Endocrine. 1995 Oct;3(10):711-6. doi: 10.1007/BF03000202.

Pituitary physiological and ultrastructural changes during aging.

Endocrine

A C Nessi, G De Hoz, C Tanoira, E Guaraglia, G Consens

PMID: 21153159 DOI: 10.1007/BF03000202

Abstract

Although it is known that both aged human beings and animals exhibit a decrease in pituitary hormone production and release, there is controversy about the true nature of these changes. Whereas some authors postulate an extra pituitary cause, i.e., a dopaminergic failure, others consider that the problem is at the level of the gland itself. CFW mice 2, 6, 12 and 18 months old, were i.p. inoculated withL: -Dopa. The pituitary gland was removed and sectioned, then observed and photographed in an electron microscope. Photomicrographs were scanned into a computer and digital image analysis made to determine secretory granules and organelle kinetics. Normal GH and TSH cells of elder mice responded to stimulation withL: -Dopa in a similar way as did cells of juveniles. The responsiveness rate of those cells to the amine precursor during the first hour of treatment was 38±3.5% and 26±0.3% of the studied cells in young and aged animals, respectively. Fully functional cells, i.e., GH and TSH cells showing 5 to 90% of their cytoplasm occupied by secretory granules (some of them immature), with a developed RER, and with absence of cell damage, were seen to be reduced from 98% in younger to 65.7% in aged animals. In successive steps, cells showed cell desquamation, darkened cytoplasm, differential swollen endoplasmic reticulum without secretory granules, increased number of secondary lysosomes (more than two per cell in a cross-section), differential swollen mitochondria, cytoplasm only containing two to five giant secondary lysosomes and finally, a complete loss of cell architecture. Therefore, GH and TSH cells at the end of their life-span were seen to derive into apoptotic images. In the whole gland, an increasing number of those pathologic images were seen as aging proceeded, thus reducing the number of normal and productive cells. From the results presented here it is proposed that an extrapituitary failure is insufficient to explain the reduced production of GH and TSH, and that the problem evolves also at the level of the gland itself.

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