BRAIN ANTIOXIDANT CAPACITY IN RAT MODELS OF BETACYTOTOXIC-INDUCED EXPERIMENTAL SPORADIC ALZHEIMER'S DISEASE AND DIABETES MELLITUS I. Tahirovic 1 , E. Sofic 1 , A. Sapcanin 1 , I. Gavrankapetanovic 2 , l. Bach-Rojecky 3 M. Salkovic-Petrisic 4 , Z. Lackovic 4 , S. Hoyer 5 , P. Riederer 6 1 Department of Chemistry, Faculty of Science, University of Sarajevo, Sarajevo, Bosnia and Herzegovina 2 School of Medicine, University of Sarajevo, Sarajevo, Bosnia and Herzegovina 3 Department of Pharmacology, School of Pharmacy and Biochemistry, University of Zagreb, Zagreb, Croatia 4 Department of Pharmacology and Croatian Institute for Brain Research, School of Medicine, University of Zagreb, Zagreb, Croatia 5 Department of Pathology, University Clinic, University of Heidelberg, Heidelberg, Germany 6 Clinical Neurochemistry, Clinic and Policlinic for Psychiatry, University of Wuerzburg, Wuerzburg, Germany Summary COMMENT: I had to re-write the Summary, please check if everything is OK and maybe add some more «oxidative stress-related» data. Oxidative stress 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 Alzhmeimer's disease (sAD). Representative experimental models of these diseases are streptozotocin (STZ)- induced diabetic rats and STZ-intracerebroventricularly (STZ-icv) treated rats, repsectively, in which antioxidative capacity (AC) against peroxyl (ORAC -ROO ) and hydroxyl (ORAC -OH ) free radicals 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 AC against the particular free radical has been found demonstrating regionally specific distribution. In the diabetic rats these abnormalities were not depenedent on 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 of STZ-induced central effects from those at the periphery. Similarities of the oxidative stress 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.
Introduction COMMENT: I think that it is important to give a background that would suggest relationship between all these models, diabetic and «cerebrally diabetic» ones. In line with that I completely rearranged the Introduction. However, although I did my best and wrote some general things, I am complete ingnorat regarding the oxidative stress, free radicals and antioxidative capacity, therefore, this issue should be inserted in the Introduction by those who are familiar with the topic.
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- Summer '07
- Diabetes, Blood sugar, oxidative stress, Diabetic neuropathy