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In fluence of proliferaling stimuli by cell growth factor on carcinogcn-induced chromosumo aberrations and sister chromatid exchanges.

细胞生长因子增殖刺激对致癌诱导的染色体畸变和姐妹染色单体交换的影响。

基本信息

批准号：
06670229
负责人：
UEDA Norifumi
金额：
$ 1.34万
依托单位：
Ehime University School of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1995
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06670229/
关键词：
Mutagen Carcinogen Sister chromatid exchange Chromosome aberrations Cell growth factor DNA repair 標的細胞

项目摘要

Acute chromosome-damaging and chromatid-rearranging capacities of various mutagens and carcinogenes such as 7,12-dimethy 1 benz (a) anthracene (DMBA), and N-nitroso-N-methylurea (NMU) were studied using rat bone marrow cells, liver cells and fibroblasts in vivo and in vitro. The frequency of chromosome aberrations (CA) and sister chromatid exchange (SCE) after administration of above-mentioned carcinogens was tested under various stimuli. Athough the incidence of DMBA- and NMU-induced CA in the normal rats was 28% and 33%, it was 17% and 24% in the polycythemic rats. However, the incidence of CA in anemic rats was 45% and 56% and in polycythmic rats administrated with 6 Units of erythropietin at the time of DMBA injection was 41% and 47%. In the other words, the induction of CA by DMBA was enhanced by anemia and suppressed by polycythemia. The low incidence of CA in polycythmic rats was reversed by stimulation of erythropoietin injected at the time of DMBA and NMU treatment. CA were distributed nonrandomly in chromo somes 1 and 2. One region, the 40% region from the centromere (1q31), of the long arm of chromosome 1, and three regions, 30,55 and 80% from the centromere (2q21,2q25,2q41), of chromosome 2 were extremely susceptible to DMBA and NMU in the hematopoietic state. The frequency of SCE was increased under the condition of anemia and that of SCE was decresed under the condition of polycythemia. In liver cell obtained hepatectomized rats, the frequency of SCE induced by DMBA was enhanced with addition of the LGF in vivo (from 13.5% to 28.3%). In fibroblasts, the frequency of SCE induced by NMU was enhanced inthe ratio of 1.5 times with addition of the FGF in cultured medium in vitro.

使用大鼠骨髓细胞、肝细胞和成纤维细胞在体内和体外研究了各种诱变剂和致癌物如 7,12-二甲基 1 苯并 (a) 蒽 (DMBA) 和 N-亚硝基-N-甲基脲 (NMU) 的急性染色体损伤和染色单体重排能力。测试了在各种刺激下给予上述致癌物质后染色体畸变（CA）和姐妹染色单体交换（SCE）的频率。正常大鼠中DMBA和NMU诱导的CA发生率分别为28%和33%，而红细胞增多症大鼠中CA发生率分别为17%和24%。然而，贫血大鼠中CA的发生率为45％和56％，而在注射DMBA时给予6单位促红细胞生成素的红细胞增多症大鼠中CA的发生率为41％和47％。换句话说，DMBA对CA的诱导因贫血而增强，因红细胞增多症而受到抑制。通过在 DMBA 和 NMU 治疗时注射促红细胞生成素刺激，可以逆转多红细胞大鼠中 CA 的低发生率。 CA非随机分布在1号和2号染色体上。1号染色体长臂的一个区域，即距着丝粒（1q31）40%的区域，和2号染色体的三个区域，距着丝粒（2q21,2q25,2q41）的30,55和80%，在造血状态下对DMBA和NMU极其敏感。贫血时SCE频率升高，红细胞增多时SCE频率降低。在肝切除大鼠的肝细胞中，体内添加LGF后，DMBA诱导的SCE频率增加（从13.5％增加到28.3％）。在成纤维细胞中，体外培养液中添加FGF后，NMU诱导的SCE频率提高了1.5倍。