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无机砷的主要代谢产物二甲基胂酸给药后,小鼠肺小静脉内皮细胞中异染色质优先增加。

Preferential increase of heterochromatin in venular endothelium of lung in mice after administration of dimethylarsinic acid, a major metabolite of inorganic arsenics.

作者信息

Nakano M, Yamanaka K, Hasegawa A, Sawamura R, Okada S

机构信息

Department of Chemicobiological Interaction, Chiba University, Japan.

出版信息

Carcinogenesis. 1992 Mar;13(3):391-3. doi: 10.1093/carcin/13.3.391.

Abstract

Dimethylarsinic acid (DMAA) administration induced the preferential increase of the heterochromatic area forming the inside of the interphase nucleus. A histopathological study of the lung and liver in mice after DMAA administration was carried out by transmission electron microscopy. Ultrastructural alterations in the endothelial nuclei of the alveolar wall were observed 12-48 h after administration. Heterochromatin tended to collect in a dense, compact mass lining the inner walls of the nucleus. A significant increase in heterochromatin induced by DMAA administration was observed by morphometric analysis. However, no substantial differences appeared in the sinusoidal endothelium of the liver. This study suggests that the much greater induction of morphological alterations, such as increased heterochromatin, in lung endothelial nuclei than in the liver might explain the high risk of lung cancer by arsenics, and that there may be a close relationship between heterochromatin alteration and DNA damages.

摘要

给予二甲基胂酸(DMAA)会导致形成间期核内部的异染色质区域优先增加。通过透射电子显微镜对给予DMAA后的小鼠肺和肝脏进行了组织病理学研究。给药后12 - 48小时观察到肺泡壁内皮细胞核的超微结构改变。异染色质倾向于聚集在细胞核内壁的致密、紧实团块中。通过形态计量分析观察到给予DMAA后异染色质显著增加。然而,肝脏的窦状内皮没有出现实质性差异。本研究表明,与肝脏相比,肺内皮细胞核中异染色质增加等形态学改变的诱导程度要大得多,这可能解释了砷导致肺癌的高风险,并且异染色质改变与DNA损伤之间可能存在密切关系。

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