title: Potential role of reactive oxygen species in pancreatitis-associated multiple organ dysfunction.
abstract: BACKGROUND
  Severe acute pancreatitis is still associated with substantial morbidity and mortality. Experimental and clinical studies have demonstrated that reactive oxygen species (ROS) represent early occurring inflammatory mediators contributing to cell dysfunction, both locally in the pancreas and remote organs.
  
  
  METHODS
  A systematic literature review was conducted to investigate the potential roles of intra- and intercellular, as well as interorgan signaling of ROS in the development of pancreatitis-associated multiple organ dysfunction syndrome (MODS). A text word search of the Medline, PubMed and Cochrane databases, and a manual search of the citations from these references, was performed.
  
  
  RESULTS
  ROS directly compromise cellular damage and regulate intercellular signals in pancreatitis-associated MODS. ROS are involved in leukocyte activation, production of cytokines, endothelial barrier dysfunction, and microcirculatory barrier dysfunction in acute pancreatitis. Beside effects on intercellular signaling, ROS also affect intracellular events and activate the transcription factor nuclear factor kappa B that regulates inflammatory cytokine expression.
  
  
  CONCLUSIONS
  ROS is a critical factor responsible for the development of pancreatitis-induced remote organ dysfunction via intercellular and interorgan signaling. The role of antioxidant treatment, included as a part of multimodal management, remains to be investigated.
authors: Department of Surgery, Lund University Hospital, Lund, Sweden.
authors: Changbin
authors: C
authors: Shi
authors: Roland
authors: R
authors: Andersson
authors: Xia
authors: X
authors: Zhao
authors: Xiangdong
authors: X
authors: Wang
mesh_terms: D006801:Humans; D016239:MEDLINE; D009102:Multiple Organ Failure / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D019283:Pancreatitis, Acute Necrotizing / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D039781:PubMed; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D017382:Reactive Oxygen Species