Oxidative stress in liver tissues in HCC patients after TACE / 中华普通外科杂志

ABSTRACT

Objective To investigate the levels of oxidative stress in liver tissues of hepatocelluar carcinoma(HCC)patients after transcatheter arterial chemotherapy(TAC).Methods Immunohistochemistry streptavidin biotinylated peroxidase(S-P)method was used to detect the cellular levels of 8-hydroxy-2'-deoxyguanosine(8-OHdG),p53 and p21~(waf1/cip1).Eighty-nine HCC patients were divided into TAC group(39 cases)and Non-TAC group(50 cases).15 Non-HCC liver tissues served as controls.Result 8-OHdG level was higher in Non-TAC group than that in TAC group in tumor tissues (F=9.516,P＜0.05),with that being the lowest in control group(F=9.516,P＜0.01);8-OHdG levels in cancer tissues were significantly higher than that in tumor surrounding tissues in both TAC group (t=7.101,P＜0.001)and Non-TAC group(t=8.020,P＜0.001),there was no significant difference of 8-OHdG levels between para-tumor tissues and controls.The levels of 8-OHdG between tumor and its surrounding tissues in TAC group(r=0.651,P＜0.001)and non-TAC group(r=0.493,P＜0.01)was in positive correlation.The difference of p53 levels in cancer tissues in TAC group and Non-TAC group were not statistically significant and p53 was not detected in para-tumor tissues.The difference of p21~(waf1/cip1) levels among TAC group,Non-TAC group and controls was statistically significant,the levels of p21~(waf1/cip1) in normal group was the highest(F=13.459,P＜0.001),followed by that in TAC and Non-TAC group in cancer tissues(TAC vs.Non-TAC group,P＜0.01);p21~(waf1/cip1) expression in normal controls was significantly higher than that in both TAC and Non-TAC group in para-tumor tissues(F=16.613,P＜0.001).The correlation of p21 ~(waf1/cip1) levels between tumor and its surrounding tissues was significant in non-TAC group(r=0.872,P＜0.001).Conclusions Oxidative stress levels in HCC tumor tissues were higher than in para-tumor tissues and non-HCC liver tissues.Cancer cells probably survive chemotherapy by fortifying oxidative stress repair mechanism.