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2,5-己二酮暴露会改变成年大鼠睾丸中微管运动蛋白的分布。

2,5-Hexanedione exposure alters microtubule motor distribution in adult rat testis.

作者信息

Hall E S, Hall S J, Boekelheide K

机构信息

Department of Pathology and Laboratory Medicine, Brown University, Providence, Rhode Island 02912, USA.

出版信息

Fundam Appl Toxicol. 1995 Feb;24(2):173-82. doi: 10.1006/faat.1995.1021.

Abstract

2,5-Hexanedione (2,5-HD) exposure in rats causes a progressive Sertoli cell injury culminating in testicular atrophy. Morphological injury is preceded by alterations in the assembly characteristics of tubulin isolated from exposed rat testes. This is followed by decreased seminiferous tubule fluid (STF) secretion by Sertoli cells and an increase in the number and size of Sertoli cell vacuoles. The possible involvement of microtubules and microtubule motor-dependent transport processes in STF secretion by Sertoli cells prompted us to examine the immunodistribution of the microtubule motors cytoplasmic dynein and kinesin during and after 2,5-HD exposure in rats. Three weeks following the commencement of exposure (1% 2,5-HD in the drinking water), the intensity of apical Sertoli cell cytoplasmic dynein immunofluorescence declined. This staining deficit became statistically significant by 4 weeks of exposure. Accompanying this change, there was progressive disruption of the immunodistribution of cisternal Golgi elements and associated kinesin immunoreactivity. The decrease in apical Sertoli cell cytoplasmic dynein immunofluorescence and disruption of Golgi and kinesin immunoreactivity suggest that 2,5-HD-induced alterations in Sertoli cell-mediated transport and secretory events could involve deficits in microtubule-dependent motor function.

摘要

大鼠暴露于2,5 -己二酮(2,5 - HD)会导致支持细胞逐渐受损,最终导致睾丸萎缩。在形态学损伤之前,从暴露大鼠睾丸中分离出的微管蛋白组装特性会发生改变。随后,支持细胞分泌的生精小管液(STF)减少,支持细胞液泡的数量和大小增加。微管和微管运动依赖的运输过程可能参与支持细胞分泌STF,这促使我们研究大鼠在暴露于2,5 - HD期间及之后微管运动蛋白胞质动力蛋白和驱动蛋白的免疫分布。暴露开始后三周(饮用水中含1% 2,5 - HD),支持细胞顶端胞质动力蛋白免疫荧光强度下降。到暴露4周时,这种染色缺陷具有统计学意义。伴随这一变化,高尔基体池元件的免疫分布及相关驱动蛋白免疫反应性逐渐受到破坏。支持细胞顶端胞质动力蛋白免疫荧光的减少以及高尔基体和驱动蛋白免疫反应性的破坏表明,2,5 - HD诱导的支持细胞介导的运输和分泌事件改变可能涉及微管依赖的运动功能缺陷。

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