Iron In Ischemic Injury

[ironjustice]

Trace Element, Antioxidant Activity, and Lipid Peroxidation Levels in
Brain Cortex of Gerbils After Cerebral Ischemic Injury.
Fang KM, Cheng FC, … Lin MC
Biol Trace Elem Res 2013 Jan 19
Abstract
Proper trace element level and antioxidant enzyme activity are crucial
for the brain in maintaining normal neurological functions.
To our knowledge, alteration of lipid peroxidation status, trace
element level, and antioxidant activity in the homogenates of brain
cortex after cerebral ischemia in gerbil, however, has not been
investigated so far.
Male Mongolian gerbils were divided into control and ischemic
subjects.
Cerebral ischemia was induced by occlusion of the right middle
cerebral artery and right common carotid artery for 1 h.
Experimental results showed that a significant increase (P < 0.01) of
the malondialdehyde level was found in the ischemic brain as compared
with the control group.
Trace element analysis indicated that a remarkable elevation (P <
0.01) of the level of iron (Fe), chromium (Cr), and a statistical
decrease of selenium (Se) and zinc (Zn) (P < 0.05) concentration were
observed in the ischemic brain as compared with the control subject.
No significant change (P > 0.05) of the copper (Cu) level was found in
both experimental groups.
Additionally, antioxidant activity of superoxide dismutase (P < 0.01)
and catalase (P < 0.05) was significantly decreased in the ischemic
brain as compared with the control subject.
Taking all results together, it is conceivable to manifest the
experimental findings that cerebral ischemia not only may result in an
enhanced oxidative stress but also may lead to further oxidative
injury.
Moreover, disturbance of trace element level combined with declined
antioxidant activity seems to play a significant role in responsible
for the etiology of cerebral ischemia.

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Deferoxamine attenuates iron-induced long-term neurotoxicity in rats
with traumatic brain injury.
Zhang L, Hu R, Li M, Li F, Meng H, Zhu G, Lin J, Feng H
Neurol Sci 2012 Apr 27.

This study investigated whether deferoxamine (DFO), an iron chelator
attenuates iron-induced toxicity in rats with traumatic brain injury.
In this study, three groups of Sprague-Dawley rats (sham, injury and
DFO groups) were examined.
Rats were killed on day 28 after Morris water maze testing and brains
perfused for either non-heme brain binding or hemosiderin staining.
Western blotting was used to measure protein levels of ferritin,
transferrin and transient receptor potential canonical channel 6
(TRPC6).
In TBI rats, there was a significant increase in brain iron on day
28,
ferritin L, ferritin H, transferrin and TRPC6 levels were all
significantly elevated post-TB1.
There were also deficits in spatial learning and memory; however, DFO
administration attenuated these effects in TBI rats supporting the
notion that DFO may reduce brain injury accentuated by iron overload.


Neurological sciences : official journal of the Italian Neurological
Society and of the Italian Society of Clinical Neurophysiology
[Neurol
Sci]


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