Format

Send to

Choose Destination
Tohoku J Exp Med. 1987 Jul;152(3):221-9.

Effects of vitamin E deficiency on the hormone secretion of the pituitary-gonadal axis of the rat.

Author information

1
Department of Home Economics, Faculty of Education, Iwate University, Morioka.

Abstract

Chronological changes of gonadotropin (FSH and LH) and testosterone concentrations 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 Leydig cells were also investigated. The results obtained in the present study are as follows: 1) The vitamin E deficient rats showed almost complete hemolysis and extremely increased TBA reacting substances (TBARS) 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 did not differ significantly from that in vitamin E supplemented group, but became significantly higher than that in the latter at 186 days of experiment. 4) The serum testosterone concentration was always lower in the vitamin E deficient group than in the control. 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.

PMID:
2821655
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for J-STAGE, Japan Science and Technology Information Aggregator, Electronic
Loading ...
Support Center