Bensoussan K, Morales C R, Hermo L
Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec, Canada.
J Androl. 1998 May-Jun;19(3):266-88.
The effects of vitamin E deficiency on the rat testis and epididymis were examined in a light- and electron-microscopic analysis. Various groups of animals were made vitamin E-deficient, beginning at postnatal day 10, via their lactating mothers, until day 21, when they were separated from their mothers. The groups were maintained thereafter on either a vitamin E-deficient or a normal diet (controls). The vitamin E-deficient animals of group A, sacrificed at day 42, revealed testes that were normal in appearance, with a full complement of germ cells when compared to their controls (group B). Group C, however, sacrificed at day 48, revealed major abnormalities in the testes, unlike both their controls (group D) and normal, untreated animals (group E). Spermatogenesis was incomplete; the most advanced cell type was predominantly step-7 spermatids. However, many of these cells, as well as earlier spermatids, appeared to undergo degeneration, evidenced by large pale areas in their nuclei, disrupted acrosomes, and a cytoplasm with uncharacteristic organelles. Multinucleated cells, characterized by their chromatoid bodies as spermatids, were often seen in the seminiferous tubule lumen. Sertoli cells were normal in appearance, except for numerous, large lipid droplets in their basal region, at stages I-VIII; in appropriate controls (group D), such droplets were absent at these stages. These lipid inclusions presumably represented the final breakdown products of the late spermatids, which were phagocytosed by Sertoli cells between days 42 and 48. However, numerous germ cells, often recognized as round spermatids, and multinucleated cells were noted in the epididymal lumen, which indicates that such cells were spared from Sertoli cell phagocytosis. These data suggest that vitamin E plays a key role in the maintenance and survival of spermatids. In the epididymis, vitamin E deficiency resulted in principal, narrow, and apical cells that showed a poorly developed secretory and endocytic apparatus at days 42 (group A) and 48 (group C), unlike those of normal, untreated animals (group E). On the other hand, clear cells of groups A and C showed a highly developed endocytic apparatus in the cauda region only, whereas in the caput and corpus regions, endocytic apparatuses were small and undifferentiated, unlike those of group E. Thus, in the epididymis, vitamin E plays a role in the structural differentiation of principal cells along the entire epididymis, whereas, in the case of clear cells, its role is region-specific. Readministration of vitamin E to the diet restored a normal appearance to both the testis and the epididymis, which indicates that the effects on these tissues are reversible. Taken together, these data indicate that vitamin E plays important roles in maintaining the viability of the spermatid population and in allowing epithelial epididymal cells to acquire their fully differentiated structural appearance.
通过光学显微镜和电子显微镜分析，研究了维生素E缺乏对大鼠睾丸和附睾的影响。从出生后第10天开始，通过哺乳期的母亲使不同组的动物维生素E缺乏，直至第21天与母亲分离。此后，这些组分别维持在维生素E缺乏或正常饮食（对照组）中。A组维生素E缺乏的动物在第42天处死，其睾丸外观正常，与对照组（B组）相比，生殖细胞数量完整。然而，C组在第48天处死时，其睾丸出现了严重异常，与对照组（D组）和正常未处理动物（E组）均不同。精子发生不完全；最成熟的细胞类型主要是7期精子细胞。然而，许多这些细胞以及早期精子细胞似乎发生了退化，表现为细胞核内大片浅色区域、顶体破裂以及含有异常细胞器的细胞质。在曲细精管腔中经常可见以精子细胞的类核体为特征的多核细胞。支持细胞外观正常，只是在I - VIII期其基部区域有大量大脂滴；在适当的对照组（D组）中，这些阶段没有此类脂滴。这些脂质包涵体可能代表晚期精子细胞的最终分解产物，在第42天至48天之间被支持细胞吞噬。然而，在附睾管腔中发现了许多通常被识别为圆形精子细胞的生殖细胞和多核细胞，这表明这些细胞未被支持细胞吞噬。这些数据表明维生素E在精子细胞的维持和存活中起关键作用。在附睾中，维生素E缺乏导致主细胞、窄细胞和顶细胞在第42天（A组）和第48天（C组）时分泌和内吞装置发育不良，与正常未处理动物（E组）不同。另一方面，A组和C组的透明细胞仅在附睾尾部区域显示高度发达的内吞装置，而在附睾头部和体部区域，内吞装置小且未分化，与E组不同。因此，在附睾中，维生素E在整个附睾主细胞的结构分化中起作用，而对于透明细胞，其作用具有区域特异性。在饮食中重新添加维生素E可使睾丸和附睾恢复正常外观，这表明对这些组织的影响是可逆的。综上所述，这些数据表明维生素E在维持精子细胞群体的活力以及使附睾上皮细胞获得其完全分化的结构外观方面发挥重要作用。
