Ceruloplasmin Protects Against Rotenone-Induced Oxidative Stress and Neurotoxicity |
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Authors: | Hineno Akiyo Kaneko Kazuma Yoshida Kunihiro Ikeda Shu-ichi |
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Institution: | (1) Department of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine, Matsumoto 390-8621, Japan;(2) Division of Neurogenetics, Department of Brain Disease Research, Shinshu University School of Medicine, Matsumoto 390-8621, Japan; |
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Abstract: | To clarify the neuroprotective property of ceruloplasmin and the pathogenesis of aceruloplasminemia, we generated ceruloplasmin-deficient
(CP
−/−) mice on the C57BL/10 genetic background and further treated them with a mitochondrial complex I inhibitor, rotenone. There
was no iron accumulation in the brains of CP
−/− mice at least up to 60 weeks of age. Without rotenone treatment, CP
−/− mice showed slight motor dysfunction compared with CP
+/+ mice, but there were no detectable differences in the levels of oxidative stress markers between these two groups. A low
dose of rotenone did not affect the mitochondrial complex I activity in our mice, however, it caused a significant change
in motor behavior, neuropathology, or the levels of oxidative stress markers in CP
−/− mice, but not in CP
+/+ mice. Our data support that ceruloplasmin protects against rotenone-induced oxidative stress and neurotoxicity, probably
through its antioxidant properties independently of its function of iron metabolism. |
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Keywords: | |
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