Noguchi Junko, Nakai Michiko, Kikuchi Kazuhiro, Kaneko Hiroyuki, Imaeda Noriaki
Division of Animal Sciences, National Institute of Agrobiological Sciences, Tsukuba, Ibaraki 305-8602, Japan.
J Reprod Dev. 2013;59(3):273-81. doi: 10.1262/jrd.2012-176. Epub 2013 Feb 22.
In the process of establishment of an inbred Duroc pig strain, males with size asymmetry of the testes were frequently observed. To clarify the possible causes of this asymmetry, we examined the testes and epididymides of 67 males of the F4-F7 generations at 35-100 weeks of age. Testicular weights showed a wide variation (120-610 g). When the weights of the testes were compared bilaterally, 35 of the 67 males showed more than a 10% difference. Histological examination of testes from this asymmetry group revealed a range of seminiferous tubule disruption including disappearance of all germ cells, but not Sertoli cells, in the epithelium. Focal lesions associated with the degenerated tubules were observed. Trends of incident fibrosis or hyalinization of these lesions were seen in aged males of the asymmetry group. Besides this abnormality of spermatogenesis, infiltration of mononuclear inflammatory cells around the tubule was frequently observed in the asymmetry group (32.9%, compared with 1.6% in males showing testis symmetry). In severe cases, the inflammatory cells were concentrated in the intertubular region instead of Leydig cells. Cellular infiltration was also observed around the epididymal duct and blood vessels, but its incidence did not differ between the symmetry and asymmetry groups. Testicular testosterone levels were significantly increased in the asymmetry group, but those of E2 and inhibin did not differ between the two groups. These histopathological features indicate that disruption of spermatogenesis after orchitis/epididymo-orchitis could induce testicular atrophy. Genetic predispositions for this trait may cause prevalent retrograde infections, resulting in orchitis/epididymo-orchitis.
在建立近交杜洛克猪品系的过程中，经常观察到睾丸大小不对称的雄性猪。为了阐明这种不对称的可能原因，我们检查了67只F4 - F7代雄性猪在35 - 100周龄时的睾丸和附睾。睾丸重量显示出很大的差异（120 - 610克）。当双侧比较睾丸重量时，67只雄性猪中有35只显示出超过10%的差异。对来自这个不对称组的睾丸进行组织学检查发现，生精小管有一系列破坏，包括上皮中所有生殖细胞消失，但支持细胞未消失。观察到与退化小管相关的局灶性病变。在不对称组的老年雄性猪中可见这些病变的纤维化或透明化趋势。除了这种精子发生异常外，在不对称组中经常观察到小管周围单核炎性细胞浸润（32.9%，而睾丸对称的雄性猪中为1.6%）。在严重情况下，炎性细胞集中在小管间区域而非睾丸间质细胞。在附睾管和血管周围也观察到细胞浸润，但对称组和不对称组之间其发生率没有差异。不对称组的睾丸睾酮水平显著升高，但两组之间的雌二醇和抑制素水平没有差异。这些组织病理学特征表明，睾丸炎/附睾炎后精子发生的破坏可导致睾丸萎缩。该性状的遗传易感性可能导致普遍的逆行感染，从而引发睾丸炎/附睾炎。
