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Iron Accumulation and DNA Damage in a Pig Model of Intracerebral Hemorrhage

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Part of the book series: Acta Neurochirurgica Supplementum ((NEUROCHIRURGICA,volume 111))

Abstract

Cerebral iron overload causes brain injury after intracerebral hemorrhage (ICH) in rats and pigs. The current study examined whether an iron chelator, deferoxamine, can reduce ICH-induced DNA damage in pigs. Pigs received an injection of autologous blood into the right frontal lobe. Deferoxamine (50 mg/kg, i.m.) or vehicle was given 2 h after ICH and then every 12 h up to 7 days. Animals were killed at day 3 or day 7 after ICH to examine iron accumulation and DNA damage. We found that ICH resulted in the development of a reddish perihematomal zone, with iron accumulation and DNA damage within that zone. Deferoxamine treatment reduced the perihematomal reddish zone, and the number of Perls’ (p < 0.01) and TUNEL (p < 0.01) positive cells. In conclusion, iron accumulates in the perihematomal zone and causes DNA damage. Systemic deferoxamine treatment reduces ICH-induced iron overload and DNA damage in pigs.

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Acknowledgment

This study was supported by grants NS-017760, NS-039866, NS-052510 and NS-057539 from the National Institutes of Health (NIH) and 0840016N from the American Heart Association (AHA). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH and AHA. Dr. Gu was supported by a grant 30700864 from the China National Natural Science Foundation.

Conflict of interest statement We declare that we have no conflict of interest.

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Correspondence to Guohua Xi .

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Gu, Y. et al. (2011). Iron Accumulation and DNA Damage in a Pig Model of Intracerebral Hemorrhage. In: Zhang, J., Colohan, A. (eds) Intracerebral Hemorrhage Research. Acta Neurochirurgica Supplementum, vol 111. Springer, Vienna. https://doi.org/10.1007/978-3-7091-0693-8_20

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  • DOI: https://doi.org/10.1007/978-3-7091-0693-8_20

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  • Publisher Name: Springer, Vienna

  • Print ISBN: 978-3-7091-0692-1

  • Online ISBN: 978-3-7091-0693-8

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