Restraint stress-induced oxidative damage and its amelioration with selenium

Fahim Atif, Seema Yousuf, Sandeep Kumar Agrawal

Research output: Contribution to journalArticle

50 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)59-63
Number of pages5
JournalEuropean Journal of Pharmacology
Volume600
Issue number1-3
DOIs
StatePublished - Dec 14 2008

Fingerprint

Selenium
Oxidative Stress
Frontal Lobe
Hippocampus
Lipid Peroxidation
Glutathione Reductase
Antioxidants
Glutathione Peroxidase
Glutathione Transferase
Catalase
Enzymes
Sodium Selenite
Brain
Free Radicals
Glutathione
Homeostasis

Keywords

  • Oxidative stress
  • Restraint stress
  • Selenium

ASJC Scopus subject areas

  • Pharmacology

Cite this

Restraint stress-induced oxidative damage and its amelioration with selenium. / Atif, Fahim; Yousuf, Seema; Agrawal, Sandeep Kumar.

In: European Journal of Pharmacology, Vol. 600, No. 1-3, 14.12.2008, p. 59-63.

Research output: Contribution to journalArticle

@article{df842744f7ce4e2ea7f23a13458c7b13,
title = "Restraint stress-induced oxidative damage and its amelioration with selenium",
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.",
keywords = "Oxidative stress, Restraint stress, Selenium",
author = "Fahim Atif and Seema Yousuf and Agrawal, {Sandeep Kumar}",
year = "2008",
month = "12",
day = "14",
doi = "10.1016/j.ejphar.2008.09.029",
language = "English (US)",
volume = "600",
pages = "59--63",
journal = "European Journal of Pharmacology",
issn = "0014-2999",
publisher = "Elsevier",
number = "1-3",

}

TY - JOUR

T1 - Restraint stress-induced oxidative damage and its amelioration with selenium

AU - Atif, Fahim

AU - Yousuf, Seema

AU - Agrawal, Sandeep Kumar

PY - 2008/12/14

Y1 - 2008/12/14

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.

AB - 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.

KW - Oxidative stress

KW - Restraint stress

KW - Selenium

UR - http://www.scopus.com/inward/record.url?scp=55949086831&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=55949086831&partnerID=8YFLogxK

U2 - 10.1016/j.ejphar.2008.09.029

DO - 10.1016/j.ejphar.2008.09.029

M3 - Article

VL - 600

SP - 59

EP - 63

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

IS - 1-3

ER -