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Oxidative changes in the rat brain by intraperitoneal injection of ferric nitrilotriacetate.

作者信息

Nakatsuka Ichiro, Maeda Shigeru, Andoh Tsugunobu, Hayashi Yukiko, Mizuno Ryuichiro, Higuchi Hitoshi, Miyawaki Takuya

机构信息

Department of Dental Anesthesiology, Okayama University Hospital, Okayama, Japan.

出版信息

Redox Rep. 2009;14(3):109-14. doi: 10.1179/135100009X392575.

DOI:10.1179/135100009X392575
PMID:19490752
Abstract

Iron is known to be involved in neuronal diseases such as neurodegenerative diseases, brain ischemia and epilepsy. However, it is unclear if a high level of peripheral iron induces these pathological conditions. Since ferric nitrilotriacetate (Fe-NTA), a low molecule iron chelate, causes kidney carcinoma and diabetes in animals due to its strong and unique oxidative stress, it is also considered to cause pathological conditions in the brain. Therefore, we studied brain changes after intraperitoneal (i.p.) injection of Fe-NTA. We investigated iron distribution in the brain and evaluated heme oxygenase (HO)-1 mRNA, IL-6 mRNA and 4-hydroxy-2-nonenal (4-HNE) quantitatively. In addition, changes in muscarinic acetylcholine receptor mRNAs were measured. It was found that iron was localized in the cortex and the hypothalamus, but not in other areas of the brain. HO-1 was induced in both the cortex and hypothalamus, and the levels of IL-6 and 4-HNE were raised in the hypothalamus, but not in the cortex. In the cortex, expression in M1 and M2 mAChRs were suppressed. In conclusion, iron reached the brain parenchyma after i.p. injection of Fe-NTA, and Fe-NTA caused oxidative reactions and suppression of mAChRs in the brain.

摘要

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