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首页> 外文期刊>The Journal of toxicological sciences >Aberrant activation of ubiquitin D at G2 phase and apoptosis by carcinogens that evoke cell proliferation after 28-day administration in rats.
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Aberrant activation of ubiquitin D at G2 phase and apoptosis by carcinogens that evoke cell proliferation after 28-day administration in rats.

机译：在大鼠中给药28天后，引起细胞增殖的致癌物在G2期引起了泛素D的异常活化和凋亡。

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We have previously reported that renal carcinogens examined in rats increase tubular cell proliferation and topoisomerase (Topo) IIα(+) cells. The present study was aimed at identifying early prediction markers of carcinogens after 28-day treatment in rats. Following gene expression screening by microarrays in renal tubules with renal carcinogens, immunohistochemical analysis and TUNEL-assay were performed with carcinogens targeting different organs. All renal carcinogens tested (ferric nitrilotriacetic acid, ochratoxin A (OTA), monuron, tris(2-chloroethyl) phosphate, and potassium bromate) increased tubular cells immunoreactive for minichromosome maintenance 3 (Mcm3) or ubiquitin D (Ubd) or those showing apoptosis, compared with untreated controls or non-carcinogenic renal toxicants. Carcinogens targeting the liver (thioacetamide (TAA), fenbendazole, piperonyl butoxide (PBO) and methyleugenol), thyroid (sulfadimethoxine), urinary bladder (phenylethyl isothiocyanate), forestomach (butylated hydroxyanisole), glandular stomach (catechol), and colon (chenodeoxycholic acid and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine) were examined for induction of Mcm3, Ubd, Topo IIα, Ki-67 and apoptosis using non-carcinogenic toxicants as negative controls. All carcinogens increased Mcm3(+), Ubd(+), Topo IIα(+), Ki-67(+) or TUNEL(+) cells, except for hepatocarcinogen PBO and both colon carcinogens, which did not increase cell proliferation. Ubd(+) cells co-expressing Topo IIα was increased without changing phospho-Histone H3-co-expressing cell population as examined with OTA and TAA. Results revealed cooperative responses of Topo IIα, Ubd and apoptosis by carcinogens inducing high proliferation activity, irrespective of target organs, examined here after a 28-day administration. Aberrant expression of Ubd at G(2) phase and increased apoptosis reflecting aberrant cell cycle regulation may be the common feature of these carcinogens.
机译：我们以前曾报道过，在大鼠中检查的肾致癌物会增加肾小管细胞增殖和拓扑异构酶（Topo）IIα（+）细胞。本研究旨在确定大鼠28天治疗后致癌物的早期预测标记。在通过微阵列技术在具有肾致癌物的肾小管中筛选基因表达后，针对靶向不同器官的致癌物进行了免疫组织化学分析和TUNEL测定。测试的所有肾致癌物（亚硝酸三乙酸铁，曲霉毒素A（OTA），莫罗隆，磷酸三（2-氯乙基）酯和溴酸钾）均增加了对微小染色体维持3（Mcm3）或泛素D（Ubd）或显示凋亡的细胞的免疫反应性，与未治疗的对照或非致癌性肾脏毒素相比。靶向肝的致癌物（硫代乙酰胺（TAA），芬苯达唑，胡椒基丁醚（PBO）和甲基丁香酚），甲状腺（磺胺二甲肟），膀胱膀胱（异硫氰酸苯乙基酯），前胃部（丁基化羟基茴香醚），腺胃（儿茶酚）和结肠（鹅去氧胆酸）使用非致癌性毒物作为阴性对照，检测了2-氨基-1-甲基-6-苯基咪唑并[4,5-b]吡啶和Mg3，Ubd，TopoIIα，Ki-67和细胞凋亡的情况。除肝癌原PBO和两种结肠癌原均增加细胞增殖外，所有致癌物均增加了Mcm3（+），Ubd（+），TopoIIα（+），Ki-67（+）或TUNEL（+）细胞。如通过OTA和TAA检测，共表达TopoIIα的Ubd（+）细胞增加而没有改变磷酸组蛋白H3共表达的细胞群体。结果显示，不论目标器官如何，致癌物诱导高增殖活性的TopoIIα，Ubd和细胞凋亡的协同反应，在给药28天后均在此处进行了研究。在G（2）阶段Ubd的异常表达和反映异常细胞周期调控的凋亡增加可能是这些致癌物的共同特征。

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