Abstract
Bile pigment including bilirubin and biliverdin is the main bile pigment causing jaundice and considered to be toxic. Recently, the protective effects of these bile pigments have been discovered and their physiologic role is studied intensively regarding its antioxidant property. These bile pigments are actively generated as end products of heme catabolism by heme oxygenases. Biliverdin is very rapidly converted to bilirubin by the enzyme biliverdin reductase. Bilirubin, when oxidized, reverts to become biliverdin once again. This cycle may further explain the potent antioxidant activity of these bile pigments. Accumulating evidence indicates that biliverdin/bilirubin can mediate the protective effects via its antioxidant property in many disease conditions in critical care medicine, such as neonatal jaundice, brain ischemia, ischemia/reperfusion injury, sepsis, acute lung injury and malignancy. This review attempts to summarize these protective roles as well as the molecular mechanisms and its clinical feasibility.
