Abstract
CNS trauma has been associated with an increase in free radical production, but the cellular sources of this increase or the mechanism involved in the production of free radicals are not known. We, therefore, investigated the effects of trauma on free radical production in cultured neurons, astrocytes and BV-2 microglial cells. Free radicals were measured with the fluorescent dye DCFDA following in vitro trauma. At 30 and 60 min following trauma, there was a 132% and 64% increase, respectively, in free radical production in neurons when compared to controls. In astrocytes, there was a 94% and 133% increase at 30 and 60 min, respectively. Microglial cells, however, displayed no significant increase in free radicals at 30, 60 or 120 min following trauma. Since trauma can induce the mitochondrial permeability transition (MPT), a process associated with mitochondrial dysfunction, we further investigated whether cyclosporin A (CsA), an agent known to block the MPT, could prevent free radical formation following trauma. In neurons CsA did not block free radical production at 30 min but blocked it by 90% at 60 min. In contrast, in astrocytes CsA completely blocked free radical production at 30 min but did not block it at 60 min. Our results indicate that a differential sensitivity to trauma-induced free radical production exists in neural cells; that the MPT may be involved in the production of free radical post-trauma; and that the CsA-sensitive phase of free radical production is different in neurons and astrocytes.
| Original language | English |
|---|---|
| Pages (from-to) | 161-166 |
| Number of pages | 6 |
| Journal | Neurochemical Research |
| Volume | 27 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - Apr 3 2002 |
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Keywords
- Astrocytes
- CNS trauma
- Cyclosporin A
- Free radicals
- Microglia
- Mitochondrial permeability transition
- Neurons
ASJC Scopus subject areas
- Neuroscience(all)
- Biochemistry
Cite this
Differential response of neural cells to trauma-induced free radical production in vitro. / Panickar, K. S.; Jayakumar, A. R.; Norenberg, Michael D.
In: Neurochemical Research, Vol. 27, No. 1-2, 03.04.2002, p. 161-166.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Differential response of neural cells to trauma-induced free radical production in vitro
AU - Panickar, K. S.
AU - Jayakumar, A. R.
AU - Norenberg, Michael D
PY - 2002/4/3
Y1 - 2002/4/3
N2 - CNS trauma has been associated with an increase in free radical production, but the cellular sources of this increase or the mechanism involved in the production of free radicals are not known. We, therefore, investigated the effects of trauma on free radical production in cultured neurons, astrocytes and BV-2 microglial cells. Free radicals were measured with the fluorescent dye DCFDA following in vitro trauma. At 30 and 60 min following trauma, there was a 132% and 64% increase, respectively, in free radical production in neurons when compared to controls. In astrocytes, there was a 94% and 133% increase at 30 and 60 min, respectively. Microglial cells, however, displayed no significant increase in free radicals at 30, 60 or 120 min following trauma. Since trauma can induce the mitochondrial permeability transition (MPT), a process associated with mitochondrial dysfunction, we further investigated whether cyclosporin A (CsA), an agent known to block the MPT, could prevent free radical formation following trauma. In neurons CsA did not block free radical production at 30 min but blocked it by 90% at 60 min. In contrast, in astrocytes CsA completely blocked free radical production at 30 min but did not block it at 60 min. Our results indicate that a differential sensitivity to trauma-induced free radical production exists in neural cells; that the MPT may be involved in the production of free radical post-trauma; and that the CsA-sensitive phase of free radical production is different in neurons and astrocytes.
AB - CNS trauma has been associated with an increase in free radical production, but the cellular sources of this increase or the mechanism involved in the production of free radicals are not known. We, therefore, investigated the effects of trauma on free radical production in cultured neurons, astrocytes and BV-2 microglial cells. Free radicals were measured with the fluorescent dye DCFDA following in vitro trauma. At 30 and 60 min following trauma, there was a 132% and 64% increase, respectively, in free radical production in neurons when compared to controls. In astrocytes, there was a 94% and 133% increase at 30 and 60 min, respectively. Microglial cells, however, displayed no significant increase in free radicals at 30, 60 or 120 min following trauma. Since trauma can induce the mitochondrial permeability transition (MPT), a process associated with mitochondrial dysfunction, we further investigated whether cyclosporin A (CsA), an agent known to block the MPT, could prevent free radical formation following trauma. In neurons CsA did not block free radical production at 30 min but blocked it by 90% at 60 min. In contrast, in astrocytes CsA completely blocked free radical production at 30 min but did not block it at 60 min. Our results indicate that a differential sensitivity to trauma-induced free radical production exists in neural cells; that the MPT may be involved in the production of free radical post-trauma; and that the CsA-sensitive phase of free radical production is different in neurons and astrocytes.
KW - Astrocytes
KW - CNS trauma
KW - Cyclosporin A
KW - Free radicals
KW - Microglia
KW - Mitochondrial permeability transition
KW - Neurons
UR - http://www.scopus.com/inward/record.url?scp=0036131371&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036131371&partnerID=8YFLogxK
U2 - 10.1023/A:1014875210852
DO - 10.1023/A:1014875210852
M3 - Article
VL - 27
SP - 161
EP - 166
JO - Neurochemical Research
JF - Neurochemical Research
SN - 0364-3190
IS - 1-2
ER -