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Pregled bibliografske jedinice broj: 328484

Časopis

Autori: Diana, Andrea; Šimić, Goran; Sinforiani, Elena; Orrù, Nicola; Pichiri, Giuseppina; Bono, Giorgio
Naslov: Mitochondria morphology and DNA content upon sublethal exposure to beta-amyloid 1-42 peptide
Izvornik: Collegium Antropologicum (0350-6134) 32 (2008), S1; 51-58
Vrsta rada: članak
Ključne riječi: amyloid toxicity; mitochondrial DNA; neuroblastoma cell culture; oxidative stress
Sažetak:
Brains affected by Alzheimer's disease (AD) show a large spectrum of mitochondrial alterations at both morphological and genetic level. The causal link between amyloid beta peptides (A beta) and mitochondrial dysfunction has been established in cellular models of AD using A beta concentrations capable of triggering massive neuronal death. However, mitochondrial changes related to sublethal exposure to A beta are less known. Here we show that subtoxic, 1 micromolar A beta(1-42) exposure does not change the mitochondrial shape of living cells, as visualized upon the uptake of the non-potentiometric fluorescent probe Mitotracker Green and enhanced yellow fluorescent protein (EYFP)-tagged cytochrome c oxidase expression. Immunolocalization of oxidative adducts 8-hydroxy-2'-deoxyguanosine, 8-hydroxyguanine and 8-hydroxyguanosine demonstrates that one-micromolar concentration of A beta(1-42) is also not sufficient to elicit dramatic qualitative changes in the RNA/DNA oxidative products. However, in comparison with controls, semi-quantitative analysis of the overall mitochondrial mass by integrated fluorescence intensity reveals an ongoing down-regulation in mitochondrial biosynthesis or, conversely, an enhanced autophagic demise of A beta treated cells. Furthermore, a significant increase of the full-length mitochondrial DNA (mtDNA) from A beta-treated versus control cells is found, as measured by long range polymerase chain reaction (PCR). Such up-regulation is accompanied by extensive fragmentation of the unamplified mtDNA, probably due to the detrimental effect of A beta. We interpret these results as a sequence of compensatory responses induced by mtDNA damage, which are devoted to repression of oxidative burst. In conclusion, our findings suggest that early therapeutic interventions aimed at prevention of mitochondrial oxidative damage may delay AD progression and help in treating AD patients.
Projekt / tema: 108-1081870-1942
Izvorni jezik: ENG
Rad je citiran u
bazama podataka:
Web of Science: Science Citation
Current Contents Citation Index
Web of Science: Social Science Citation Index
MEDLINE
Scopus
Kategorija: Znanstveni
Znanstvena područja:
Temeljne medicinske znanosti,Kliničke medicinske znanosti,Psihologija
URL Internet adrese: http://hrcak.srce.hr/index.php?show=clanak&id_clanak_jezik=38679
http://dementia.hiim.hr/2008%20CollAntropol%202.pdf
URL cjelovitog teksta:
Google Scholar: Mitochondria morphology and DNA content upon sublethal exposure to beta-amyloid 1-42 peptide
Upisao u CROSBI: Goran Šimić (), 11. Tra. 2008. u 11:20 sati



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