title: Serum amyloid P component induces TUNEL-positive nuclei in rat brain after intrahippocampal administration.
abstract: Serum amyloid P component (SAP)-induced neuronal apoptosis has been demonstrated on the primary culture of embryonic rat cerebral cortex in vitro. Here we present pieces of evidence that cell death is also induced by serum amyloid P component in living rat brain similarly to that in cell culture. Intrahippocampally administered SAP diffuses from the site of injection to the cortical and subcortical area of the rat brain and enters the cells of brain tissue in 1 week. It induces elevation of the number of in situ TdT-mediated dUTP-X nick end-labeled nuclei in the hippocampus, cortex and subcortical structures of rat central nervous system. DNA fragmentation, which is detected by the end labeling reaction, is characteristic to apoptosis. It develops in 4 weeks following exposure. Apoptosis is an important form of cell death in different neurodegenerative diseases including Alzheimer's disease. Our present work reveals that apoptosis can be induced by SAP beyond other hitherto known apoptosis inducing components of neurodegeneration. Hereby SAP seems to be an important component of the process, which leads to expanded neuronal loss in the pathomechanism of neurodegenerative diseases.
authors.affiliation: Pharmacological and Drug Safety Research, Gedeon Richter Plc., POB 27, H-1475 Budapest 10, Hungary. z.urbanyi@richter.hu
authors.forename: Zoltán
authors.initials: Z
authors.lastname: Urbányi
authors.forename: Miklós
authors.initials: M
authors.lastname: Sass
authors.forename: Judit
authors.initials: J
authors.lastname: Laszy
authors.forename: Viktor
authors.initials: V
authors.lastname: Takács
authors.forename: István
authors.initials: I
authors.lastname: Gyertyán
authors.forename: Tamás
authors.initials: T
authors.lastname: Pázmány
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D053938:DNA Fragmentation / Q000187:drug effects; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D020287:In Situ Nick-End Labeling; D008297:Male; D009410:Nerve Degeneration / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D019636:Neurodegenerative Diseases / Q000378:metabolism / Q000503:physiopathology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D009498:Neurotoxins / Q000378:metabolism* / Q000633:toxicity; D058225:Plaque, Amyloid / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D000683:Serum Amyloid P-Component / Q000378:metabolism* / Q000633:toxicity; D013997:Time Factors
chemical_list: D009498:Neurotoxins; D000683:Serum Amyloid P-Component