Miesel R, Zuber M
Deutsches Rheumaforschungszentrum, Berlin, Germany.
Inflammation. 1993 Oct;17(5):551-61. doi: 10.1007/BF00914193.
Sera of patients with various inflammatory and autoimmune rheumatic diseases were screened for the presence of xanthine oxidase (XOD) and compared to sera from healthy donors and patients with nonrheumatic diseases including AIDS, internal diseases, and different carcinomas. Up to 50-fold higher levels of XOD were detected in rheumatic sera (P < 0.001). In addition, serum sulfhydryls (SH) were determined as sensitive markers of oxidative stress. The SH status in rheumatic patients was diminished by 45-75% (P < 0.001) and inversely correlated to the concentration of serum XOD (R = 0.73), suggesting a causal interrelation. The depletion of serum sulfhydryls by the oxyradical-producing XOD/acetaldehyde system was mimicked successfully ex vivo in human serum from healthy donors. Cortisone treatment of patients suffering from systemic lupus erythematosus and rheumatoid arthritis impressively normalized elevated XOD concentrations in rheumatic sera to those of healthy controls. The participation of xanthine oxidase in the depletion of serum antioxidants in rheumatic patients is discussed in the light of substrate availability and Km values.
对患有各种炎症性和自身免疫性风湿性疾病患者的血清进行黄嘌呤氧化酶(XOD)检测,并与健康供体以及患有非风湿性疾病(包括艾滋病、内科疾病和不同癌症)患者的血清进行比较。在风湿性疾病患者的血清中检测到XOD水平高达健康对照组的50倍(P < 0.001)。此外,测定血清巯基(SH)作为氧化应激的敏感标志物。风湿性疾病患者的SH水平降低了45 - 75%(P < 0.001),且与血清XOD浓度呈负相关(R = 0.73),提示二者存在因果关系。在健康供体的人血清中,体外成功模拟了由产氧自由基的XOD/乙醛系统导致的血清巯基消耗。对系统性红斑狼疮和类风湿关节炎患者进行可的松治疗后,风湿性疾病患者血清中升高的XOD浓度显著恢复至健康对照组水平。根据底物可用性和Km值,讨论了黄嘌呤氧化酶在风湿性疾病患者血清抗氧化剂消耗中的作用。