[SOME DATA ON CHANGES IN ADRENAL CORTEX FUNCTION IN ANIMALS DURING THE DEVELOPMENT OF STRESS].
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The authors report the clinico-anatomical analysis of 23 observations on malignant tumors of the adrenal cortex. The greatest diagnostic difficulties are encountered in the so-called "non-functioning" tumors, devoid of normal activity and mostly observed in adults. To pinpoint further the diagnosis, a wide use of morphological methods, especially needle biopsy, is recommended. A prolonged preclinical period, a tendency to predominantly hematogenic metastases spread, the fibrinolytic activity of parenchymal cells, pyrogenic and allergic effects of the catabolism products should be referred to as the biological features of the tumor. Bilateral involvement of adrenal glands sometimes depends on multicentric growth of a hormone-dependent tumor.
We isolated a cDNA clone encoding the human prohormone convertase PC5 from human adrenal gland mRNA. The deduced protein sequence would encode a 915 amino acid preproPC5 that shares a very high degree of homology with previously cloned rat and mouse homologues. PC5 mRNA was detected in multiple human tissues, including the brain, adrenal and thyroid glands, heart, placenta, lung, and testes. PC5 mRNA was undetectable in the liver and was present at lower levels in skeletal muscle, kidney, pancreas, small intestine, and stomach. Co-transfection of human PC5 and human prorenin expression vectors in cultured GH4C1 cells led to secretion of active renin. The activation of human prorenin by PC5 depended on a pair of basic amino acids at positions 42 and 43 of the prorenin prosegment and occurred only in cells containing dense core secretory granules. Human PC5 was colocalized with renin by immunohistochemistry in the zona glomerulosa of the adrenal gland, suggesting that it could participate in the activation of a local renin-angiotensin system in the human adrenal cortex.
Forty-one autopsies in newborns with hyaline membrane were studied. In fourteen cases (34.1%) cystic degeneration of the outermost portion of the adrenal cortex was found. Our results differ from other studies as the lesions were observed in newborns at various gestational ages, with a higher incidence in the group of pre-term babies, small for their gestational age. The constant association of hyaline membrane and adrenal cortex cystic degeneration seem to suggest that both processes may share a common etiopathogenic mechanism, namely hypoxia followed by increased ACTH secretion.
The possibility of functioning of microsomal steroid hydroxylases in the adrenal cortex in the presence of the electron-transporting proteins in mitochondrial monooxygenase systems has been studied. It was found that adrenodoxin reductase stimulates both the 21- and 17 alpha-steroid hydroxylation activities in microsomes of the adrenal cortex with the same efficiency as does NADPH-dependent cytochrome P-450 reductase. Using cytochrome b5 and its specific antibody, an attempt has been made to investigate possible mechanisms of the stimulating effect of adrenodoxin reductase.
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