Yamaguchi T, Terakado M, Horio F, Aoki K, Tanaka M, Nakajima H
Department of Biochemical Genetics, Tokyo Medical and Dental University, Japan.
Biochem Biophys Res Commun. 1996 Jun 5;223(1):129-35. doi: 10.1006/bbrc.1996.0857.
The anti-oxidative effect of bilirubin was investigated in an ischemia-reperfusion model of rat liver. The rat portal vessel and liver artery were ligated with a vascular clip, and after reperfusion the urine was collected at intervals. The amount of biopyrrins, the oxidative metabolites of bilirubin, in rat urine reached a maximum 4 hours after reperfusion. Biotripyrrin-a and -b which are biopyrrins isolated from human urine were included in urinary bilirubin oxidative metabolites of rats after reperfusion. The hepatic mRNA level of heme oxygenase-1 (HO-1), the rate limiting enzyme of bilirubin biosynthesis, reached a maximum after 4 hours. Furthermore, the hepatic activity of HO began to rise 4 hours after treatment and remained high until 24 hours posttreatment. These findings suggest that bilirubin acts as a physiological antioxidant in vivo in ischemia-reperfusion and that bilirubin biosynthesis is evoked by oxidative stress.
在大鼠肝脏缺血再灌注模型中研究了胆红素的抗氧化作用。用血管夹结扎大鼠门静脉和肝动脉，再灌注后每隔一段时间收集尿液。大鼠尿液中胆红素的氧化代谢产物胆色素原的量在再灌注后4小时达到最大值。从人尿中分离出的胆色素原-a和-b包含在再灌注后大鼠尿胆红素氧化代谢产物中。胆红素生物合成的限速酶血红素加氧酶-1（HO-1）的肝脏mRNA水平在4小时后达到最大值。此外，HO的肝脏活性在处理后4小时开始升高，并一直保持高水平直到处理后24小时。这些发现表明，胆红素在体内缺血再灌注中起生理抗氧化剂的作用，并且氧化应激可诱发胆红素生物合成。
