Paniagua R, Nistal M, Sáez F J, Fraile B
Department of Cell Biology and Genetics, University of Alcalá de Henares, Madrid, Spain.
J Electron Microsc Tech. 1991 Oct;19(2):241-60. doi: 10.1002/jemt.1060190209.
The ultrastructure of the progressive testicular involution with advancing age in men is reviewed. There is no definite age at which testicular involution begins, and the onset and severity of testicular lesions are subjected to pronounced individual variations. Hormone studies also indicate great individual variations, and subtle changes in both the testis and the pituitary develop progressively with age. Testicular size, sperm quality, and numbers of all germ cell types, Sertoli cells, and Leydig cells decrease with age. The volume occupied by the seminiferous tubules decreases, whereas that occupied by the testicular interstitium remains constant. The most frequent histological pattern of the aging testis is a mosaic of different seminiferous tubule lesions, varying from tubules with complete, although reduced, spermatogenesis, to completely sclerosed tubules. The tubules with complete spermatogenesis may show numerous morphological abnormalities in the germ cells, including multinucleation. Abnormal germ cells degenerate causing Sertoli cell vacuolation. These vacuoles correspond to dilations of the extracellular spaces resulting from the premature exfoliation of germ cells. Degenerating cells that are phagocytosed by the Sertoli cells give rise to an accumulation of lipid droplets in the Sertoli cell cytoplasm. The loss of germ cells begins with the spermatids, but progressively affects the earlier germ cell types, and tubules with maturation arrest at the level of the spermatocytes or spermatogonia are observed. The Sertoli cells show morphological abnormalities such as dedifferentiation, mitochondrial metaplasia, and multinucleation. Germ cell loss is associated with thickening of the tunica propria. When all seminiferous epithelial cells have disappeared, only an intensely collagenized tunica propria with myoid cells remains (sclerosed tubules). The Leydig cells progressively dedifferentiate with a decrease in the quantity of both smooth endoplasmic reticulum and mitochondria, together with an accumulation of lipid droplets, crystalline inclusions, and residual bodies, and formation of multinucleate cells. The development of tubular involution with age is similar to that observed after experimental ischemia, suggesting that vascular lesions may play an important role in age-related testicular atrophy.
本文综述了男性随着年龄增长睾丸进行性退化的超微结构。睾丸退化开始的确切年龄尚无定论，睾丸病变的发生和严重程度存在明显的个体差异。激素研究也表明个体差异很大，睾丸和垂体的细微变化会随着年龄的增长而逐渐发展。睾丸大小、精子质量以及所有生殖细胞类型、支持细胞和间质细胞的数量都会随着年龄的增长而减少。生精小管所占体积减小，而睾丸间质所占体积保持不变。衰老睾丸最常见的组织学模式是不同生精小管病变的镶嵌，从具有完整（尽管减少）生精功能的小管到完全硬化的小管不等。具有完整生精功能的小管可能在生殖细胞中表现出许多形态异常，包括多核化。异常生殖细胞退化导致支持细胞空泡化。这些空泡对应于生殖细胞过早脱落导致的细胞外间隙扩张。被支持细胞吞噬的退化细胞会导致支持细胞胞质中脂质小滴的积累。生殖细胞的丢失始于精子细胞，但逐渐影响更早的生殖细胞类型，并且观察到生精小管在精母细胞或精原细胞水平出现成熟停滞。支持细胞表现出形态异常，如去分化、线粒体化生和多核化。生殖细胞丢失与固有膜增厚有关。当所有生精上皮细胞消失后，只剩下含有肌样细胞的高度胶原化的固有膜（硬化小管）。间质细胞随着滑面内质网和线粒体数量的减少而逐渐去分化，同时伴有脂质小滴、结晶包涵体和残余体的积累以及多核细胞的形成。随着年龄增长小管退化的发展与实验性缺血后观察到的情况相似，这表明血管病变可能在与年龄相关的睾丸萎缩中起重要作用。
