Ekmekci A, Sayl A, Dönmez H, Bal F
Department of Medical Biology and Genetics, Faculty of Medicine, Gazi University, Ankara, Turkey.
Mutat Res. 1995 Apr;328(1):49-53. doi: 10.1016/0027-5107(94)00196-c.
In this study, the individual and combined effects of prostaglandin E1 (PGE1) and Indomethacin on mitomycin C (MMC)-induced SCEs in human lymphocytes was investigated in vitro. All MMC-treated cultures showed a great increase of SCEs (approximately two-fold), indicating its ability to induce mutations. SCE data showed that MMC-induced SCEs were reduced significantly in the presence of PGE1 in pooled analysis of six experiments (60.55% reduction of SCEs at 10(-6) M, 34.13% reduction of SCEs at 10(-9) M). In contrast the presence of indomethacin in the medium during MMC treatment of cells failed to show a significant reduction of SCEs in pooled analysis (21.17%). However, individual analyses revealed only two of six donors with a significant SCE response. Thus, the findings suggest that PGE1 can modify the DNA damaging effect of carcinogens and thereby may prevent the initiation of the carcinogenic process.
在本研究中，体外研究了前列腺素E1（PGE1）和吲哚美辛单独及联合应用对丝裂霉素C（MMC）诱导的人淋巴细胞姐妹染色单体交换（SCE）的影响。所有经MMC处理的培养物均显示SCE显著增加（约两倍），表明其诱导突变的能力。SCE数据显示，在六项实验的汇总分析中，PGE1存在时MMC诱导的SCE显著降低（10^(-6) M时SCE降低60.55%，10^(-9) M时SCE降低34.13%）。相比之下，在细胞用MMC处理期间培养基中存在吲哚美辛，在汇总分析中未显示SCE显著降低（21.17%）。然而，个体分析显示六个供体中只有两个有显著的SCE反应。因此，研究结果表明PGE1可以改变致癌物的DNA损伤作用，从而可能预防致癌过程的启动。
