[논문]Modulatory effects of <tex>$\\alpha$</tex>- and <tex>$\\gamma$</tex>-tocopherols on 4-hydroxyestradiol induced oxidative stresses in MCF-10A breast epithelial cells

Lee, Eun-Ju; Oh, Seung-Yeon; Kim, Mi-Kyung; Ahn, Sei-Hyun; Son, Byung-Ho; Sung, Mi-Kyung

doi:10.4162/nrp.2009.3.3.185

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

Nutrition research and practice, v.3 no.3, 2009년, pp.185 - 191

Lee, Eun-Ju (Department of Food and Nutrition, Sookmyung Women's University) , Oh, Seung-Yeon (Department of Food and Nutrition, Sookmyung Women's University) , Kim, Mi-Kyung (National Cancer Center Institute) , Ahn, Sei-Hyun (Department of Surgery, College of Medicine and Asan Medical Center) , Son, Byung-Ho (Department of Surgery, College of Medicine and Asan Medical Center) , Sung, Mi-Kyung (Department of Food and Nutrition, Sookmyung Women's University)

Abstract ▼ AI-Helper

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-$OHE_2$) 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-$OHE_2$, either with or without $30{\mu}M$ tocopherols for 96 h. 4-$OHE_2$ 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-$OHE_2$ treatment also changed the levels of DNA repair proteins, BRCA1 and PARP-1. $\gamma$-Tocopherol suppressed the 4-$OHE_2$-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-$OHE_2$ 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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