在具有代谢活性的人肝癌细胞系HepG2细胞中，持久性有机污染物（POPs）调节了苯并(a)芘诱导的微核形成。

Benzo(a)pyrene induced micronucleus formation was modulated by persistent organic pollutants (POPs) in metabolically competent human HepG2 cells.

作者信息

Wu Xin-jiang, Lu Wen-qing, Mersch-Sundermann Volker

机构信息

Institute of Indoor and Environmental Toxicology, Justus-Liebig-University of Giessen, University Hospital, Aulweg 123, D-35385 Giessen, Germany.

出版信息

Toxicol Lett. 2003 Sep 30;144(2):143-50. doi: 10.1016/s0378-4274(03)00198-x.

DOI:10.1016/s0378-4274(03)00198-x

PMID:12927358

Abstract

Due to their bioaccumulation and their biological properties persistent organic pollutants (POPs) attract wide attention. In the present study we investigated the genotoxicity, cogenotoxicity and antigenotoxicity of three selected POPs (DDT, aroclor-1254 and toxaphene) in the HepG2 micronucleus assay. Exposure of HepG2 cells to DDT (17.8-60 microM) and aroclor-1254 (23-184 microM) alone did not increase the micronucleus-frequencies. A slight genotoxic effect could be observed after exposure to toxaphene (20-40 microM). Additionally, the ability of POPs to enhance/decrease the benzo(a)pyrene (BaP)-induced micronucleus formation was investigated. Exposure of HepG2 cells to 50 microM BaP alone led to a more than 2-fold increase of micronuclei (MN) compared with the background frequency. But when the cells were pretreated with 23-181 microM aroclor-1254 or 10-20 microM toxaphene, BaP exposure caused significantly more MN than BaP alone. In contrast, DDT (17.8-60 microM) reduced BaP-induced micronucleus induction by 6-38%. Mechanisms of action are discussed.

摘要

由于其生物累积性及其生物学特性，持久性有机污染物（POPs）引起了广泛关注。在本研究中，我们在HepG2微核试验中研究了三种选定的持久性有机污染物（滴滴涕、多氯联苯混合物1254和毒杀芬）的遗传毒性、共遗传毒性和抗遗传毒性。单独将HepG2细胞暴露于滴滴涕（17.8 - 60微摩尔）和多氯联苯混合物1254（23 - 184微摩尔）不会增加微核频率。暴露于毒杀芬（20 - 40微摩尔）后可观察到轻微的遗传毒性作用。此外，还研究了持久性有机污染物增强/降低苯并(a)芘（BaP）诱导的微核形成的能力。与背景频率相比，单独将HepG2细胞暴露于50微摩尔BaP会导致微核（MN）增加超过2倍。但是当细胞用23 - 181微摩尔多氯联苯混合物1254或10 - 20微摩尔毒杀芬预处理时，BaP暴露导致的微核明显多于单独的BaP。相比之下，滴滴涕（17.8 - 60微摩尔）使BaP诱导的微核诱导减少了6 - 38%。本文讨论了作用机制。