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Oxidative Medicine and Cellular Longevity
Volume 2014 (2014), Article ID 730301, 15 pages
Review Article

Human AP Endonuclease 1: A Potential Marker for the Prediction of Environmental Carcinogenesis Risk

1Environmental Health Research Department, National Institute of Environmental Research, 42 Hwangyeong-ro, Seo-gu, Incheon 404-708, Republic of Korea
2School of Public Health, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul 151-742, Republic of Korea
3Department of Life Science, Institute of Environmental Medicine, Dongguk University, 30 Pildong-ro 1-gil, Jung-gu, Seoul 100-715, Republic of Korea
4Department of Safety Engineering, Dongguk University, Gyeongju, Gyeongbuk 780-714, Republic of Korea
5Department of Food and Nutrition, Sookmyung Women’s University, Cheong-ro 47-gil 100, Youngsan-gu, Seoul 140-742, Republic of Korea

Received 25 April 2014; Accepted 30 June 2014; Published 26 August 2014

Academic Editor: Jing Yi

Copyright © 2014 Jae Sung Park et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Human apurinic/apyrimidinic endonuclease 1 (APE1) functions mainly in DNA repair as an enzyme removing AP sites and in redox signaling as a coactivator of various transcription factors. Based on these multifunctions of APE1 within cells, numerous studies have reported that the alteration of APE1 could be a crucial factor in development of human diseases such as cancer and neurodegeneration. In fact, the study on the combination of an individual’s genetic make-up with environmental factors (gene-environment interaction) is of great importance to understand the development of diseases, especially lethal diseases including cancer. Recent reports have suggested that the human carcinogenic risk following exposure to environmental toxicants is affected by APE1 alterations in terms of gene-environment interactions. In this review, we initially outline the critical APE1 functions in the various intracellular mechanisms including DNA repair and redox regulation and its roles in human diseases. Several findings demonstrate that the change in expression and activity as well as genetic variability of APE1 caused by environmental chemical (e.g., heavy metals and cigarette smoke) and physical carcinogens (ultraviolet and ionizing radiation) is likely associated with various cancers. These enable us to ultimately suggest APE1 as a vital marker for the prediction of environmental carcinogenesis risk.