PMID- 17605105
OWN - NLM
STAT- MEDLINE
DCOM- 20071120
LR  - 20220223
IS  - 0364-3190 (Print)
IS  - 0364-3190 (Linking)
VI  - 32
IP  - 10
DP  - 2007 Oct
TI  - Reduced brain antioxidant capacity in rat models of betacytotoxic-induced 
      experimental sporadic Alzheimer's disease and diabetes mellitus.
PG  - 1709-17
AB  - 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.
FAU - Tahirovic, Ismet
AU  - Tahirovic I
AD  - Department of Chemistry, Faculty of Science, University of Sarajevo, Zmaja od 
      Bosne 35, 71 000, Sarajevo, Bosnia and Herzegovina
FAU - Sofic, Emin
AU  - Sofic E
FAU - Sapcanin, Aida
AU  - Sapcanin A
FAU - Gavrankapetanovic, Ismet
AU  - Gavrankapetanovic I
FAU - Bach-Rojecky, Lidija
AU  - Bach-Rojecky L
FAU - Salkovic-Petrisic, Melita
AU  - Salkovic-Petrisic M
FAU - Lackovic, Zdravko
AU  - Lackovic Z
FAU - Hoyer, Siegfried
AU  - Hoyer S
FAU - Riederer, Peter
AU  - Riederer P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070629
PL  - United States
TA  - Neurochem Res
JT  - Neurochemical research
JID - 7613461
RN  - 0 (Antibiotics, Antineoplastic)
RN  - 0 (Antioxidants)
RN  - 0 (Free Radicals)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Peroxides)
RN  - 0 (Reactive Oxygen Species)
RN  - 3352-57-6 (Hydroxyl Radical)
RN  - 5W494URQ81 (Streptozocin)
SB  - IM
MH  - Alzheimer Disease/*chemically induced/*metabolism
MH  - Animals
MH  - Antibiotics, Antineoplastic/administration & dosage
MH  - Antioxidants/*metabolism
MH  - Brain Chemistry/*physiology
MH  - Diabetes Mellitus, Experimental/*chemically induced/metabolism
MH  - Diabetic Neuropathies/metabolism/pathology
MH  - Free Radicals/metabolism
MH  - Hydroxyl Radical/metabolism
MH  - Injections, Intraventricular
MH  - Insulin-Secreting Cells/drug effects/*physiology
MH  - Male
MH  - Nerve Tissue Proteins/metabolism
MH  - Oxidative Stress/*physiology
MH  - Pain Measurement/drug effects
MH  - Peroxides/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Reactive Oxygen Species/metabolism
MH  - Streptozocin/administration & dosage
EDAT- 2007/07/03 09:00
MHDA- 2007/12/06 09:00
CRDT- 2007/07/03 09:00
PHST- 2007/03/02 00:00 [received]
PHST- 2007/06/07 00:00 [accepted]
PHST- 2007/07/03 09:00 [pubmed]
PHST- 2007/12/06 09:00 [medline]
PHST- 2007/07/03 09:00 [entrez]
AID - 10.1007/s11064-007-9410-1 [doi]
PST - ppublish
SO  - Neurochem Res. 2007 Oct;32(10):1709-17. doi: 10.1007/s11064-007-9410-1. Epub 2007 
      Jun 29.