Acute effects of spinal cord injury on the pituitary-testicular hormone axis and Sertoli cell functions: a time course study.
Acute effects of spinal cord injury on the pituitary-testicular hormone axis and Sertoli cell functions: a time course study.
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DOI：
10.1002/j.1939-4640.1995.tb01746.x
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发表时间：
1995-03
影响因子：
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通讯作者：
Hosea F. S. Huang;T. Linsenmeyer;Ming-tang Li;W. Giglio;R. Anesetti;J. V. Hagen;J. Ottenweller;C. Serenas;L. Pogach
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文献类型：
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作者：
Hosea F. S. Huang;T. Linsenmeyer;Ming-tang Li;W. Giglio;R. Anesetti;J. V. Hagen;J. Ottenweller;C. Serenas;L. Pogach
本研究探讨了脊髓损伤后精子发生异常发生的时程及其与垂体-睾丸激素轴和支持细胞功能变化的关系。以成年雄性大鼠T9、L1椎体水平脊髓横断为模型，建立脊髓损伤模型。动物在手术后3、7和14天被处死。早在脊髓损伤后3天，T9和L1动物就观察到精子发生的异常，包括精子成熟延迟和精子细胞核空泡化。到了第14天，其他病变变得明显，包括成熟精子细胞的吞噬、不完全的细胞联合和生精上皮的完全退化。并发一过性但意义重大(P<0.10)。Northern印迹分析显示，术后3天，T9和L1组大鼠睾丸中2.7kb支持细胞转铁蛋白mRNA转录水平短暂但显著降低(P<；0.05)。另一方面，在为期两周的研究期间，1.7kb的雄激素结合蛋白(ABP)mRNA保持不受影响。生精细胞特异性半铁蛋白和精子细胞特异性转移蛋白2和鱼精蛋白1的稳定转录水平也保持不变。这些结果表明，脊髓损伤将对垂体-睾丸激素轴产生暂时但深远的影响。这些变化可能会损害支持细胞功能的某些方面，使这些细胞无法支持正常的精子发生。然而，生精损伤的严重性和两种主要支持细胞蛋白的不同反应使得激素缺乏不可能是脊髓损伤后精子发生障碍的唯一机制。
The present study investigated the time course of the onset of the abnormalities in spermatogenesis following spinal cord injury, and their relationship to changes in the pituitary testicular hormonal axis and Sertoli cell function. Spinal cord injury (SCI) was induced in adult male rats by surgical transection of the spinal cord at the level of T9 and L1 vertebrae. Animals were killed 3, 7, and 14 days after the operation. As early as 3 days following SCI, abnormalities in spermatogenesis, including delayed spermiation and vacuolization of the nucleus of spermatids, were noted in both the T9 and L1 animals. By 14 days, other lesions, including phagocytosis of mature spermatids, incomplete cellular associations, and total regression of seminiferous epithelium, became apparent. Concurrently a transient but significant (P 0.10). Northern blot analysis of testicular poly(A)+ RNA revealed a transient but significant reduction in the steady-state level of the 2.7-kilobase (kb) Sertoli cell transferrin mRNA transcript in both the T9 and the L1 animals 3 days after the operation (P < 0.05). On the other hand, the 1.7-kb androgen binding protein (ABP) mRNA remained unaffected during the 2-week study period. The steady-state level of mRNA transcripts for spermatogenic cell-specific hemiferrin and spermatid specific transition protein 2 and protamine 1 also remained unchanged. These results suggest that spinal cord injury will result in a temporary, but profound, effect on the pituitary-testicular hormone axis. These changes may impair certain aspects of Sertoli cell function that could render these cells incapable of supporting normal spermatogenesis. However, the severity of spermatogenic lesions and the disparate responses of the two major Sertoli cell proteins make it unlikely that hormone deficiency is the only mechanism responsible for the impaired spermatogenesis following spinal cord injury.