Pregled bibliografske jedinice broj: 339146
Brain antioxidant capacity in rat models of betacytotoxic-induced experimental sporadic Alzheimer's disease and diabetes mellitus
Brain antioxidant capacity in rat models of betacytotoxic-induced experimental sporadic Alzheimer's disease and diabetes mellitus // Journal of Neural Transmission. Supplementum, 2007 (2007), Suppl. 72; 235-240 (međunarodna recenzija, članak, znanstveni)
CROSBI ID: 339146 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
Brain antioxidant capacity in rat models of betacytotoxic-induced experimental sporadic Alzheimer's disease and diabetes mellitus
Autori
Tahirović, Ismet ; Sofić, Emin ; Šapčanin, Aida ; Gavrankapetanović, Ismet ; Bach-Rojecky, Lidija ; Šalković-Petrišić, Melita ; Lacković, Zdravko ; Hoyer, Siegfried ; Riederer, Peter
Izvornik
Journal of Neural Transmission. Supplementum (0303-6995) 2007
(2007), Suppl. 72;
235-240
Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni
Ključne riječi
Rat; Streptozotocin; Diabetes Mellitus; Antioxidant Capacity; Oxidative Stress
Sažetak
It is believed that oxidative stress plays a central role ini the pathogenesis of metabolic diseases like diabetes mellitus (DM) and its complications (like peripheral neuropathy) as well as in neurodegenerative disorders like sporadic Alzheimer's disease (sAD). Representative experimental models of these diseases are streptozotocin (STZ)-induced diabetic rats and STZ-intracerebroventricularly (STZ-icv) treated rats, in whichantioxidant caoacity against peroxyl (ORAC-ROO*) and hydroxyl (ORAC-OH*) free radical was measured in three different brain regions (hippocampus, cerebellum, and brain stem) by means of oxygen radical absorbance capacity (ORAC) assay. in the brain of both STZ-induced diabetic and STZ-icv treated rats decreased antioxidant capacity has been found demonstrating regionally specific distribution. In the diabetic rats these abnormalities were not associated with the development of peripheral diabetic neuropathy. Also, these abnormalities were not prevented by the icv pretreatment of glucose transport inhibitor 5-thio-D-glucose in the STZ-icv treated rats, suggesting different mechanism for STZ-induced central effects from those at the periphery. Similarities in the oxidative stress alterations in the brain of STZ-icv rats and humans with sAD could be useful in the search for new drugs in the treatment of sAD that have antioxidant activity.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti
Napomena
Rad je sličan prvotno objavljenom radu Tahirovic et al., Neurochemical Res 2007 ; 32:1709-1717, a objavljen je uz dozvolu ko-autora i glavnog urednika J Neural Transm.
POVEZANOST RADA
Projekti:
108-1080003-0001 - NEUROTRANSMITORI I NOVI MEHANIZMI DJELOVANJA LIJEKOVA I OTROVA (Lackovic, Zdravko, MZOS ) ( CroRIS)
108-1080003-0020 - Mozak, eksperimentalni i cerebralni dijabetes i kognitivni i drugi poremećaji (Šalković-Petrišić, Melita, MZOS ) ( CroRIS)
Ustanove:
Medicinski fakultet, Zagreb
Citiraj ovu publikaciju:
Časopis indeksira:
- Current Contents Connect (CCC)
- Web of Science Core Collection (WoSCC)
- Science Citation Index Expanded (SCI-EXP)
- SCI-EXP, SSCI i/ili A&HCI
- Scopus
- MEDLINE