Vettenranta K, Raivio K O
Children's Hospital, University of Helsinki, Finland.
Pediatr Res. 1990 Mar;27(3):286-8. doi: 10.1203/00006450-199003000-00017.
Through oxygen free-radical production, xanthine oxidase (XOD, E.C.1.2.3.2) has been implicated in the pathogenesis of postischemic and hyperoxic tissue injuries among newborn. We measured the activity and evaluated the kinetic characteristics of XOD in human fetal liver, intestine, brain, and myocardium. Both the fetal liver and intestine contain a high XOD activity through gestation. The activity increases in the liver and decreases in the intestine with advancing gestation. The apparent Km for hypoxanthine is 4.8-5.5 microM in the intestine throughout gestation and in the liver at term but higher than 30 microM in the liver during the first half of pregnancy. The activity is undetectable both in the fetal brain and myocardium throughout gestation. Thus, XOD activity is present at least in the liver and intestine to account for the oxidation of hypoxanthine and xanthine. However, direct evidence for adenine nucleotide catabolism, followed by oxidation of the accumulated hypoxanthine during tissue reoxygenation in the human liver or intestine is not available.
通过产生氧自由基，黄嘌呤氧化酶（XOD，E.C.1.2.3.2）被认为与新生儿缺血后和高氧组织损伤的发病机制有关。我们测量了人胎儿肝脏、肠道、大脑和心肌中XOD的活性，并评估了其动力学特征。在整个妊娠期，胎儿肝脏和肠道均含有较高的XOD活性。随着妊娠进展，肝脏中的活性增加，而肠道中的活性降低。在整个妊娠期，肠道中次黄嘌呤的表观Km为4.8 - 5.5微摩尔，足月时肝脏中的表观Km为4.8 - 5.5微摩尔，但在妊娠前半期肝脏中的表观Km高于30微摩尔。在整个妊娠期，胎儿大脑和心肌中均未检测到该活性。因此，至少在肝脏和肠道中存在XOD活性，以解释次黄嘌呤和黄嘌呤的氧化。然而，在人类肝脏或肠道组织再氧合过程中，腺嘌呤核苷酸分解代谢以及随后积累的次黄嘌呤氧化的直接证据尚不可得。
