Clinical application of a biodefense reaction against oxidative stress using mAb.

点击翻译按钮获取中文摘要

We examined the possibility that bilirubin oxidation is provoked in vivo by using scurvy-prone ODS-odlod rats treated with endotoxin (lipopolysaccharide). Recently, bilirubin oxidative metabolites were isolated from human urine and named biotripyrrin-a and biotripyrrin-b. In ODS-odlod rats fed an ascorbicacid-free diet, the concentration of bilirubin metabolites in urine was increased 7.0-fold at 3 h after injection of lipopolysaccharide and 4.4-fold at 10 h compared to the control rats injected with saline. The dietary supplement of ascorbic acid, the physiological antioxidant, suppressed the increase in bilirubin metabolites in urine after lipopolysaccharide injection : concentrations of biotripyrrin-a and biotripyrrin-b in urine collected 6.5- 1O h after the injection were lower in rats fed an ascorbic-acid-supplemented diet than in rats fed an ascorbic-acid-free diet. Moreover, feeding of ascorbic acid suppressed the hepatic mRNA level of heme oxygenase-1, the rate-limiting enzyme of bilirubin biosynthesis, in rats injected with lipopolysaccharide. These findings indicate that bilirubin oxidation is markedly stimulated in lipo-polysaccharide-treated rats and suggest that bilirubin and ascorbic acid have physio1ogically protective effects against oxidative stress.