Blood-derived iron mediates free radical production and neuronal death in the hippocampal CA1 area following transient forebrain ischemia in rat View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2010-12-01

AUTHORS

Ui Jin Park, Young Ae Lee, Sun Mi Won, Jin Hwan Lee, Seung-Hee Kang, Joe E. Springer, Yong Beom Lee, Byoung Joo Gwag

ABSTRACT

Abnormal brain iron homeostasis has been proposed as a pathological event leading to oxidative stress and neuronal injury under pathological conditions. We examined the possibility that neuronal iron overload would mediate free radical production and delayed neuronal death (DND) in hippocampal CA1 area after transient forebrain ischemia (TFI). Mitochondrial free radicals (MFR) were biphasically generated in CA1 neurons 0.5–8 and 48–60 h after TFI. Treatment with Neu2000, a potent spin trapping molecule, as well as trolox, a vitamin E analogue, blocked the biphasic MFR production and attenuated DND in the CA1, regardless of whether it was administered immediately or even 24 h after reperfusion. The late increase in MFR was accompanied by iron accumulation and blocked by the administration of deferoxamine—an iron chelator. Iron accumulation was attributable to prolonged upregulation of the transferrin receptor and to increased uptake of peripheral iron through a leaky blood–brain barrier. Infiltration of iron-containing cells and iron accumulation were attenuated by depletion of circulating blood cells through X-ray irradiation of the whole body except the head. The present findings suggest that excessive iron transported from blood mediates slowly evolving oxidative stress and neuronal death in CA1 after TFI, and that targeting iron-mediated oxidative stress holds extended therapeutic time window against an ischemic event. More... »

PAGES

459-473

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00401-010-0785-8

DOI

http://dx.doi.org/10.1007/s00401-010-0785-8

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1031858667

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21120509


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40 schema:description Abnormal brain iron homeostasis has been proposed as a pathological event leading to oxidative stress and neuronal injury under pathological conditions. We examined the possibility that neuronal iron overload would mediate free radical production and delayed neuronal death (DND) in hippocampal CA1 area after transient forebrain ischemia (TFI). Mitochondrial free radicals (MFR) were biphasically generated in CA1 neurons 0.5–8 and 48–60 h after TFI. Treatment with Neu2000, a potent spin trapping molecule, as well as trolox, a vitamin E analogue, blocked the biphasic MFR production and attenuated DND in the CA1, regardless of whether it was administered immediately or even 24 h after reperfusion. The late increase in MFR was accompanied by iron accumulation and blocked by the administration of deferoxamine—an iron chelator. Iron accumulation was attributable to prolonged upregulation of the transferrin receptor and to increased uptake of peripheral iron through a leaky blood–brain barrier. Infiltration of iron-containing cells and iron accumulation were attenuated by depletion of circulating blood cells through X-ray irradiation of the whole body except the head. The present findings suggest that excessive iron transported from blood mediates slowly evolving oxidative stress and neuronal death in CA1 after TFI, and that targeting iron-mediated oxidative stress holds extended therapeutic time window against an ischemic event.
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47 schema:keywords Abnormal brain iron homeostasis
48 Blood-derived iron
49 CA1
50 CA1 area
51 CA1 neurons 0.5
52 DND
53 E analogue
54 MFR production
55 Neu2000
56 accumulation
57 administration
58 administration of deferoxamine
59 analogues
60 area
61 barriers
62 biphasic MFR production
63 blood cells
64 blood mediates
65 blood-brain barrier
66 body
67 brain iron homeostasis
68 cells
69 chelators
70 conditions
71 death
72 deferoxamine
73 depletion
74 events
75 excessive iron
76 findings
77 forebrain ischemia
78 free radical production
79 free radicals
80 head
81 hippocampal CA1 area
82 homeostasis
83 increase
84 infiltration
85 injury
86 iron
87 iron accumulation
88 iron chelators
89 iron homeostasis
90 iron overload
91 iron-containing cells
92 iron-mediated oxidative stress
93 irradiation
94 ischemia
95 ischemic events
96 late increase
97 leaky blood-brain barrier
98 mediates
99 mitochondrial free radicals
100 molecules
101 neuronal death
102 neuronal injury
103 neuronal iron overload
104 neurons 0.5
105 overload
106 oxidative stress
107 pathological conditions
108 pathological events
109 peripheral iron
110 possibility
111 potent spin
112 present findings
113 production
114 prolonged upregulation
115 radical production
116 radicals
117 rats
118 ray irradiation
119 receptors
120 reperfusion
121 spin
122 stress
123 therapeutic time window
124 time window
125 transferrin receptor
126 transient forebrain ischemia
127 treatment
128 upregulation
129 uptake
130 vitamin E analogue
131 whole body
132 window
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