Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activation.
In near-physiological concentrations, glucocorticoid hormones cause the death of several types of normal and neoplastic lymphoid cell, but the mechanisms involved are unknown. One of the earliest structural changes in the dying cell is widespread chromatin condensation, of the type characteristic of apoptosis, the mode of death frequently observed where cell deletion seems to be 'programmed'. It is shown here that this morphological change is closely associated with excision of nucleosome chains from nuclear chromatin, apparently through activation of an intracellular, but non-lysosomal, endonuclease.
D000818:Animals; D002843:Chromatin / Q000187:drug effects* / Q000648:ultrastructure; D003851:Deoxyribonucleases / Q000378:metabolism; D004720:Endonucleases / Q000378:metabolism*; D008775:Methylprednisolone / Q000031:analogs & derivatives*; D008776:Methylprednisolone Hemisuccinate / Q000494:pharmacology*; D008970:Molecular Weight; D009707:Nucleosomes / Q000378:metabolism; D051381:Rats; D013950:Thymus Gland / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology
D002843:Chromatin; D009707:Nucleosomes; D008776:Methylprednisolone Hemisuccinate; D003851:Deoxyribonucleases; D004720:Endonucleases; D008775:Methylprednisolone