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Restraint stress-induced oxidative damage and its amelioration with selenium.
Eur J Pharmacol. 2008 Dec 14; 600(1-3):59-63.EJ

Abstract

Stress is a state of threatened cellular homeostasis which results in free radical generations and subsequent oxidative damage. The aim of this study was to evaluate the effect of selenium on restraint stress-induced oxidative damage in hippocampus, striatum and frontal cortex. Rats were pre-treated with sodium selenite (0.3 mg/kg; intraperitoneally) for 15 days and divided into six groups (n=8). Rats were then subjected to restraint stress for 1 h and 4 h. Lipid peroxidation, glutathione (GSH) and activities of antioxidant enzymes viz. selenium-dependent glutathione peroxidase (Se-GPx), glutathione reductase (GR), glutathione S-transferase (GST) and catalase were evaluated in the frontal cortex, striatum and hippocampus. Restraint stress-induced for 1 h and 4 h caused a significant decrease (P<0.001) in intracellular GSH content and the activity of Se-GPx, GR, GST and catalase with a significant increase (P<0.001) in the level of lipid peroxidation in all 3 regions of the brain. Selenium pre-treatment exhibited restoration of antioxidant enzymes activity, GSH content and decrease in the level of lipid peroxidation in hippocampus, striatum and frontal cortex in both 1 h and 4 h restraint stress groups. Protective effect of selenium pre-treatment was found to be more pronounced in 4 h restraint stress group as compared to 1 h restraint stress group. Selenium per se had no effect on GSH, lipid peroxidation level or activities of antioxidant enzymes in hippocampus, striatum and frontal cortex. In conclusion, selenium pre-treatment protected the brain against restraint stress-induced oxidative damage at 4 h in hippocampus, striatum and frontal cortex.

Authors+Show Affiliations

Department of Surgery, Section of Neurosurgery, University of Nebraska Medical Center, Omaha, Nebraska 68198-6250 USA. atiftox@yahoo.comNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18854182

Citation

Atif, Fahim, et al. "Restraint Stress-induced Oxidative Damage and Its Amelioration With Selenium." European Journal of Pharmacology, vol. 600, no. 1-3, 2008, pp. 59-63.
Atif F, Yousuf S, Agrawal SK. Restraint stress-induced oxidative damage and its amelioration with selenium. Eur J Pharmacol. 2008;600(1-3):59-63.
Atif, F., Yousuf, S., & Agrawal, S. K. (2008). Restraint stress-induced oxidative damage and its amelioration with selenium. European Journal of Pharmacology, 600(1-3), 59-63. https://doi.org/10.1016/j.ejphar.2008.09.029
Atif F, Yousuf S, Agrawal SK. Restraint Stress-induced Oxidative Damage and Its Amelioration With Selenium. Eur J Pharmacol. 2008 Dec 14;600(1-3):59-63. PubMed PMID: 18854182.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Restraint stress-induced oxidative damage and its amelioration with selenium. AU - Atif,Fahim, AU - Yousuf,Seema, AU - Agrawal,Sandeep K, Y1 - 2008/09/30/ PY - 2008/03/30/received PY - 2008/09/02/revised PY - 2008/09/18/accepted PY - 2008/10/16/pubmed PY - 2009/3/28/medline PY - 2008/10/16/entrez SP - 59 EP - 63 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 600 IS - 1-3 N2 - Stress is a state of threatened cellular homeostasis which results in free radical generations and subsequent oxidative damage. The aim of this study was to evaluate the effect of selenium on restraint stress-induced oxidative damage in hippocampus, striatum and frontal cortex. Rats were pre-treated with sodium selenite (0.3 mg/kg; intraperitoneally) for 15 days and divided into six groups (n=8). Rats were then subjected to restraint stress for 1 h and 4 h. Lipid peroxidation, glutathione (GSH) and activities of antioxidant enzymes viz. selenium-dependent glutathione peroxidase (Se-GPx), glutathione reductase (GR), glutathione S-transferase (GST) and catalase were evaluated in the frontal cortex, striatum and hippocampus. Restraint stress-induced for 1 h and 4 h caused a significant decrease (P<0.001) in intracellular GSH content and the activity of Se-GPx, GR, GST and catalase with a significant increase (P<0.001) in the level of lipid peroxidation in all 3 regions of the brain. Selenium pre-treatment exhibited restoration of antioxidant enzymes activity, GSH content and decrease in the level of lipid peroxidation in hippocampus, striatum and frontal cortex in both 1 h and 4 h restraint stress groups. Protective effect of selenium pre-treatment was found to be more pronounced in 4 h restraint stress group as compared to 1 h restraint stress group. Selenium per se had no effect on GSH, lipid peroxidation level or activities of antioxidant enzymes in hippocampus, striatum and frontal cortex. In conclusion, selenium pre-treatment protected the brain against restraint stress-induced oxidative damage at 4 h in hippocampus, striatum and frontal cortex. SN - 1879-0712 UR - https://www.unboundmedicine.com/medline/citation/18854182/Restraint_stress_induced_oxidative_damage_and_its_amelioration_with_selenium_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(08)00964-3 DB - PRIME DP - Unbound Medicine ER -