High doses of nicotinamide prevent oxidative mitochondrial dysfunction in a cellular model and improve motor deficit in a drosophila model of parkinson's disease
文献类型：期刊论文
| 作者 | Jia, Haiqun1,2; Li, Xin1; Gao, Hongxiang1; Feng, Zhihui1,2; Li, Xuesen1,2; Zhao, Lei1; Jia, Xu1; Zhang, Hongyu1; Liu, Jiankang3 |
| 刊名 | Journal of neuroscience research
 |
| 出版日期 | 2008-07-01 |
| 卷号 | 86期号:9页码:2083-2090 |
| 关键词 | Climbing ability Complex i Dna damage Alpha-ketoglutarate dehydrogenase Protein oxidation |
| ISSN号 | 0360-4012 |
| DOI | 10.1002/jnr.21650 |
| 通讯作者 | Liu, jiankang(j.hu@uci.edu) |
| 英文摘要 | Nicotinamide, the principal form of niacin (vitamin b3), has been proposed to be neuroprotective in parkinson's disease. however, the effects and mechanisms of nicotinamide on motor function in animals and on mitochondrial function in cellular systems have not been well studied. we hypothesized that niacin-derived nad(p)h as antioxidants and enzyme cofactors could inhibit oxidative damage and improve mitochondrial function and thus protect neurodegeneration and improve motor function. in the present study, the effects of nicotinamide on mitochondrial function and oxidative stress were studied in a 1-methyl-4-phenylpyridinium (mpp+)-induced cellular model of parkinson's disease, and the effects of improving motor dysfunction were studied in an alpha-synuclein transgenic drosophila parkinson's model. mitochondrial function was tested by measuring the activity of mitochondrial complex i and alpha-ketoglutarate dehydrogenase, and oxidative damage was tested by measuring reactive oxygen species, dna damage (8-oxo-7,8-dihydro-2'-deoxyguanosine and comet assay), and protein oxidation (protein carbonyls) levels. nicotinamide at a relatively higher concentration, that is, 100-fold of the level in the cell culture medium (101 mg/l), significantly protected sk-n-mc human neuroblastoma cells from an mpp+-induced decrease in cell viability, complex i and alpha-ketoglutarate dehydrogenase activity, and an increase in oxidant generation, dna damage, and protein oxidation. in the drosophila model, nicotinamide at 15 and 30 mg/100 g diet significantly improved climbing ability. these results suggest that nutritional supplementation of nicotinamide at high doses decreases oxidative stress and improves mitochondrial and motor function in cellular and/or drosophila models and may be an effective strategy for preventing and ameliorating parkinson's disease. (c) 2008 wiley-liss, inc. |
| WOS关键词 | ALPHA-LIPOIC ACID ; COENZYME Q(10) ; COGNITIVE DYSFUNCTION ; NADH ; DAMAGE ; NEUROPROTECTION ; BIOSYNTHESIS ; ALZHEIMERS ; TOXIN ; CELLS |
| WOS研究方向 | Neurosciences & Neurology |
| WOS类目 | Neurosciences |
| 语种 | 英语 |
| WOS记录号 | WOS:000257722400018 |
| 出版者 | WILEY-LISS |
| URI标识 | http://www.irgrid.ac.cn/handle/1471x/2385279 |
| 专题 | 中国科学院大学 |
| 通讯作者 | Liu, Jiankang |
| 作者单位 | 1.Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Nutrit Sci, Shanghai, Peoples R China 2.Chinese Acad Sci, Grad Sch, Beijing, Peoples R China 3.Univ Calif Irvine, Inst Brain Aging & Dementia, Irvine, CA USA |
| 推荐引用方式 GB/T 7714 | Jia, Haiqun,Li, Xin,Gao, Hongxiang,et al. High doses of nicotinamide prevent oxidative mitochondrial dysfunction in a cellular model and improve motor deficit in a drosophila model of parkinson's disease[J]. Journal of neuroscience research,2008,86(9):2083-2090. |
| APA | Jia, Haiqun.,Li, Xin.,Gao, Hongxiang.,Feng, Zhihui.,Li, Xuesen.,...&Liu, Jiankang.(2008).High doses of nicotinamide prevent oxidative mitochondrial dysfunction in a cellular model and improve motor deficit in a drosophila model of parkinson's disease.Journal of neuroscience research,86(9),2083-2090. |
| MLA | Jia, Haiqun,et al."High doses of nicotinamide prevent oxidative mitochondrial dysfunction in a cellular model and improve motor deficit in a drosophila model of parkinson's disease".Journal of neuroscience research 86.9(2008):2083-2090. |
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来源：中国科学院大学
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