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Modulatory effects of alpha- and gamma-tocopherols on 4-hydroxyestradiol induced oxidative stresses in MCF-10A breast epithelial cells

Authors
Lee, Eun-JuOh, Seung-YeonKim, Mi-KyungAhn, Sei HyunSon, Byung HoSung, Mi-Kyung
Issue Date
Sep-2009
Publisher
KOREAN NUTRITION SOC
Keywords
Breast cancer; DNA damage; 4-hydroxyestradiol; oxidative stress; tocopherol
Citation
NUTRITION RESEARCH AND PRACTICE, v.3, no.3, pp 185 - 191
Pages
7
Journal Title
NUTRITION RESEARCH AND PRACTICE
Volume
3
Number
3
Start Page
185
End Page
191
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13624
DOI
10.4162/nrp.2009.3.3.185
ISSN
1976-1457
2005-6168
Abstract
The elevated level of circulating estradiol increases the risk of breast tumor development. To gain Further insight into mechanisms involved in their actions, we investigated the molecular mechanisms of 4-hydroxyestradiol (4-OHE2) to initiate and/or promote abnormal cell growth, and of alpha- or gamma-tocopherol to inhibit this process. MCF-10A, human breast epithelial cells were incubated with 0.1 mu M 4-OHE2, either with or without 30 mu M tocopherols for 96 h. 4-OHE2 caused the accumulation of intracellular ROS. while cellular GSH/GSSG ratio and MnSOD protein levels were decreased, indicating that there was an oxidative burden. 4-OHE2 treatment also changed the levels of DNA repair proteins, BRCA1 and PARP-1. gamma-Tocopherol suppressed the 4-OHE2-induced increases in ROS, GSH/GSSG ratio, and MnSOD protein expression, while alpha-tocopherol up-regulated BRCA1 and PARP-1 protein expression. In conclusion, 4-OHE2 increases oxidative stress reducing the level of proteins related to DNA repair. Tocopherols suppressed oxidative stress by scavenging ROS or up-regulating DNA repair elements.
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