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饮食钴诱导的睾丸变性和坏死

Testicular degeneration and necrosis induced by dietary cobalt.

作者信息

Corrier D E, Mollenhauer H H, Clark D E, Hare M F, Elissalde M H

出版信息

Vet Pathol. 1985 Nov;22(6):610-6. doi: 10.1177/030098588502200616.

Abstract

Dietary cobalt (265 ppm Co) induced polycythemia and consistent degenerative and necrotic lesions in the seminiferous tubules of rats. Cyanosis and engorgement of testicular vasculature on day 35 and thereafter was followed on day 70 by degenerative and necrotic changes in the germinal epithelium and Sertoli cells. Spermatogonia, primary spermatocytes and round spermatids were markedly affected, while elongated spermatids, spermatozoa, and sertoli cells were more resistant. Damaged tubules, often present side by side with normal tubules, contained multinucleated giant cells composed of degenerated and necrotic spermatocytes and/or spermatids, sloughed germinal and Sertoli cells, and calcified necrotic debris. Necrotic tubules were frequently collapsed and devoid of epithelium except for occasional spermatogonia and surviving Sertoli cells. Lesions were not observed in the Leydig cells, cauda epididymis or seminal vesicles.

摘要

饮食中的钴(265 ppm钴)可诱发大鼠红细胞增多症,并在大鼠的生精小管中引发持续的退行性和坏死性病变。在第35天及之后,睾丸血管出现发绀和充血,到第70天时,生精上皮和支持细胞出现退行性和坏死性变化。精原细胞、初级精母细胞和圆形精子细胞受到明显影响,而延长型精子细胞、精子和支持细胞则更具抵抗力。受损的小管通常与正常小管并排出现,其中含有由退化和坏死的精母细胞和/或精子细胞、脱落的生精细胞和支持细胞以及钙化的坏死碎片组成的多核巨细胞。坏死的小管经常塌陷,除偶尔可见的精原细胞和存活的支持细胞外,上皮细胞缺失。在睾丸间质细胞、附睾尾部或精囊中未观察到病变。

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