Aflatoxin B1 damages peripheral blood lymphocytes in patients with primary hepatocellular carcinoma by inducing peroxidation

Objective: The aim of this study was to examine the effect of aflatoxin B1 (AFB1) on lymphocytes in patients with primary hepatocellular carcinoma (HCC) and the underlying mechanism. Methods: Peripheral blood from 20 HCC patients (liver cancer group) and 10 healthy individuals (control group) were collected for isolating peripheral blood lymphocytes. The peripheral blood lymphocytes of each patient were cultured in vitro and divided into four subgroups; blank control subgroup and subgroups treated with AFB1 doses of 0.2 mu g/mL (low toxicity), 2 mu g/mL (mild toxicity), and 20 mu g/mL (high toxicity). After incubation for 24 h, the level of the DNA damage marker, 8-hydroxyguanine (8-oxoG), was detected in the cells using flow cytometry and the activity of oxidative damage markers, hydroxy radical (OH-) and oxygen free radical, were detected using Fenton method and Xanthine oxidase method, respectively. Results: The content of 8-oxoG in liver cancer group was significantly higher than that in the control group (P < 0.05). It increased in an AFB1-dose-dependent manner in both groups. The same trend was also found with respect to the OH-content. However, the total superoxide dismutase (T-SOD) activity decreased with increasing dose of AFB1. Partial correlation analysis showed that the content of 8-oxoG was negatively correlated with the T-SOD activity (r = 0.5539, P = 0.001), but positively correlated with the content of OH-(r = 0.3812, P = 0.038). Conclusion: AFB1 causes more oxidative damage in lymphocytes of patients with HCC, by inducing peroxidation, than in lymphocytes of healthy individuals.