Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 3714913

Adrenocortical function and suicidal behavior in depressive disorders.

R P Brown·B Mason·P Stoll·D Brizer·J Kocsis·P E Stokes·J J Mann
View original source ↗Export metadata ↓

Abstract

In order to examine the hypothesis that abnormal adrenocortical function is associated with suicidal behavior, morning and afternoon plasma cortisols and 1-mg dexamethasone suppression tests (DSTs) were performed in 65 patients with primary major depressive disorder. Patients with recent suicide attempts (within 28 days before DST) were compared to patients who had made past attempts and those who had never made suicide attempts with respect to age, gender, severity of depression, and plasma cortisol levels. Plasma cortisol levels did not differ significantly among the three groups. Nonsuppression on the DST was associated with presence of delusions, increasing age, and global severity of depression, but not with suicide attempts.

Explore related subjects

Adrenal CortexAdultAge FactorsAgedDelusionsDepressive DisorderDexamethasoneFemaleHumansHydrocortisoneMaleMiddle AgedSuicide, AttemptedJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R P Brown, B Mason, P Stoll, D Brizer, J Kocsis, P E Stokes, J J Mann. 1986. Adrenocortical function and suicidal behavior in depressive disorders.. https://doi.org/10.1016/0165-1781(86)90079-x

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

KEEP EXPLORING

Related citations

PubMed2007

Immunohistochemical Jun/Fos protein localization and DNA synthesis in rat adrenal cortex after treatment with ACTH or FGF2.

In vitro and in vivo studies have suggested that the expression of the early response genes for Jun and Fos proteins plays an important role in adrenal cell proliferation. In order to study the expression pattern of the activating protein-1 (AP-1) family of oncogenes in the adrenal gland, we have used immunohistochemistry to localize Jun and Fos protein expression in rat adrenal cortex infused in situ with adrenocorticotropic hormone (ACTH), fibroblast growth factor 2 (FGF2), or both. The expression of AP-1 factors has been found to be correlated with in vivo ACTH and FGF2 proliferation in rats treated with dexamethasone and bromodeoxyuridine (BrdU). Induction of c-Jun and c-Fos in the zona fasciculata and of FosB in the zona reticularis suggests that, after ACTH stimulation, these proteins are the main AP-1 components in these zones. In vivo, ACTH increases BrdU-positive cells in the zona fasciculata and zona reticularis suggesting that the composition of AP-1 complexes in these zones is correlated with proliferation. Patterns of Fos and Jun induction by FGF2 do not resemble those after ACTH induction. However, in isolation, neither affects the zona glomerulosa. In the zona fasciculata, and more so in the zona reticularis, FGF2 modulates responses to ACTH, reducing the numbers of Jun-positive cells, Fos-positive cells, and DNA synthesis. This indicates that FGF2 antagonizes ACTH, and that ACTH thus controls the trophic effect independently of exogenous FGF2. Our results implicate the AP-1 family of transcription factors in the regulation of cell progression and the control of ACTH-induced proliferation in the zona fasciculata and zona reticularis.

Adrenal Cortex↗
PubMed2007

Tyrosine phosphatases in steroidogenic cells: regulation and function.

In adrenocortical and Leydig cells PKA activation by trophic hormones increases the activity of protein tyrosine phosphatases and also induces the expression of MAP kinase phosphatase 1 (MKP-1), a dual activity protein phosphatase (serine/threonine and tyrosine). This work summarizes the knowledge on the regulation and the role played by cAMP-activated tyrosine phosphatases as well as MKP-1 in the hormonal activation of the acute and chronic phases of steroidogenesis.

Adrenal Cortex↗
PubMed2007

Stimulation of the pituitary-adrenal axis and of adrenocortical steroidogenesis ex vivo by administration of di-2-ethylhexyl phthalate to prepubertal male rats.

Phthalate esters exert deleterious effects on testicular physiology and, consequently, on reproduction and fertility. However, little is presently known concerning potential adverse effects of these environmental pollutants on the hormonal functions of the adrenal gland. Therefore, we have investigated the effects of administering to rats of different developmental ages di-2-ethylhexyl phthalate (DEHP) on the hypothalamic-pituitary-adrenal axis in vivo, as well as on adrenocortical steroidogenesis ex vivo. Oral exposure to DEHP once daily for 4 days elevated the serum levels of ACTH and corticosterone in rats 20 and 40 days of age, but not in adult, 60-day-old animals. Furthermore, primary cultures of adrenocortical cells isolated from 20- and 40-day-old rats treated with DEHP exhibited an enhanced capacity to produce corticosterone in response to ACTH, dibutyryl cAMP, and 22R-hydroxycholesterol, as well as increased ACTH-stimulated transport of endogenous cholesterol into mitochondria. Neither DEHP nor its major metabolite mono-2-ethylhexyl phthalate altered steroidogenesis in cultures of adrenocortical cells isolated from untreated rats. These findings demonstrate that in male rats, DEHP exerts an age-dependent influence on the pituitary-adrenocortical axis in vivo and adrenocortical steroidogenesis ex vivo. Such perturbation may be of pathological significance in connection with disorders of the hormonal stress response, especially in very young human beings.

Adrenal Cortex↗