Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ADRENAL CORTEX”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,279 records · Page 71Linked to original sources
PubMed1994

[Effect of kidney tonifying herbs on morphological changes of adrenal cortex in androgen-sterilized rats].

Young rats of 9-day old with testosterone propionate subcutaneously injected were used as an androgen sterilized rats (ASR) model. On 80th day, herbal extract of tonifying the Kidney was fed for 14 days, all animals were sacrificed by cardiac perfusion method on 100 days of ages. Morphological studies with light and electron microscope, immunohistochemical studies with argyrophilic nucleolar organiser region (AgNOR) and proliferating cell nucleolar antigen (PCNA) were used for observations on the morphological change of adrenal cortex. In control group (treated with testosterone propionate only) the reticular zone of the adrenal cortex extented widely in which cellular fatty drops, AgNOR and PCNA increased apparently. In animal treated with herbs, the width of the reticular zone, the numbers of AgNOR and PCNA reduced significantly to normal levels (P < 0.01, P < 0.01, P < 0.01) and numbers of fatty drops also decreased. It suggests that during inducing ovulation in ASR tonifying Kidney herbs simultaneously regulated the adrenal function besides the chief function on pituitary-ovary regulation.

Adrenal Cortex↗
PubMed1996

Expression of p21(WAF1/CIP1/SDI1) and p53 in apoptotic cells in the adrenal cortex and induction by ischemia/reperfusion injury.

p21(WAF1/CIP1/SDI1), an inhibitor of cyclin-dependent kinases, is expressed at varying levels in human adrenal glands removed during surgery or organ recovery. In glands with p21 mRNA, nuclear p21 immunoreactivity, which was occasionally extensive, colocalized with p53 immunoreactivity and DNA damage, as evidenced by in situ end-labeling. Many cells showed morphological features of apoptosis when observed by fluorescent DNA dye staining and electron microscopy. This pattern was also associated with high levels of cytoplasmic heat shock protein 70. To address the question of the origin of p21 expression in some human adrenal glands, rat adrenal glands were subjected to 30 min of ischemia followed by 8 h of reperfusion. Cells with nuclear p21 and p53 appeared in the adrenal cortex together with DNA damage detected by in situ end-labeling. Nuclear p21 immunoreactivity was also produced in adrenal tissue fragments incubated at 37 degrees C in vitro. However, in this case, p21 expression was confined to the cut edge of the tissue. In contrast, p21 in human adrenal glands, as in ischemic rat glands, was within the inner regions of the cortex, supporting an origin of the protein in vivo rather than postmortem. The p53/p21 pathway of reaction to cellular injury, potentially leading to apoptosis, may play a role in tissue damage such as that resulting from ischemia/reperfusion. In the human adrenal cortex this process may be a precursor of adrenal failure.

Adrenal Cortex↗
PubMed1976

Plasma cortisol level is an index for functional state of adrenal cortex during pregnancy.

Measurement of plasma cortisol is necessary in assessing the functional state of the adrenal cortex and the availability of other active steroids to the tissues during pregnancy. Coupled with clinical endocrine tests, these determinations can give the physician a good indication of the type of disorder present e.g. Addison's diseases, panhypopituitarism and adrenal hyperfunction. The method used for estimation of venous plasma cortisol when adequately controlled, is very sensitive and accurate.

Addison Disease↗
PubMed1995

Ultrastructural changes in mitochondria of the adrenal cortex of iron-deficient rats.

Male Sprague-Dawley rats aged 3 weeks that were maintained on an iron-deficient diet for 4-5 weeks developed severe anemia with markedly reduced hemoglobin levels (4.11 +/- 0.20 Hb g% versus controls 12.74 +/- 0.15 Hb g%). On sacrifice, the adrenal glands were removed and processed for light and transmission electron microscopy and enzyme cytochemistry. The major histological and ultrastructural changes in the adrenal cortex in response to the iron deficiency were seen in cells of the zona fasciculata, especially in its outer region, and to a lesser degree in cells of the zona reticularis. Structural changes were seen in the mitochondria of these cells, which often became grossly enlarged and developed unusual electron-dense inclusions. In addition, the lipid droplets in the iron-deficient cells of these regions were much less developed and less prominent compared with controls. Quantitative cytochemical localization of succinic dehydrogenase (SDH) activity in the adrenal glands showed that in iron-deficient rats there was an increase in SDH activity in the zona fasciculata (46%) and in the zona reticularis (74%), whereas there was a reduction of approximately 41% in SDH activity in the zona glomerulosa. Serum corticosterone levels were significantly raised in the iron-deficient rats compared with the control rats. Our results indicate that severe nutritional iron deficiency in rats causes ultrastructural and cytochemical changes in the mitochondria of the adrenal cortex accompanied by increased secretion of corticosterone.

Adrenal Cortex↗