Search PubMed⌕ Search

PubMed · 6301034

[Hormones and aging. 2].

Abstract

The main hormonal disturbances in ageing are: 1) a slight decrease in the secretion of all hormones, with the exception of gonadotropins in women whose production increases sharply as a result of the almost complete suppression of ovarian activity; 2) a slight but substantial resistance of tissues to the action of most hormones; 3) the cessation of estrogen secretion with an important decrease in androgen secretion in the ovaries; 4) a decrease in androgen secretion with a lesser reduction in estrogen secretion in the testicles; 5) an important decrease in adrenal androgen secretion in both sexes. These findings are the consequence and not the cause of ageing which, to some degree, they do promote, especially in bone, muscle, skin and mucous membranes. Therapeutic incidences of the hormonal disturbances in ageing, though not negligeable, are still limited.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J Vague. 1983-01-13. [Hormones and aging. 2].. https://pubmed.ncbi.nlm.nih.gov/6301034/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

The p53 codon 249 mutant--derived from human functional adrenal tumors--can modify the cell shape of normal adrenocortical transfected cells.

Our previous study has indicated that p53 gene mutation occurred in 73% of human functional adrenal tumors, and the mutation hot spots were focused on codons 100, 102 (exon 4), and 249 (exon 7). Furthermore, a transcriptional activity study revealed that the mutant p53 protein derived from human functional adrenal tumors lost 90% transcriptional activity and the ability to bind with the p53 sequence. In order to investigate the influence of the mutant protein extracted from adrenocortical tumors on normal adrenal cells, we first cloned p53 cDNA from the human primary aldosteronism and constituted it with isopropyl thiogalactoside (IPTG) inducible expression vector as recombinant plasmid. The recombinant plasmid was then transfected to normal bovine adrenocortical cells through electroporation. The results showed that the p53 protein mutations at codons 100 and 102 could neither affect the cell morphology nor enable cell growth on the soft agar. In addition, no significant difference was found in cortisol level between the p53 transfected and the control cells. On the other hand, cell morphological changes and cell proliferation rate increase were observed when we used IPTG to induce the expression of the p53 protein, which mutated at codon 249, in adrenocortical cells. The cell morphology changes included less flattened and decreased elongation when compared to non-transfected cells. However, the cortisol level in transfected cells was not affected by the p53 mutants. Taken together, we concluded that the mutant p53 protein indeed participates in adrenal carcinogenesis; however, it has no influence on hormone production and secretion.

Adrenal Cortex↗

Primary culture system of adrenocortical cells from dogs to evaluate direct effects of chemicals on steroidogenesis.

The present study was conducted to confirm the usefulness of a primary culture system of adrenocortical cells from dogs for detecting the direct effects of the chemicals on adrenal cortex. Corticosteroid levels in the culture supernatant were measured using high-performance liquid chromatography (HPLC) following 24-h incubation with the chemicals. Ketoconazole, miconazole, metyrapone, aminoglutethimide, and 1-(o-chlorophenyl)-1-(p-chlorophenyl)-2,2-dichloroethane (o,p-DDD), which were known to inhibit cortisol production were evaluated in this system. Both viable cells and corticosteroid levels were decreased by o,p-DDD treatment. Other chemicals showed various inhibition patterns of corticosteroid levels as follows without affecting cell viability. Ketoconazole decreased total corticosteroids level by mainly due to the decreases in cortisol and 11-deoxycortisol levels. Miconazole decreased cortisol and 11-deoxycortisol levels, however, slightly increased corticosterone level. Metyrapone decreased cortisol and corticosterone levels as 11-deoxycortisol and 11-deoxycorticosterone levels were increased. Aminoglutethimide decreased total corticosteroids level by mainly decreasing cortisol, corticosterone and 11-deoxycortisol levels. These results suggested that determination of the pattern of corticosteroid levels by HPLC in this system well reflected the mode of their action on steroidogenesis. Thus, we conclude this simple system was useful to determine the direct effects of chemicals on steroidogenesis in the adrenal cortex.

Adrenal Cortex↗

Electrical stimulation of the dorsal hippocampus caused a long lasting inhibition of ACTH and adrenocortical responses to photic stimuli in freely moving rats.

The effect of a single train of electrical hippocampal stimulation on ACTH and corticosterone (CS) responses to subsequent photic stimulation was studied in freely moving male rats. The hippocampal stimulation inhibited the stress-induced rise [corrected] in serum CS levels up to 150 h when compared to sham stimulated animals. This effect did not exist at 300 h following stimulation. This sustained hippocampal inhibitory effect on the adrenocortical response, which was not reported previously, was partially abolished by section of the dorsal fornix. The present data demonstrate that dorsal hippocampal stimulation has a long lasting inhibitory effect on pituitary adrenocortical secretion following neural stimuli and this is partially mediated by the dorsal fornix.

Adrenal Cortex↗