Selenium plays a modulatory role against cerebral ischemia-induced neuronal damage in rat hippocampus

Seema Yousuf, Fahim Atif, Muzamil Ahmad, Md Nasrul Hoda, M. Badruzzaman Khan, Tauheed Ishrat, Fakhrul Islam

Research output: Contribution to journalArticle

54 Citations (Scopus)

Abstract

During cerebral ischemic cascade, a unifying factor which leads to mitochondrial dysfunctions is lack of oxygen followed by decrease in ATP production. The present study demonstrates the effect of selenium pretreatment (0.1 mg/kg as sodium selenite, i.p, 7 days) on cerebral ischemia-induced altered levels of mitochondrial ATP content, intracellular calcium (Cai 2+) in synaptosomes, expression of heat stress protein (Hsp70) and caspase-3 activity in hippocampus followed by neurobehavioral deficits and histopathological changes in Wistar rats. Cerebral ischemia was induced for 2 h followed by reperfusion for 22 h. It was observed that levels of (Cai 2+), Hsp70 and caspase-3 activity were significantly (p < 0.01-0.001) higher with a marked decrease in ATP level in hippocampus of ischemic group as compared to sham values. Subsequently, a marked change was observed in neurobehavioral activities in ischemic animals as compared to control one. As a result of selenium pretreatment, a significant (p < 0.05-0.001) trend of restoration was observed in the level of ATP, (Cai 2+), Hsp70, caspase-3 and behavioral outputs as compared to ischemic group. Histopathological analysis confirmed the protective effect of selenium against cerebral ischemia induced histological alterations as evidenced by lesser edema formation and separation of cells with minimal microglial cell infiltration in selenium pretreated group as compared to ischemic animals. The present study suggests that selenium may be able to salvage the ischemic penumbral zone neurons, thereby limiting ischemic cell death.

Original languageEnglish (US)
Pages (from-to)218-225
Number of pages8
JournalBrain Research
Volume1147
Issue number1
DOIs
StatePublished - May 25 2007
Externally publishedYes

Fingerprint

Selenium
Brain Ischemia
Hippocampus
Adenosine Triphosphate
Caspase 3
Sodium Selenite
Synaptosomes
Cell Separation
Heat-Shock Proteins
Reperfusion
Wistar Rats
Edema
Cell Death
Hot Temperature
Oxygen
Calcium
Neurons

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

Cite this

Selenium plays a modulatory role against cerebral ischemia-induced neuronal damage in rat hippocampus. / Yousuf, Seema; Atif, Fahim; Ahmad, Muzamil; Nasrul Hoda, Md; Badruzzaman Khan, M.; Ishrat, Tauheed; Islam, Fakhrul.

In: Brain Research, Vol. 1147, No. 1, 25.05.2007, p. 218-225.

Research output: Contribution to journalArticle

Yousuf, S, Atif, F, Ahmad, M, Nasrul Hoda, M, Badruzzaman Khan, M, Ishrat, T & Islam, F 2007, 'Selenium plays a modulatory role against cerebral ischemia-induced neuronal damage in rat hippocampus', Brain Research, vol. 1147, no. 1, pp. 218-225. https://doi.org/10.1016/j.brainres.2007.01.143
Yousuf, Seema ; Atif, Fahim ; Ahmad, Muzamil ; Nasrul Hoda, Md ; Badruzzaman Khan, M. ; Ishrat, Tauheed ; Islam, Fakhrul. / Selenium plays a modulatory role against cerebral ischemia-induced neuronal damage in rat hippocampus. In: Brain Research. 2007 ; Vol. 1147, No. 1. pp. 218-225.
@article{39a509ea725c4d439d89193f55a7f8c9,
title = "Selenium plays a modulatory role against cerebral ischemia-induced neuronal damage in rat hippocampus",
abstract = "During cerebral ischemic cascade, a unifying factor which leads to mitochondrial dysfunctions is lack of oxygen followed by decrease in ATP production. The present study demonstrates the effect of selenium pretreatment (0.1 mg/kg as sodium selenite, i.p, 7 days) on cerebral ischemia-induced altered levels of mitochondrial ATP content, intracellular calcium (Cai 2+) in synaptosomes, expression of heat stress protein (Hsp70) and caspase-3 activity in hippocampus followed by neurobehavioral deficits and histopathological changes in Wistar rats. Cerebral ischemia was induced for 2 h followed by reperfusion for 22 h. It was observed that levels of (Cai 2+), Hsp70 and caspase-3 activity were significantly (p < 0.01-0.001) higher with a marked decrease in ATP level in hippocampus of ischemic group as compared to sham values. Subsequently, a marked change was observed in neurobehavioral activities in ischemic animals as compared to control one. As a result of selenium pretreatment, a significant (p < 0.05-0.001) trend of restoration was observed in the level of ATP, (Cai 2+), Hsp70, caspase-3 and behavioral outputs as compared to ischemic group. Histopathological analysis confirmed the protective effect of selenium against cerebral ischemia induced histological alterations as evidenced by lesser edema formation and separation of cells with minimal microglial cell infiltration in selenium pretreated group as compared to ischemic animals. The present study suggests that selenium may be able to salvage the ischemic penumbral zone neurons, thereby limiting ischemic cell death.",
author = "Seema Yousuf and Fahim Atif and Muzamil Ahmad and {Nasrul Hoda}, Md and {Badruzzaman Khan}, M. and Tauheed Ishrat and Fakhrul Islam",
year = "2007",
month = "5",
day = "25",
doi = "10.1016/j.brainres.2007.01.143",
language = "English (US)",
volume = "1147",
pages = "218--225",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - Selenium plays a modulatory role against cerebral ischemia-induced neuronal damage in rat hippocampus

AU - Yousuf, Seema

AU - Atif, Fahim

AU - Ahmad, Muzamil

AU - Nasrul Hoda, Md

AU - Badruzzaman Khan, M.

AU - Ishrat, Tauheed

AU - Islam, Fakhrul

PY - 2007/5/25

Y1 - 2007/5/25

N2 - During cerebral ischemic cascade, a unifying factor which leads to mitochondrial dysfunctions is lack of oxygen followed by decrease in ATP production. The present study demonstrates the effect of selenium pretreatment (0.1 mg/kg as sodium selenite, i.p, 7 days) on cerebral ischemia-induced altered levels of mitochondrial ATP content, intracellular calcium (Cai 2+) in synaptosomes, expression of heat stress protein (Hsp70) and caspase-3 activity in hippocampus followed by neurobehavioral deficits and histopathological changes in Wistar rats. Cerebral ischemia was induced for 2 h followed by reperfusion for 22 h. It was observed that levels of (Cai 2+), Hsp70 and caspase-3 activity were significantly (p < 0.01-0.001) higher with a marked decrease in ATP level in hippocampus of ischemic group as compared to sham values. Subsequently, a marked change was observed in neurobehavioral activities in ischemic animals as compared to control one. As a result of selenium pretreatment, a significant (p < 0.05-0.001) trend of restoration was observed in the level of ATP, (Cai 2+), Hsp70, caspase-3 and behavioral outputs as compared to ischemic group. Histopathological analysis confirmed the protective effect of selenium against cerebral ischemia induced histological alterations as evidenced by lesser edema formation and separation of cells with minimal microglial cell infiltration in selenium pretreated group as compared to ischemic animals. The present study suggests that selenium may be able to salvage the ischemic penumbral zone neurons, thereby limiting ischemic cell death.

AB - During cerebral ischemic cascade, a unifying factor which leads to mitochondrial dysfunctions is lack of oxygen followed by decrease in ATP production. The present study demonstrates the effect of selenium pretreatment (0.1 mg/kg as sodium selenite, i.p, 7 days) on cerebral ischemia-induced altered levels of mitochondrial ATP content, intracellular calcium (Cai 2+) in synaptosomes, expression of heat stress protein (Hsp70) and caspase-3 activity in hippocampus followed by neurobehavioral deficits and histopathological changes in Wistar rats. Cerebral ischemia was induced for 2 h followed by reperfusion for 22 h. It was observed that levels of (Cai 2+), Hsp70 and caspase-3 activity were significantly (p < 0.01-0.001) higher with a marked decrease in ATP level in hippocampus of ischemic group as compared to sham values. Subsequently, a marked change was observed in neurobehavioral activities in ischemic animals as compared to control one. As a result of selenium pretreatment, a significant (p < 0.05-0.001) trend of restoration was observed in the level of ATP, (Cai 2+), Hsp70, caspase-3 and behavioral outputs as compared to ischemic group. Histopathological analysis confirmed the protective effect of selenium against cerebral ischemia induced histological alterations as evidenced by lesser edema formation and separation of cells with minimal microglial cell infiltration in selenium pretreated group as compared to ischemic animals. The present study suggests that selenium may be able to salvage the ischemic penumbral zone neurons, thereby limiting ischemic cell death.

UR - http://www.scopus.com/inward/record.url?scp=34147152673&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34147152673&partnerID=8YFLogxK

U2 - 10.1016/j.brainres.2007.01.143

DO - 10.1016/j.brainres.2007.01.143

M3 - Article

VL - 1147

SP - 218

EP - 225

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1

ER -