Evaluation of Oxidative Stress in the Late Postoperative Stage of Liver Transplantation

Augusto, Viviane S.; Rodrigues, Alfredo José; Reis, Graziela Saraiva; Silveira, Ana Paula Cassiano; Silva, O. de Castro e; Mente, Ênio David; Jordão, Alceu Afonso; Évora, Paulo Roberto Barbosa

doi:10.1016/j.transproceed.2013.12.058

Cited by 11 publications

(10 citation statements)

References 12 publications

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“…Recent clinical researches show that also in humans during ischemia the amounts of ROS increase resulting in oxidative stress imbalance as evidenced by an increase in oxidative stress markers and antioxidant response [67], [68], [69] and this oxidative imbalance persist in late post-operative stage (1 year after liver transplant) [70]. Additionally, as noted above, steatotic livers have poor prognosis in liver transplant that is associated to evidence of mitochondrial dysfunction and enhanced production of ROS [71].…”

Section: Translation Into the Clinical Settingmentioning

confidence: 95%

ROS homeostasis, a key determinant in liver ischemic-preconditioning

Prieto

Monsalve

2017

Redox Biology

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Reactive Oxygen Species (ROS) are key mediators of ischemia-reperfusion injury but also required for the induction of the stress response that limits tissue injury and underlies the protection provided by ischemic-preconditioning protocols. Liver steatosis is an important risk factor for liver transplant failure. Liver steatosis is associated with mitochondrial dysfunction and excessive mitochondrial ROS production. Studies aiming at decreasing the sensibility of the steatotic liver to ischemia-reperfusion injury using pre-conditioning protocols, have shown that the steatotic liver has a reduced capacity to respond to these protocols. Recent studies indicate that these effects are related to a reduced capacity of the steatotic liver to respond to elevated ROS levels following reperfusion by inducing a compensatory response. This failure to respond to ROS is associated with reduced levels of antioxidants, mitochondrial damage, hepatocyte cell death, activation of the immune system and induction of pro-fibrotic mediators.

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Section: Translation Into the Clinical Settingmentioning

confidence: 95%

ROS homeostasis, a key determinant in liver ischemic-preconditioning

Prieto

Monsalve

2017

Redox Biology

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“…In NHBD, NAC was thought to be effective in reducing the injurious consequences of IRI on bile ducts, but these data have not been reproducible . Use of free radical scavengers and antioxidants such as S‐adenosyl‐methionine and Vitamin E has shown no clinical value in liver transplantation …”

Section: Therapeutics For Hepatic Irimentioning

confidence: 99%

“…139,140 Use of free radical scavengers and antioxidants such as S-adenosyl-methionine and Vitamin E has shown no clinical value in liver transplantation. 141 A complex network of cytokine expression underlies the response to hepatic IRI. Modulating the cytokine response would be a logical way to blunt the effects of hepatic IRI in liver transplantation.…”

Section: Ther Apeuti C S For Hepati C Irimentioning

confidence: 99%

Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms

Dar

Sullivan

Bynon

et al. 2019

Liver International

273

245

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Liver disease causing end organ failure is a growing cause of mortality. In most cases, the only therapy is liver transplantation. However, liver transplantation is a complex undertaking and its success is dependent on a number of factors. In particular, liver transplantation is subject to the risks of ischaemia‐reperfusion injury (IRI). Liver IRI has significant effects on the function of a liver after transplantation. The cellular and molecular mechanisms governing IRI in liver transplantation are numerous. They involve multiple cells types such as liver sinusoidal endothelial cells, hepatocytes, Kupffer cells, neutrophils and platelets acting via an interconnected network of molecular pathways such as activation of toll‐like receptor signalling, alterations in micro‐RNA expression, production of ROS, regulation of autophagy and activation of hypoxia‐inducible factors. Interestingly, the cellular and molecular events in liver IRI can be correlated with clinical risk factors for IRI in liver transplantation such as donor organ steatosis, ischaemic times, donor age, and donor and recipient coagulopathy. Thus, understanding the relationship of the clinical risk factors for liver IRI to the cellular and molecular mechanisms that govern it is critical to higher levels of success after liver transplantation. This in turn will help in the discovery of therapeutics for IRI in liver transplantation – a process that will lead to improved outcomes for patients suffering from end‐stage liver disease.

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“…During reperfusion of engrafted livers, a significant increase in oxidative stress is seen, consistently with ischemia/reperfusion injury. Intriguingly, although these levels decrease immediately within the first days postoperatively; results on long-term levels are conflicting: In one study [37], urinary isoprostanes measured 6 to 12 months after transplantation were still significantly increased compared to normal values, while another report [39] interestingly showed not only lower MDA levels > 12 months after transplantation compared to those of healthy volunteers but also a concurrent decrease in GSH. Although the underlying cause remains unclear, two hypotheses are postulated, including interfering effects of gradual corticosteroid withdrawal and modification of other immunosuppressants or influence by recurrence of underlying liver disease.…”

Section: Oxidative Stress In Liver Transplantationmentioning

confidence: 99%

Associations of Oxidative Stress and Postoperative Outcome in Liver Surgery with an Outlook to Future Potential Therapeutic Options

Senoner

Schindler

Stättner

et al. 2019

Oxidative Medicine and Cellular Longevity

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Several types of surgical procedures have shown to elicit an inflammatory stress response, leading to substantial cytokine production and formation of oxygen-based or nitrogen-based free radicals. Chronic liver diseases including cancers are almost always characterized by increased oxidative stress, in which hepatic surgery is likely to potentiate at least in the short term and hereby furthermore impair the hepatic redox state. During liver resection, intermittent inflow occlusion is commonly applied to prevent excessive blood loss but resulting ischemia and reperfusion of the liver have been linked to increased oxidative stress, leading to impairment of cell functions and subsequent cell death. In the field of liver transplantation, ischemia/reperfusion injury has extensively been investigated in the last decades and has recently been in the scientific focus again due to increased use of marginal donor organs and new machine perfusion concepts. Therefore, given the intriguing role of oxidative stress in the pathogenesis of numerous diseases and in the perioperative setting, the interest for a therapeutic antioxidative agent has been present for several years. This review is aimed at giving an introduction to oxidative stress in surgical procedures in general and then examines the role of oxidative stress in liver surgery in particular, discussing both transplantation and resection. Results from studies in the animal and human settings are included. Finally, potential therapeutic agents that might be beneficial in reducing the burden of oxidative stress in hepatic diseases and during surgery are presented. While there is compelling evidence from animal models and a limited number of clinical studies showing that oxidative stress plays a major role in both liver resection and transplantation and several recent studies have suggested a potential for antioxidative treatment in chronic liver disease (e.g., steatosis), the search for effective antioxidants in the field of liver surgery is still ongoing.

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Evaluation of Oxidative Stress in the Late Postoperative Stage of Liver Transplantation

Cited by 11 publications

References 12 publications

ROS homeostasis, a key determinant in liver ischemic-preconditioning

ROS homeostasis, a key determinant in liver ischemic-preconditioning

Ischaemia reperfusion injury in liver transplantation: Cellular and molecular mechanisms

Associations of Oxidative Stress and Postoperative Outcome in Liver Surgery with an Outlook to Future Potential Therapeutic Options

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