Polychlorinated biphenyl induced ROS signaling delays the entry of quiescent human breast epithelial cells into the proliferative cycle.
Polychlorinated biphenyl induced ROS signaling delays the entry of quiescent human breast epithelial cells into the proliferative cycle.
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DOI：
10.1016/j.freeradbiomed.2010.03.012
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发表时间：
2010-07-01
影响因子：
7.4
通讯作者：
Goswami, Prabhat C.
中科院分区：
文献类型：
--
作者：
Chaudhuri, Leena;Sarsour, Ehab H.;Kalen, Amanda L.;Aykin-Burns, Nukhet;Spitz, Douglas R.;Goswami, Prabhat C.
关键词：
多氯联苯（PCBs）是一种环境化学污染物，可通过自身氧化和氧化还原循环产生活性氧（ROS）。我们调查的假设，PCB诱导的ROS信号的扰动调节进入静止细胞的增殖周期。将静止的MCF-10A人乳腺上皮细胞与0-3微摩尔的2-（4-氯苯基）苯并-1，4-醌（4-Cl-BQ）、2，2′，4，4′，5，5′-六氯联苯（PCB 153）和Aroclor 1254孵育4天。以较低密度重新接种细胞，并分析细胞周期时相分布、ROS水平、MnSOD表达和细胞周期蛋白D1蛋白水平。4-Cl-BQ孵育的静止期细胞进入S期的延迟最大。这种延迟与MnSOD活性、蛋白质和mRNA水平的降低以及细胞ROS水平的增加有关。结果表明，4-Cl-BQ处理选择性地促进了4.2kb MnSOD转录物的降解，而1.5kb转录物的半衰期没有改变。在用4-Cl-BQ处理的细胞中，再铺板细胞中细胞周期蛋白D1蛋白水平的积累受到抑制。用聚乙二醇结合的超氧化物歧化酶和过氧化氢酶预处理静止细胞抑制4-Cl-BQ诱导的ROS水平增加，这与细胞周期蛋白D1积累的增加一致，并进入S期。这些结果表明，4-Cl-BQ诱导的ROS信号的扰动抑制静止细胞进入S期。
Polychlorinated biphenyls (PCBs) are environmental chemical contaminants that can produce reactive oxygen species (ROS) by autoxidation of dihydroxy-PCBs and redox-cycling. We investigate the hypothesis that PCB induced perturbations in ROS signaling regulate the entry of quiescent cells into the proliferative cycle. Quiescent MCF-10A human breast epithelial cells were incubated with 0–3 micromolar of 2-(4-chlorophenyl)benzo-1,4-quinone (4-Cl-BQ), 2, 2′, 4, 4′, 5, 5′-hexachlorobiphenyl (PCB 153), and Aroclor 1254 for 4 days. Cells were replated at a lower density and analyzed for cell cycle phase distributions, ROS levels, MnSOD expression, and cyclin D1 protein levels. Quiescent cells incubated with 4-Cl-BQ showed the maximal delay in entering S phase. This delay was associated with a decrease in MnSOD activity, protein and mRNA levels, and an increase in cellular ROS levels. Results from the mRNA turnover assay showed that the 4-Cl-BQ treatment selectively enhanced the degradation of the 4.2 kb MnSOD transcript, while the half-life of the 1.5 kb transcript did not change. Accumulation of cyclin D1 protein levels in replated cells was suppressed in cells treated with 4-Cl-BQ. Pretreatment of quiescent cells with polyethylene glycol-conjugated superoxide dismutase and catalase suppressed 4-Cl-BQ induced increase in ROS levels, which was consistent with an increase in cyclin D1 accumulation, and entry into S phase. These results showed 4-Cl-BQ induced perturbations in ROS signaling inhibit the entry of quiescent cells into S phase.
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影响因子：
4.8
作者：
Sarsour, EH;Agarwal, M;Goswami, PC
通讯作者：
Goswami, PC
DOI：
10.1080/15287399409531870
发表时间：
1994-06-01
期刊：
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH
影响因子：
--
作者：
JOHANSEN, HR;BECHER, G;SKAARE, JU
通讯作者：
SKAARE, JU
影响因子：
7.8
作者：
Busuttil, RA;Rubio, M;Vijg, J
通讯作者：
Vijg, J
影响因子：
64.5
作者：
Mayr C;Bartel DP
通讯作者：
Bartel DP
影响因子：
4.1
作者：
Amaro, AR;Oakley, GG;Robertson, LW
通讯作者：
Robertson, LW