. Med.

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The effects of hyperbaric oxygen (HBO) therapy on oxidant/antioxidant metabolism are controversial and its effects on hepatic regeneration are not known. In this study, we investigated a possible beneficial effect of HBO therapy on oxidant and antioxidants levels during liver regeneration. To conduct this study, seventy percent hepatectomy was performed on forty-eight SpraggueDawley rats and the rats were divided into two equal groups: HBO-treated group and untreated group (non-HBO group). We determined the levels of malondialdehyde (MDA), an oxidative stress marker, and the levels of antioxidant enzymes/reagents, including glutathione (GSH), superoxide dismutase (SOD) activitiy, copper (Cu) and zinc (Zn), in the remnant liver samples. We also measured mitotic index (MI) and proliferating cell nuclear antigen (PCNA) levels to assess the degree of liver regeneration. HBO treatment significantly decreased MDA levels, whereas it increased SOD activity, GSH and Zn levels. In contrast, Cu levels were lower in the HBO-treated livers than the levels in the untreated remnant livers. The effect of HBO treatment may be mediated by the suppression of certain enzymes that are responsible for lipid peroxidation. In addition, HBO treatment may induce the production of antioxidant enzymes/reagents by remnant liver tissues. The HBO-treated rats maintained their body weights but the untreated rats lost body weights. HBO treatment also increased MI and PCNA levels, indicating HBO treatment enhances liver regeneration. These

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“…[8][9][10] Hepatic reperfusion injury after cold preservation involves the release of oxygen radicals, and the loss of viability of endothelial cells and hepatocytes. 11,12 Recently, apoptosis has been identified as a mechanism of hepatic injury after ischemia and reperfusion 13,14 and proposed to be critical in liver graft after transplantation. Apoptosis involves the interplay of several proapoptotic factors such as caspases and antiapoptotic factors such as members of the Bcl family.…”

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confidence: 99%

Extended preservation of rat liver graft by induction of heme oxygenase-1

et al. 2002

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Livers can be preserved only for a short period without jeopardizing the transplantation outcome. Heat shock proteins (HSPs) protect against ischemia and reperfusion injury. We studied whether their induction and, in particular, the induction of heme oxygenase 1 (HO-1), improves transplantation survival after an extended time of cold storage. Rats were subjected to heat preconditioning (42°C for 20 minutes). Livers were harvested 24 hours later, preserved in cold University of Wisconsin solution for 44 hours, and transplanted in isogeneic rats (arterialized transplantation). HO-1 was specifically induced and inhibited by cobalt protoporphyrin and tin protoporphyrin, respectively. All animals receiving a graft without preconditioning and subjected to 44 hours of cold preservation died within 3 days, whereas 89% of rats who received a graft exposed to heat survived for 3 weeks (P ‫؍‬ .0004). Preconditioning reduced serum aspartate transaminase (AST) and lactate dehydrogenase activities after reperfusion, improved bile flow, and decreased the histologic lesions of reperfusion injury. These significant effects of heat preconditioning were prevented by administration of tin protoporphyrin and could be reproduced by administration of cobalt protoporphyrin. In grafts without preconditioning, only a small fraction (<5%) of hepatocytes were positive with the terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) assay, and even less expressed activated caspase 3. Preconditioning tended to reduce the number of positive cells and to stimulate the expression of antiapoptotic Bcl-X L . In conclusion, heat preconditioning and, specifically, overexpression of HO-1 improve posttransplantation survival and graft function after prolonged cold ischemia preservation. The mechanism underlying these beneficial effects does not appear to be prevention of apoptosis. (HEPATOLOGY 2002;35:1082-1092

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Preservation injury of the liver: mechanisms and novel therapeutic strategies

Cited by 168 publications

References 94 publications

Biochemical assessment of oxidative status versus liver enzymes in patients with chronic fascioliasis

Biochemical assessment of oxidative status versus liver enzymes in patients with chronic fascioliasis

The Effects of Hyperbaric Oxygen Treatment on Oxidant and Antioxidants Levels during Liver Regeneration in Rats

Extended preservation of rat liver graft by induction of heme oxygenase-1

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