Diallyl trisulfide as an inhibitor of benzo(a)pyrene-induced precancerous carcinogenesis in MCF-10A cells

详细信息	查看全文 | 推荐本文 |

• 作者：Yasmeen M. Nkrumah-Elie^a ; ^{yasmeen1.barnesnkrum@famu.edu} ; Jayne S. Reuben^b ; ^{jreuben@ghs.org} ; Alicia Hudson^a ; ^{atucker78@aol.com} ; Equar Taka^a ; ^{equar.taka@famu.edu} ; Ramesh Badisa^a ; ^{ramesh.badisa@famu.edu} ; Tiffany Ardley^a ; ^{tiffany.ardley@famu.edu} ; Bridg&rsquo ; ette Israel^a ; ^{bridgette.israel@famu.edu} ; Sakeenah Y. Sadrud-Din^c ; ^{ssadrud690@aol.com} ; Ebenezer Oriaku^a ; ^{ebenezer.oriaku@famu.edu} ; Selina F. Darling-Reed^a ; ^{selina.darling@famu.edu}
• 关键词：Benzo(a)pyrene ; Diallyl trisulfide ; Early carcinogenesis ; Breast cancer ; MCF-10A ; In vitro
• 刊名：Food and Chemical Toxicology
• 出版年：2012
• 期刊代码：20_02786915
• 类别：pha
• 出版时间：July, 2012
• 卷：50
• 期：7
• 页码：2524-2530
• 文件大小：637 K

摘要

Diallyl trisulfide (DATS) is a garlic organosulfide that is toxic to cancer cells, however, little is known about its effect in the initiation phase of carcinogenesis. We sought to determine whether DATS could inhibit the carcinogen, benzo(a)pyrene (BaP), from inducing precancerous activity, in vitro. MCF-10A cells were either pre-treated (PreTx) or concurrently treated (CoTx) with 1 渭M BaP, and 6 or 60 渭M DATS for up to 24 h. The DATS 6 and 60 渭M CoTx inhibited BaP-induced cell proliferation by an average of 71.1%and 120.8%, respectively, at 6 h. The 60 渭M DATS pretreatment decreased BaP-induced G2/M cell cycle transition by 127%, and reduced the increase in cells in the S-phase by 42%; whereas 60 渭M DATS CoTx induced a 177%increase in cells in G1. DATS effectively inhibited (P < 0.001) BaP-induced peroxide formation by at least 54%, which may have prevented the formation of BaP-induced DNA strand breaks. In this study, we reveal mechanisms involved in DATS inhibition of BaP-induced carcinogenesis, including inhibition of cell proliferation, regulation of cell cycle, attenuation of ROS formation, and inhibition of DNA damage. At the doses evaluated, DATS appears to be an effective attenuator of BaP-induced breast carcinogenesis, in vitro.