Investigations on the turnover of adrenocortical mitochondria. XII. Studies on the mechanism of the ACTH-induced elongation of the half-life of rat zona fasciculata mitochondria.
The half-life of rat adrenocortical mitochondria was determined by high resolution autoradiography and liquid scintillation spectroscopy as previously described (Mazzocchi et al., '76). The results obtained by the two approaches were in good agreement. In the normal rats the half-life of adrenocortical mitochondria averaged 11 days. ACTH significantly increased mitochondrial half-life to about 16 days, and chloramphenicol significantly decreased this parameter in both untreated and ACTH-administered rats to about seven days. It is suggested that the ACTH-induced maintenance and slowing down of the degradation rate of adrenocortical mitochondria requires continuous mitochondrial DNA-dependent protein synthesis.
D000302:Adrenal Cortex / Q000648:ultrastructure*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology* / Q000502:physiology; D000818:Animals; D001345:Autoradiography; D002470:Cell Survival; D004247:DNA / Q000096:biosynthesis; D006207:Half-Life; D008297:Male; D008928:Mitochondria / Q000254:growth & development*; D014176:Protein Biosynthesis; D051381:Rats
D000324:Adrenocorticotropic Hormone; D004247:DNA