Differential effects of quercetin and silymarin on arsenite-induced cytotoxicity in two human breast adenocarcinoma cell lines
- 作者：Elio A. Soria ; Aldo R. Eynard ; Patricia L. Quiroga ; Guillermina A. Bongiovanni
- 关键词：Arsenite ; Breast cancer cells ; γ ; -glutamyltranspeptidase ; MCF-7 ; Oxidative stress ; Quercetin ; Sialic acid ; Silymarin ; ZR-75-1
- 刊名：Life Sciences
- 出版年：2007
- 期刊代码：62_00243205
- 类别：imm
- 出版时间：13 October 2007
- 卷：81
- 期：17-18
- 页码：1397-1402
- 文件大小：261 K
摘要
Arsenic has been proposed as a chemotherapeutic agent for leukemia and other solid tumors. However, its environmental exposure has been linked epidemiologically with an elevated carcinoma risk (i.e. skin, bladder and lung), with cellular oxidative stress being implicated in both induced-arsenic toxicity and carcinogenicity. Consequently, antioxidants may differentially interfere in these effects. The human mammary adenocarcinoma lines MCF-7 and ZR-75-1 were treated in vitro with 200 μM NaAsO2 (As), 5 μM silymarin (S) and/or 50 μM quercetin (Q). The following biomembrane parameters were assessed: sialic acid (SA) in gangliosides, γ-glutamyltranspeptidase activity (GGT), conjugated dienes and free radical activity, in order to evaluate the arsenite‑flavonoid interactions. The time-dependent arsenite toxicity was not prevented by flavonoids in ZR-75-1 cells, whereas quercetin protected MCF-7 cells for 8 h. With regard to GGT, only quercetin protected ZR-75-1 cells against stress. In MCF-7 cells, the arsenite-induced GGT activity was not counteracted by either quercetin or silymarin. S, Q, As and As + S treatments reduced the SA content only in the MCF-7 membrane, while As + Q treatment increased it in both lines. The membrane resistance to lipid oxidation in these cells enclosed the up-regulation of GGT activity and sialylglycolipid content. Taking these results together, quercetin interfered with arsenite toxicity, whereas silymarin was not able. Thus, the potential role of flavonoids as co-adjutants may differ widely in therapeutic protocols.