Oxidative Stress and Liver Ischemia–Reperfusion Injury

Garcı́a-Ruiz, Carmen; Morales, Albert; Fernández‐Checa, José C.

doi:10.1007/978-3-319-15539-5_7

Cited by 6 publications

(6 citation statements)

References 100 publications

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“…Alcohol, chemicals, and infections can cause liver damage [9,10]. Studies have shown that diseases, such as cirrhosis, liver cancer, and hepatitis, are thought to be induced by oxidative stress [11][12][13]. It can not only 2 of 11 cause liver cell injury and death by changing intracellular macromolecules (including DNA, proteins, and lipids), but also regulate the death of liver cells by altering signal transduction pathway [14,15].…”

Section: Introductionmentioning

confidence: 99%

Floridoside Exhibits Antioxidant Properties by Activating HO-1 Expression via p38/ERK MAPK Pathway

Niu

Zhou

et al. 2020

Marine Drugs

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Floridoside is a low-molecular-weight organic compound, which can be accumulated by red algae under stressful conditions to protect cells via its excellent antioxidant properties. In the present study, we investigated the antioxidant mechanism of floridoside toward human hepatocyte L-02 cells. We found that floridoside had no toxicity to L-02 cells, and no reactive oxidative species were induced by it either. However, the expression of hemoxygenase-1 (HO-1) protein was up-regulated upon exposure to floridoside, and two antioxidant enzymes, superoxide dismutase (SOD) and GSH-Px, were activated by floridoside. Moreover, we investigated the pathway involved in the production of these antioxidants, p38/extracellular signal-regulated kinase (ERK) MAPK-nuclear factor-erythroid-2-related factor 2 (Nrf2) pathway. ERK1/2 and p38 phosphorylation, nuclear translocation of Nrf2, and activation of ARE luciferase activity were observed upon exposure to floridoside. siRNA interference and inhibitor treatment suppressed the HO-1 expression and the phosphorylation of ERK1/2 and p38, respectively. These results indicated that floridoside exerted its antioxidant activity by activating HO-1 expression via p38/ERK MAPK-Nrf2 pathway in human hepatocyte L-02 cells.

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Section: Introductionmentioning

confidence: 99%

Floridoside Exhibits Antioxidant Properties by Activating HO-1 Expression via p38/ERK MAPK Pathway

Niu

Zhou

et al. 2020

Marine Drugs

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“…The liver is an organ that can tolerate ischemia to a much higher degree than other organs, such as the heart. Typically, damage from ischemia is evident in the liver after only 30 minutes [1], though, most of this damage occurs in the reperfusion phase. This is evident in the ischemia-only groups in this experiment, where statistically there is no difference from the controls.…”

Section: Discussionmentioning

confidence: 99%

“…One of the reasons for this shortage is ischemia and reperfusion injury (IRI) which has a significant negative impact on the organ functionality. IRI occurs both during hepatic surgery with clamping of the vascular pedicle of the porta hepatis (Pringle maneuver) and in LT [1]. Hepatic IRI has a profound clinical impact on graft function after LT with organs from marginal or extended criteria donors because its deleterious effects are augmented in these grafts.…”

Section: Introductionmentioning

confidence: 99%

“…Paradoxically, the return of blood flow after a period of ischemia (reperfusion) results in further hepatocyte injury due to induced oxidative stress. This occurs through a complex cascade of events that includes mitochondrial dysfunction and systemic release of inflammatory mediators, reactive oxygen species (ROS), and proteases [1,4]. These processes lead to failure in the ATP production mechanisms, causing cell death [5].…”

Section: Introductionmentioning

confidence: 99%

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Optical imaging for the assessment of hepatocyte metabolic state in ischemia and reperfusion injuries

Cour¹,

Mehrvar²,

Kim³

et al. 2017

Biomed. Opt. Express

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Deterioration in mitochondrial function leads to hepatic ischemia and reperfusion injury (IRI) in liver surgery and transplantation. 3D optical cryoimaging was used to measure the levels of mitochondrial coenzymes NADH and FAD, and their redox ratio (NADH/FAD) gave a quantitative marker for hepatocyte oxidative stress during IRI. Using a rat model, five groups were compared: control, ischemia for 60 or 90 minutes (Isc60, Isc90), ischemia for 60 or 90 minutes followed by reperfusion of 24 hours (IRI60, IRI90). Ischemia alone did not cause a significant increase in the redox ratio; however, the redox ratio in both IRI60 and IRI90 groups was significantly decreased by 29% and 71%, respectively. A significant correlation was observed between the redox ratio and other markers of injury such as serum aminotransferase levels and the tissue ATP level. The mitochondrial redox state can be successfully measured using optical cryoimaging as a quantitative marker of hepatic IR injury.

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“…Consequently, hypoxic conditions caused by ischemia let the cells suffer from ATP depletion [ 7 , 8 ]. Eventually, the lack of O 2 disrupts proper hepatic metabolic function and can trigger the initiation of cell death processes [ [9] , [10] , [11] ]. Additionally, restoration of blood flow (i.e.…”

Section: Introductionmentioning

confidence: 99%

Computational Modeling of Oxidative Stress in Fatty Livers Elucidates the Underlying Mechanism of the Increased Susceptibility to Ischemia/Reperfusion Injury

Schleicher

Dahmen

2018

Computational and Structural Biotechnology Journal

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QuestionDonor liver organs with moderate to high fat content (i.e. steatosis) suffer from an enhanced susceptibility to ischemia/reperfusion injury (IRI) during liver transplantation. Responsible for the cellular injury is an increased level of oxidative stress, however the underlying mechanistic network is still not fully understood.MethodWe developed a phenomenological mathematical model of key processes of hepatic lipid metabolism linked to pathways of oxidative stress. The model allows the simulation of hypoxia (i.e. ischemia-like conditions) and reoxygenation (i.e. reperfusion-like conditions) for various degrees of steatosis and predicts the level of hepatic lipid peroxidation (LPO) as a marker of cell damage caused by oxidative stress.Results & ConclusionsOur modeling results show that the underlying feedback loop between the formation of reactive oxygen species (ROS) and LPO leads to bistable systems behavior. Here, the first stable state corresponds to a low basal level of ROS production. The system is directed to this state for healthy, non-steatotic livers. The second stable state corresponds to a high level of oxidative stress with an enhanced formation of ROS and LPO. This state is reached, if steatotic livers with a high fat content undergo a hypoxic phase. Theoretically, our proposed mechanistic network would support the prediction of the maximal tolerable ischemia time for steatotic livers: Exceeding this limit during the transplantation process would lead to severe IRI and a considerable increased risk for liver failure.

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Oxidative Stress and Liver Ischemia–Reperfusion Injury

Cited by 6 publications

References 100 publications

Floridoside Exhibits Antioxidant Properties by Activating HO-1 Expression via p38/ERK MAPK Pathway

Floridoside Exhibits Antioxidant Properties by Activating HO-1 Expression via p38/ERK MAPK Pathway

Optical imaging for the assessment of hepatocyte metabolic state in ischemia and reperfusion injuries

Computational Modeling of Oxidative Stress in Fatty Livers Elucidates the Underlying Mechanism of the Increased Susceptibility to Ischemia/Reperfusion Injury

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