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小鼠睾丸女性化:睾丸间质细胞中过氧化物酶体数量稀少。

Testicular feminization of the mouse: paucity of peroxisomes in Leydig cell of the testis.

作者信息

Reddy J K, Ohno S

出版信息

Am J Pathol. 1981 Apr;103(1):96-104.

Abstract

The testes of mice with the X-linked testicular feminization (Tfm/y hermaphrodite) mutation are very small and cryptorchid. The spermatogenesis in the adult Tfm/y hermaphrodite mouse testes is arrested, and the testosterone biosynthesis is significantly reduced due to deficiency of 17-keto-steroid reductase, the enzyme essential for the conversion of androstanedione to testosterone. In this study the distribution of peroxisomes in the Leydig cells of adult Tfm/y hermaphrodite mice was investigated because of the suggestion that peroxisomes may participate in lipid metabolism and/or androgen biosynthesis is steroidogenic cells. Aldehyde-fixed testicular tissue of Tfm/y hermaphrodite mice was processed for the cytochemical localization of peroxisome catalase to facilitate identification of these organelles in the Leydig cells. Testes from Blo/y and CSa strain normal adult mice served as controls. Testicular Leydig cells of normal adult Blo/y and CSa mice contained abundant smooth endoplasmic reticulum (SER) in the form of complex interconnected tubules and double-walled membranous vesicles. Numerous peroxisomes, often in continuity with SER channels or in close association with lipid droplets, were observed in Leydig cells of normal males. In contrast, the peroxisomes in the Leydig cells of adult Tfm/y hermaphrodite mouse testes were either undiscernible or greatly reduced in number and size. SER in these cells was sparse, whereas mitochondria were numerous. In addition, abundant clusters of lipid droplets were encountered in a majority of Leydig cells of Tfm/y hermaphrodite mouse testes. Peroxisome and SER paucity in Leydig cells of Tfm/y hermaphrodite mice may be a reflection of reduced testosterone production. Whether excessive accumulation of lipid in the Leydig cells of Tfm/y hermaphrodite mouse testes is due to reduced utilization of cholesterol for the biosynthesis of testosterone or to impaired lipid metabolism due to reduction in peroxisome population in these cells remains to be ascertained.

摘要

具有X连锁睾丸雌性化(Tfm/y雌雄同体)突变的小鼠睾丸非常小且隐睾。成年Tfm/y雌雄同体小鼠睾丸中的精子发生停滞,由于17-酮类固醇还原酶缺乏,睾酮生物合成显著减少,该酶是雄烯二酮转化为睾酮所必需的。在本研究中,对成年Tfm/y雌雄同体小鼠睾丸间质细胞中过氧化物酶体的分布进行了研究,因为有迹象表明过氧化物酶体可能参与类固醇生成细胞的脂质代谢和/或雄激素生物合成。对Tfm/y雌雄同体小鼠经醛固定的睾丸组织进行处理,以进行过氧化物酶体过氧化氢酶的细胞化学定位,便于在间质细胞中识别这些细胞器。来自Blo/y和CSa品系正常成年小鼠的睾丸用作对照。正常成年Blo/y和CSa小鼠的睾丸间质细胞含有丰富的滑面内质网(SER),呈复杂的相互连接的小管和双壁膜泡形式。在正常雄性的间质细胞中观察到许多过氧化物酶体,它们通常与SER通道连续或与脂滴紧密相连。相比之下,成年Tfm/y雌雄同体小鼠睾丸间质细胞中的过氧化物酶体要么难以辨认,要么数量和大小大大减少。这些细胞中的SER稀少,而线粒体众多。此外,在Tfm/y雌雄同体小鼠睾丸的大多数间质细胞中发现了大量脂滴簇。Tfm/y雌雄同体小鼠间质细胞中过氧化物酶体和SER的缺乏可能反映了睾酮产生的减少。Tfm/y雌雄同体小鼠睾丸间质细胞中脂质的过度积累是由于用于睾酮生物合成的胆固醇利用减少,还是由于这些细胞中过氧化物酶体数量减少导致脂质代谢受损,仍有待确定。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/becf/1903810/76459421c2c7/amjpathol00217-0102-a.jpg

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