Effects of a prolonged treatment with aminoglutethimide on the zona fasciculata of rat adrenal cortex: a morphometric investigation.
The effects of a 7-day administration of aminoglutethimide (AG) on the adrenal zona fasciculata were examined in "normal" and dexamethasone/ACTH-treated rats. There was a 70-74% decrease in the concentration of corticosterone in blood, but no conspicuous qualitative changes suggesting cell degeneration occurred. Morphometry showed that AG induced a significant hypertrophy of the zona fasciculata and its parenchymal cells only in "normal" animals, which was due to an increase in the volume of the mitochondrial compartment and to proliferation of the smooth endoplasmic reticulum. This response to AG was considered to be non-specific and mediated by the enhanced secretion of ACTH following the decrease in the blood level of corticosterone. AG administration significantly increased the volume of the lipid-droplet compartment and the number of intramitochondrial lipid-like inclusions in both groups of animals. These changes were interpreted as the morphological counterpart of the AG-induced block of cholesterol utilization in steroid synthesis.
D000302:Adrenal Cortex / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000616:Aminoglutethimide / Q000494:pharmacology*; D000818:Animals; D003345:Corticosterone / Q000097:blood; D003907:Dexamethasone / Q000494:pharmacology; D006984:Hypertrophy; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D000616:Aminoglutethimide; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone