In this paper,we summarize the main progresses made inour group in the field of the mechanism of pigment gallstoneformation.It was found that after treatment with freeradicals,biiirubin(BR)was changed into free radical itself,and a semiquinone free radical and a superoxide free radicalbound with metal were recognized,which was detected byESR(electron spin resonance).By the means of NMR(nuclear magnetic resonance)and IR(Infra-red spectra),itwas postulated that bilirubin polymerized through thereaction between the vinyl group and the hydroxyl groupunder the attack of free radicals.It was also found thatbilirubin free radical were liable to calcify in a kinetic study.Because of its chemical properties,bilirubin free radical wasshown to be cytotoxic to hepatocyte,which wasdemonstrated based on the following facts:induction ofphospholipid peroxidation(LPO),leakage of lactatedehydrogenase(LDH)and decrease of glutathione.As tothe mechanism of bilirubin-induced cytotoxicity,it waspostulated that the main target of bilirubin free radical wasthe cell membrane,including phospholipid and membranebound proteins,especially spectrin,a content ofcytoskeleton.Based on the results mentioned above,it wasdeduced that bilirubin free radical is the key factor thatinitiates and promotes the formation of pigment gallstone,which is consistent with other researches in recent years. In this paper, we summarize the main progresses made inour group in the field of the mechanism of pigment gallstoneformation. It was found that after treatment with freeradicals, biiirubin (BR) was changed into free radical itself, and a semiquinone free radical and a superoxide free radicalbound with metal were recognized, which was detected byESR (electron spin resonance) .By the means of NMR (nuclear magnetic resonance) and IR (Infra-red spectra), itwas postulated that bilirubin polymerized through thereaction between the vinyl group and the hydroxyl groupunder the attack of free radicals.It was found also thatbilirubin free radical were liable to calcify in a kinetic study.Because of its chemical properties, birirubin free radical wasshown to be cytotoxic to hepatocyte, which wasdemonstrated based on the following facts: induction ofphospholipid peroxidation (LPO), leakage of lactate dehydrogenase (LDH) and decrease of glutathione. As tothe mechanism of bilirubin-induced cytotoxicity, it was postulated th at the main target of birirubin free radical wasthe cell membrane, including phospholipid and membranebound proteins, especially spectrin, a content of cytoskeleton. it wasdeduced that bilirubin free radical is the key factor that that associates and promotes the formation of pigment gallstone , which is consistent with other researches in recent years.