Histophysiology of the adrenal cortex.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
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A study was made of the effect of the Soviet original drug thymarin on the adrenal cortex of male CBA mice. The drug was obtained from the cattle thymus and is known to induce competence of the T lymphocyte system of immunity. Histoenzymological studies disclosed a statistically significant reduction in the activity of NAD. H- and NADP X X H-diaphorases, glucoso-6-phosphate dehydrogenase and alkaline phosphatases in adrenocortical cells. Linear dimensions and cell volumes in the glomerular, fascicular and reticular zones were also found to be reduced. Thymarin is suggested to be one of the factors that regulate the structure and function of the adrenal cortex. It is believed that thymarin may exert a repressive effect on the adrenal cortex.
The zona reticularis (ZR) cell in the human adrenal cortex is responsible for the secretion of dehydroepiandrosterone, but its biology, origin, and putative decrease in number during aging are poorly understood. In the present experiments, we investigated to what extent ZR and zona fasciculata (ZF) cells differ in patterns of gene expression. Both cell types were purified by microdissection from adult adrenal cortex specimens. After a brief period in culture, RNA was harvested from the cells and used to prepare radioactively labeled probes following amplification by PCR. Probes were used in hybridizations of arrays of cDNAs on nylon membranes (PCR products or plasmids obtained from an adrenal cDNA library). Analysis of hybridization intensities showed that 17 of the 750 genes studied differed in expression by more than 2-fold. Several genes expressed at higher levels in ZR cells encode components of the major histocompatibility complex or enzymes involved in peroxide metabolism. Members of the tubulin gene family were expressed at higher levels in ZF cells. Differential expression of four of the genes was confirmed by Northern blotting. These differences show that although ZR and ZF cells are similar in gene expression, ZR cells have a gene expression pattern related to the unique biology of this cell type.
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The paper treats of current diagnostic criteria for congenital dysfunction of the adrenal cortex in children. They include investigation of HLA-antigens, identification of heterozygote and homozygote carriership, prenatal diagnosis of the disease, and the screening tests. The leading position in the disease diagnosis is assigned to its clinical manifestations, measurement of 17-hydroxyprogesterone and testosterone in blood serum together with excretion of 17-ketosteroids with urine. Emphasis is laid on the importance of early disease diagnosis and establishment of sex appurtenance, which is promoted by studies of sex chromatin, karyotype and ultrasonic scanning of the internal genitalia. The treatment policy for patients with congenital dysfunction of the adrenal cortex has been elaborated as have been its aspects: hormonal, surgical and psychotherapeutic. The treatment protocols using current hormonal drugs with changes in conventional time of their intake are described in detail. The long-term results of hormonal therapy are provided on the basis of large clinical material (over 500 patients with congenital dysfunction of the adrenal cortex were examined).
The comparative investigation of the adrenal cortex in hypertensive (INHERITED STRESS-INDUCED ARTERIAL HYPERTENSION--ISIAH) and normotensive strain (Wistar) 12-months age rats was performed. The structural signs such as the lowering of the mitochondria volume involved in steroid synthesis in showed more notable age-related reduction of steroidogenesis in the adrenal glomerular and fascicular zones and in the ISIAH rats. The lowering of the cell steroidogenesis was compensated by the adrenal glomerular and fascicular zones and hypertrophy as a result the adrenocorticocytes hyperplasia. At the same time the more considerable sclerotic changes of the adrenal cortex periendothelial space were demonstrated in the ISIAH rats. The results obtained give evidence that reducing potential of compensatory possibilities of the adrenal cortex of the ISIAH rats in the late postnatal ontogenesis period cause high probability of adaptative-compensatory mechanisms failure and pathological process aggravation in these animals.
It is well known that plasma levels of dehydroepiandrosterone (DHEA), a steroid hormone secreted by zona reticularis (ZR) of the adrenal cortex, reach the maximal values in the third decade of life and then gradually decline with age. Moreover, the DHEA deficiency is probably responsible for several functional disturbances connected with aging. It was also found that ZR reaches its definitive volume at puberty and undergoes selective atrophy during the aging. Thus, the decline of DHEA may be a simple consequence of ZR atrophy in aged subjects. A hypothesis presented here attempts to explain the mechanism of the age-related ZR atrophy and is based on the adrenal cortex cell kinetics. In the adrenal cortex the cell proliferation indices are lower when we pass from zona glomerulosa (ZG) to the inner zones and are the lowest in ZR. In contrast, the apoptotic index is the highest in ZR. It is suggested that adrenocortical cells renew from the progenitor cells located in ZG /zona fasculata boundary and /or in subcapsular layer. These cells migrate centripetally undergoing the subsequent steps of differention and consecutive divisions - and - if not die en route - reach the most central localization in ZR. In consequence, ZR includes the "oldest" adrenocortical cells which probably in majority reached the "Hayflick's number" and cannot divide. This results in the preponderance of apoptosis over proliferation leading to progressive ZR atrophy followed by a decline of secretion of ZR-derived steroid hormones.