کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6021818 | 1580653 | 2014 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Folate deficiency-induced oxidative stress contributes to neuropathy in young and aged zebrafish - Implication in neural tube defects and Alzheimer's diseases
ترجمه فارسی عنوان
استرس اکسیداتیو ناشی از کمبود فولات موجب ایجاد نوروپاتی در ماهیان دریایی جوان و سالم می شود - پیامدهایی در نقص لوله عصبی و بیماری آلزایمر
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کلمات کلیدی
کمبود فولاد، ³-گلوتامیل هیدرولاز، ماهی قزل آلا، نقص لوله عصبی، متابولیسم یک کربن، بیماری های آلزایمر،
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
چکیده انگلیسی
Folate is a nutrient essential for the development, function and regeneration of nervous systems. Folate deficiency has been linked to many neurological disorders including neural tube defects in fetus and Alzheimer's diseases in the elderly. However, the etiology underlying these folate deficiency-associated diseases is not completely understood. In this study, zebrafish transgenic lines with timing and duration-controllable folate deficiency were developed by ectopically overexpressing a recombinant EGFP-γ-glutamyl hydrolase (γGH). Impeded neural crest cell migration was observed in the transgenic embryos when folate deficiency was induced in early stages, leading to defective neural tube closure and hematopoiesis. Adding reduced folate or N-acetylcysteine reversed the phenotypic anomalies, supporting the causal link between the increased oxidative stress and the folate deficiency-induced abnormalities. When folate deficiency was induced in aged fish accumulation of beta-amyloid and phosphorylated Tau protein were found in the fish brain cryo-sections. Increased autophagy and accumulation of acidic autolysosome were apparent in folate deficient neuroblastoma cells, which were reversed by reduced folate or N-acetylcysteine supplementation. Decreased expression of cathepsin B, a lysosomal protease, was also observed in cells and tissue with folate deficiency. We concluded that folate deficiency-induced oxidative stress contributed to the folate deficiency-associated neuropathogenesis in both early and late stages of life.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Disease - Volume 71, November 2014, Pages 234-244
Journal: Neurobiology of Disease - Volume 71, November 2014, Pages 234-244
نویسندگان
Tseng-Ting Kao, Chia-Yi Chu, Gang-Hui Lee, Tsun-Hsien Hsiao, Nai-Wei Cheng, Nan-Shan Chang, Bing-Hung Chen, Tzu-Fun Fu,