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Selenium prevents cognitive decline and oxidative damage in rat model of streptozotocin-induced experimental dementia of Alzheimer's type.
Brain Res. 2009 Jul 24; 1281:117-27.BR

Abstract

Selenium (Se), a nutritionally essential trace element with known antioxidant potential, protects the brain from oxidative damage in various models of neurodegeneration. Intracerebroventricular-streptozotocin (ICV-STZ) in rats causes impairment of brain glucose and energy metabolism along with oxidative damage and cholinergic dysfunction, and provides a relevant model for sporadic dementia of Alzheimer's type (SDAT). The present study demonstrates the therapeutic efficacy of Se on cognitive deficits and oxidative damage in ICV-STZ in rats. Male Wistar rats were pre-treated with sodium selenite, a salt of Se (0.1 mg/kg; body weight) for 7 days and then were injected bilaterally with ICV-STZ (3 mg/kg), while sham rats received the same volume of vehicle. After two ICV-STZ infusions, rats were tested for memory deficits in passive avoidance and Morris water maze (MWM) tests and then were sacrificed for biochemical and histopathological assays. ICV-STZ-infused rats showed significant loss in learning and memory ability, which were significantly improved by Se supplementation. A significant increase in thio-barbituric acid reactive species (TBARS), protein carbonyl (PC) and a significant decrease in reduced glutathione (GSH), antioxidant enzymes (glutathione peroxidase [GPx] and glutathione reductase [GR]) and adenosine triphosphate (ATP) in the hippocampus and cerebral cortex and choline acetyltransferase (ChAT) in hippocampus were observed in ICV-STZ rats. Se supplementation significantly ameliorated all alterations induced by ICV-STZ in rats. Our study reveals that Se, as a powerful antioxidant, prevents cognitive deficits, oxidative damage and morphological changes in the ICV-STZ rats. Thus, it may have a therapeutic value for the treatment of SDAT.

Authors+Show Affiliations

Department of Medical Elementology and Toxicology, Neurotoxicology Laboratory, Jamia Hamdard (Hamdard University), New Delhi, India. tauheedarshi@gmail.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19374888

Citation

Ishrat, Tauheed, et al. "Selenium Prevents Cognitive Decline and Oxidative Damage in Rat Model of Streptozotocin-induced Experimental Dementia of Alzheimer's Type." Brain Research, vol. 1281, 2009, pp. 117-27.
Ishrat T, Parveen K, Khan MM, et al. Selenium prevents cognitive decline and oxidative damage in rat model of streptozotocin-induced experimental dementia of Alzheimer's type. Brain Res. 2009;1281:117-27.
Ishrat, T., Parveen, K., Khan, M. M., Khuwaja, G., Khan, M. B., Yousuf, S., Ahmad, A., Shrivastav, P., & Islam, F. (2009). Selenium prevents cognitive decline and oxidative damage in rat model of streptozotocin-induced experimental dementia of Alzheimer's type. Brain Research, 1281, 117-27. https://doi.org/10.1016/j.brainres.2009.04.010
Ishrat T, et al. Selenium Prevents Cognitive Decline and Oxidative Damage in Rat Model of Streptozotocin-induced Experimental Dementia of Alzheimer's Type. Brain Res. 2009 Jul 24;1281:117-27. PubMed PMID: 19374888.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Selenium prevents cognitive decline and oxidative damage in rat model of streptozotocin-induced experimental dementia of Alzheimer's type. AU - Ishrat,Tauheed, AU - Parveen,Kehkashan, AU - Khan,Mohd Moshahid, AU - Khuwaja,Gulrana, AU - Khan,M Badruzzaman, AU - Yousuf,Seema, AU - Ahmad,Ajmal, AU - Shrivastav,Pallavi, AU - Islam,Fakhrul, Y1 - 2009/04/15/ PY - 2009/01/05/received PY - 2009/04/02/revised PY - 2009/04/04/accepted PY - 2009/4/21/entrez PY - 2009/4/21/pubmed PY - 2009/10/1/medline SP - 117 EP - 27 JF - Brain research JO - Brain Res VL - 1281 N2 - Selenium (Se), a nutritionally essential trace element with known antioxidant potential, protects the brain from oxidative damage in various models of neurodegeneration. Intracerebroventricular-streptozotocin (ICV-STZ) in rats causes impairment of brain glucose and energy metabolism along with oxidative damage and cholinergic dysfunction, and provides a relevant model for sporadic dementia of Alzheimer's type (SDAT). The present study demonstrates the therapeutic efficacy of Se on cognitive deficits and oxidative damage in ICV-STZ in rats. Male Wistar rats were pre-treated with sodium selenite, a salt of Se (0.1 mg/kg; body weight) for 7 days and then were injected bilaterally with ICV-STZ (3 mg/kg), while sham rats received the same volume of vehicle. After two ICV-STZ infusions, rats were tested for memory deficits in passive avoidance and Morris water maze (MWM) tests and then were sacrificed for biochemical and histopathological assays. ICV-STZ-infused rats showed significant loss in learning and memory ability, which were significantly improved by Se supplementation. A significant increase in thio-barbituric acid reactive species (TBARS), protein carbonyl (PC) and a significant decrease in reduced glutathione (GSH), antioxidant enzymes (glutathione peroxidase [GPx] and glutathione reductase [GR]) and adenosine triphosphate (ATP) in the hippocampus and cerebral cortex and choline acetyltransferase (ChAT) in hippocampus were observed in ICV-STZ rats. Se supplementation significantly ameliorated all alterations induced by ICV-STZ in rats. Our study reveals that Se, as a powerful antioxidant, prevents cognitive deficits, oxidative damage and morphological changes in the ICV-STZ rats. Thus, it may have a therapeutic value for the treatment of SDAT. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/19374888/Selenium_prevents_cognitive_decline_and_oxidative_damage_in_rat_model_of_streptozotocin_induced_experimental_dementia_of_Alzheimer's_type_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(09)00732-X DB - PRIME DP - Unbound Medicine ER -