Pregled bibliografske jedinice broj: 339217
Reduced brain antioxidant capacity in rat models of betacytotoxic-induced experimental sporadic Alzheimer’ s disease and diabetes mellitus
Reduced brain antioxidant capacity in rat models of betacytotoxic-induced experimental sporadic Alzheimer’ s disease and diabetes mellitus // Neurochemical Research, 32 (2007), 10; 1709-1717 doi:10.1007/s11064-007-9410-1 (međunarodna recenzija, članak, znanstveni)
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Naslov
Reduced 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
Neurochemical Research (0364-3190) 32
(2007), 10;
1709-1717
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 (OS) plays a central role in 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 which antioxidant capacity (AC) against peroxyl (ORAC(-ROO) (*)) and hydroxyl (ORAC(-OH) (*)) free radicals (FR) was measured in three different brain regions: the hippocampus (HPC), the cerebellum (CB), and the brain stem (BS) by means of oxygen radical absorbance capacity (ORAC) assay. In the brain of both STZ-induced diabetic and STZ-icv treated rats decreased AC has been found demonstrating regionally specific distribution. In the diabetic rats these abnormalities were not associated with the development of peripheral diabetic neuropathy (PDN). Also, these abnormalities were not prevented by the intracerebroventricularly (icv) pretreatment of glucose transport inhibitor 5-thio-D: -glucose (TG) in the STZ-icv treated rats, suggesting different mechanism of STZ-induced central effects from those at the periphery. Similarities of the OS alterations in the brain of STZ-icv rats and humans with sAD could be useful in the search for the new drugs in the treatment of sAD that have antioxidant activity. In the STZ-induced diabetic animals the existence of PDN was tested by the paw pressure test, 3 weeks following the diabetes induction. Mechanical nociceptive thresholds were measured three times at 10-min intervals by applying increased pressure to the hind paw until the paw-withdrawal or overt struggling was elicited. Only those diabetic animals which demonstrated decreased withdrawal threshold values in comparison with the control non-diabetic animals (C) were considered to have developed the PDN.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti
Napomena
The paper is published in special issue dedicated to Dr. Moussa Youdim and has similarities with the paper Tahirević at al. J Neural Transm Suppl. 2007 ; (72):235-40. However, these two publications with overlaping results are published with the knowledge of editor.
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