Effects of vitamin E deficiency on the endocrine glands especially on the function of pituitary and testis.

通过测定维生素E缺乏大鼠血清促性腺激素（FSH、LH）和睾酮浓度的时间变化，探讨维生素E缺乏对大鼠垂体-性腺功能的影响。研究了LH在leding细胞中的受体位点、结合常数（Ka）和环AMP的形成。本研究结果如下：1)维生素E缺乏大鼠几乎完全溶血，血清和肝脏中TBA反应物质急剧增加。2)试验后期，维生素E缺乏组血清LH浓度略高于维生素E补充组。3)试验第196天，维生素E缺乏组血清FSH浓度显著高于维生素E补充组。4)维生素E缺乏组血清睾酮浓度始终低于对照组。5)与维生素E补充组相比，维生素E缺乏组LH/hCG受体数量略多，Ka明显减小（低亲和力）。维生素E缺乏组间质细胞形成环状AMP的数量明显减少。上述结果提示，维生素E缺乏直接抑制性腺功能，使间质细胞激素合成减少，并通过反馈机制导致垂体LH分泌增加。

Chronological changes of gonadotropin(FSH and LH) and testosterone concentration in the serum were measured in vitamin E deficient rats to investigate the effects of vitamin E deficiency on the pituitary-gonadal function in rats. The receptor sites and association constant(Ka) for LH and the formation of cyclic AMP in the Leyding cells were also investigated. The results obtained in this research are as follows :1) The vitamin E deficient rats showed almost complete hemolysis and extremely increased TBA reacting substance in the serum and liver.2) The serum LH concentration in the vitamin E deficient group was slightly higher than in the vitamin E supplemented group during the later periods of experiment.3) The serum FSH concentration in the vitamin E deficient group became significantly higher than in the vitamin E supplemented group at 196 days of experiment.4) The serum testosterone concentration was always lower in the vitamin E deficient group than in the control. However, the decrease of testosterone in plasma and tissue was prevented by the administration of DPPD.5) The vitamin E deficient group showed slightly large number of LH/hCG receptor and significantly small Ka (low affinity), as compared with vitamin E supplemented group. The formation of cyclic AMP by Leydig cells decreased significantly in vitamin E deficient group. These results suggest that the vitamin E deficiency exerted a suppressive effect directly on the gonadal function to decrease the hormone synthesis in the Leydig cells and caused the increased secretion of pituitary LH owing to the feedback mechanism.