Schwarz K B, Kew M, Klein A, Abrams R A, Sitzmann J, Jones L, Sharma S, Britton R S, Di Bisceglie A M, Groopman J
Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.
Dig Dis Sci. 2001 Oct;46(10):2173-8. doi: 10.1023/a:1011958814371.
Since oxidative DNA damage plays a role in experimental carcinogen-induced cancers, the purpose of the present study was to determine if hepatic oxidative DNA damage was increased in patients with HCC compared to patients with benign hepatic tumors or hepatic metastases (non-HCC) or to patients with end-stage alcoholic liver disease undergoing liver transplantation. Oxidative DNA damage was assessed by 8-hydroxy-2'-deoxyguanosine (8-OH-dG). Results showed that peritumoral 8-OH-dG was markedly increased in HCC (N= 51) (180 +/- 74 vs 32 +/- 58-OH-dG/10(6)dG for tumor, P < 0.005) in contrast to patients with non-HCC (N = 17), in whom the peritumoral 8-OH-dG did not differ from that in tumor (39 +/- 7 vs. 31 +/- 108-OH-dG/10(6)dG). Oxidative DNA damage can be both mutagenic and carcinogenic; our data suggested it will be important in future studies to determine the chronology of this type of liver injury relative to hepatocarcinogenesis.
由于氧化性DNA损伤在实验性致癌物诱发的癌症中发挥作用,本研究的目的是确定与患有良性肝肿瘤或肝转移瘤(非肝癌)的患者相比,或与接受肝移植的终末期酒精性肝病患者相比,肝癌患者肝脏的氧化性DNA损伤是否增加。通过8-羟基-2'-脱氧鸟苷(8-OH-dG)评估氧化性DNA损伤。结果显示,与非肝癌患者(N = 17)相比,肝癌患者(N = 51)瘤周组织中的8-OH-dG显著增加(肿瘤组织中为180±74 vs 32±58 8-OH-dG/10(6)dG,P < 0.005),非肝癌患者瘤周组织中的8-OH-dG与肿瘤组织中的无差异(39±7 vs. 31±10 8-OH-dG/10(6)dG)。氧化性DNA损伤既具有致突变性又具有致癌性;我们的数据表明,在未来的研究中确定这种类型的肝损伤相对于肝癌发生的时间顺序将很重要。