“…Excessive production of oxygen-derived free radicals can induce alterations in intestinal permeability and absorption in acute pancreatitis by effects of lysosomal proteases and eicosanoids released by stimulated leukocytes, macrophages, dendritic cells and antigen-presenting cells in the mucosa, and by lipid peroxidation of cell membranes [75] . Extrapancreatic endothelial barrier dysfunction characterized by increased microcirculatory endothelial permeability has been noted in the early stage of acute pancreatitis [23,70,73] . High concentrations of ROS generated in the early stage of pancreatitis are responsible for such an increase in endothelial permeability by promoting expression and activation of adhesion molecules on both leukocytes and endothelial cells, leading to alterations in cell signal transduction and redox-regulated transcription factors such as activator protein-1 and NF-B.…”