Open Access

Oxidative stress-induced 1, N6-ethenodeoxyadenosine adduct formation contributes to hepatocarcinogenesis

  • Authors:
    • Lei Zhou
    • Yuzhen Yang
    • Dean Tian
    • Ying Wang
  • View Affiliations

  • Published online on: January 4, 2013     https://doi.org/10.3892/or.2013.2227
  • Pages: 875-884
  • Copyright: © Zhou et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Numerous studies have found that oxidative stress-derived 1, N6-ethenodeoxyadenosine (ε-dA) can act as a driving force towards hepatocellular carcinoma (HCC) in cancer-prone liver diseases. The aim of the present study was to determine the oxidative stress status and the occurrence of ε-dA in HCC and adjacent non-tumor liver tissue, and to clarify whether the occurrence of ε-dA is related to liver inflammatory activity, fibrosis and mutant p53 expression. Oxidative stress-related parameters were examined in tumor and (or) non-tumor liver tissues of 32 patients with HCC. ε-dA, mutant p53 and proliferating cell nuclear antigen (PCNA) were immunohistochemically investigated in control, HCC and non-tumor liver tissues. The total antioxidant capacity and total superoxide dismutase activity of HCC tissues were lower compared to those of non-tumor tissues (P<0.05 vs. P<0.001). The prevalence of ε-dA in HCC was significantly higher compared to control (P<0.0001) and non-tumor liver tissues (P<0.001). A significant correlation between the positive rate of ε-dA and mutant p53 was observed (r=0.5162, P<0.01). The positive rate of PCNA in HCC was significantly higher compared to control (P<0.0001) and non-tumor liver tissues (P<0.0001). There was a possible link between the formation of ε-dA and chronic inflammation and fibrosis. Therefore, ε-dA lesions may gradually accumulate in chronic liver diseases, and partially contribute to mutant p53 overexpression and excessive cell proliferation, making it a potential mechanism in oxidative stress-mediated hepatocarcinogenesis.
View Figures
View References

Related Articles

Journal Cover

March 2013
Volume 29 Issue 3

Print ISSN: 1021-335X
Online ISSN:1791-2431

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Zhou L, Yang Y, Tian D and Wang Y: Oxidative stress-induced 1, N6-ethenodeoxyadenosine adduct formation contributes to hepatocarcinogenesis. Oncol Rep 29: 875-884, 2013
APA
Zhou, L., Yang, Y., Tian, D., & Wang, Y. (2013). Oxidative stress-induced 1, N6-ethenodeoxyadenosine adduct formation contributes to hepatocarcinogenesis. Oncology Reports, 29, 875-884. https://doi.org/10.3892/or.2013.2227
MLA
Zhou, L., Yang, Y., Tian, D., Wang, Y."Oxidative stress-induced 1, N6-ethenodeoxyadenosine adduct formation contributes to hepatocarcinogenesis". Oncology Reports 29.3 (2013): 875-884.
Chicago
Zhou, L., Yang, Y., Tian, D., Wang, Y."Oxidative stress-induced 1, N6-ethenodeoxyadenosine adduct formation contributes to hepatocarcinogenesis". Oncology Reports 29, no. 3 (2013): 875-884. https://doi.org/10.3892/or.2013.2227