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[原代发育过程中经胎盘暴露于N-亚硝基乙基脲后BALB C小鼠体内的肿瘤]

[Tumors in BALB C mice after transplacental exposure to N-nitrosoethylurea in progenesis].

作者信息

Napalkov N P, Tomatis L, Lihachev A Ia, Kolodin V I

出版信息

Vopr Onkol. 1977;23(3):41-51.

PMID:898795
Abstract

In the experiments with transplacental exposure of mice to N-nitrosoethyl urea (NEU) an enhanced carcinogenesis was noted not only in the first but also in the second generation. This effect in mice of the second generation was manifested in earlier development, as compared with control animals, of different neoplasms as well as in somewhat increased frequency of their detection. Postnatal exposure to NEU would enhance carcinogenesis in mice of both experimental and control groups, whereas no enhancement of carcinogenesis was observed in animals exposed to NEU in progenesis, compared with control mice. Postnatal x-ray irradiation also failed to produce enhanced carcinogenesis, compared with control animals i.e. those exposed to NEU in progenesis. While in female mice of the same group, contrary to the control, ovarian tumors under the effect of irradiation did not arise. It is suggested that there is a pathogenic connection between the inheritance of carcinogenic effect by oocytes and the loss by the ovary its capacity to produce neoplasms in response to irradiation.

摘要

在将小鼠经胎盘暴露于N-亚硝基乙基脲(NEU)的实验中,不仅在第一代,而且在第二代都观察到致癌作用增强。与对照动物相比,第二代小鼠的这种效应表现为不同肿瘤的发育提前,以及其检出频率略有增加。产后暴露于NEU会增强实验组和对照组小鼠的致癌作用,而与对照小鼠相比,在胚胎期暴露于NEU的动物未观察到致癌作用增强。与对照动物(即胚胎期暴露于NEU的动物)相比,产后X射线照射也未产生增强的致癌作用。同一组的雌性小鼠与对照组相反,在辐射作用下未出现卵巢肿瘤。有人认为,卵母细胞致癌效应的遗传与卵巢丧失对辐射产生肿瘤的能力之间存在致病联系。

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