title: A morphometric study of the reversal of ACTH-induced hypertrophy of rat adrenocortical cells after cessation of treatment.
abstract: The effect of a prolonged (7-day) ACTH administration on rat zona fasciculata cells and its reversal after cessation of treatment was investigated by morphometry. ACTH treatment caused a notable cell hypertrophy, which was mainly due to the increase in the volume of the mitochondrial compartment and to smooth endoplasmic reticulum (SER) proliferation, and a conspicuous rise in the basal level of corticosterone. After cessation of ACTH administration, rat zona fasciculata cells underwent a time-dependent atrophy, so that after 5 days they resembled those of control animals, and the blood concentration of corticosterone reverted to the base-line value. The cell atrophy was provoked by the decrease in the volumes of the mitochondrial compartment and SER, and was associated with a striking time-dependent accumulation of dense bodies. Stereology demonstrated that during the first two days after ACTH withdrawal the decrease of SER prevailed over that of the mitochondrial compartment, while the reverse occurred during the remaining three days. The increase in the volume of dense-body compartment, though largely due to the accumulation of residual bodies, was mainly coupled with a rise in the volume of the microautophagic-vacuole compartment during the first two days after ACTH cessation and with an increase in that of the macroautophagic-vacuole compartment during the following three days. The hypothesis is advanced that both micro- and macroautophagy play a role in the reversal of ACTH-induced hypertrophy of rat zona fasciculata cells after cessation of treatment, the first process being mainly involved in the elimination of SER, and the second one in the degradation of mitochondria.
authors.affiliation: Department of Anatomy, University of Padua, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Rebuffat
authors.forename: L
authors.initials: L
authors.lastname: Cavallini
authors.forename: A S
authors.initials: AS
authors.lastname: Belloni
authors.forename: G
authors.initials: G
authors.lastname: Mazzocchi
authors.forename: A
authors.initials: A
authors.lastname: Coi
authors.forename: G P
authors.initials: GP
authors.lastname: De Tos
authors.forename: G G
authors.initials: GG
authors.lastname: Nussdorfer
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000633:toxicity*; D000818:Animals; D006984:Hypertrophy; D008247:Lysosomes / Q000187:drug effects / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D008928:Mitochondria / Q000187:drug effects / Q000648:ultrastructure; D015388:Organelles / Q000187:drug effects / Q000648:ultrastructure*; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values; D014617:Vacuoles / Q000187:drug effects / Q000648:ultrastructure; D015383:Zona Fasciculata / Q000187:drug effects / Q000473:pathology* / Q000648:ultrastructure
chemical_list: D000324:Adrenocorticotropic Hormone