کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1942224 | 1052595 | 2013 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Dissecting the molecular mechanism by which NH2htau and Aβ1-42 peptides impair mitochondrial ANT-1 in Alzheimer disease
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کلمات کلیدی
AβVDACCGCsNFTsβ-hydroxybutyrateDIDSantimycin AoligomycinCysUCRRCIOXPHOSXODAp5ASuccANT-1ATP D.S.ATP detecting systemATRN-ethyl-maleimidephosphate buffer saline mediumPBSUncoupling Control RatioXanthine oxidase - زانتین اکسیدازCN− - CN-mERs - mers هاROS - ROSS.D. - SD.β-Amyloid - β-آمیلوئیدatractyloside - آتراتکتیلوزیدCyanide - اسید سیاندریک و سیانورoligo - الیگوstandard deviation - انحراف معیارAlzheimer disease - بیماری آلزایمرadenine nucleotide translocator - ترجمه آدنین نوکلئوتیدیRET - حقXanthine - زانتیRespiratory chain - زنجیر تنفسیcerebellar granule cells - سلول های گرانول مخچهSuccinate - سوکینتینCysteine - سیستئینRespiratory control index - شاخص کنترل تنفسیinorganic phosphate - فسفات معدنیOxidative phosphorylation - فسفوریلاسیون اکسیداتیوMersalyl - مرسالیلreverse electron transport - معکوس حمل و نقل الکترونneurofibrillary tangles - مگس های نوروفیبریلیالMitochondria - میتوکندریاNEM - نهvoltage-dependent anion channel - کانال آنیون وابسته به ولتاژThiol group - گروه تیولThiol groups - گروه های تیولReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
دانش گیاه شناسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
To find out whether and how the adenine nucleotide translocator-1 (ANT-1) inhibition due to NH2htau and Aβ1-42 is due to an interplay between these two Alzheimer's peptides, ROS and ANT-1 thiols, use was made of mersalyl, a reversible alkylating agent of thiol groups that are oriented toward the external hydrophilic phase, to selectively block and protect, in a reversible manner, the -SH groups of ANT-1. The rate of ATP appearance outside mitochondria was measured as the increase in NADPH absorbance which occurs, following external addition of ADP, when ATP is produced by oxidative phosphorylation and exported from mitochondria in the presence of glucose, hexokinase and glucose-6-phosphate dehydrogenase. We found that the mitochondrial superoxide anions, whose production is induced at the level of Complex I by externally added Aβ1-42 and whose release from mitochondria is significantly reduced by the addition of the VDAC inhibitor DIDS, modify the thiol group/s present at the active site of mitochondrial ANT-1, impair ANT-1 in a mersalyl-prevented manner and abrogate the toxic effect of NH2htau on ANT-1 when Aβ1-42 is already present. A molecular mechanism is proposed in which the pathological Aβ-NH2htau interplay on ANT-1 in Alzheimer's neurons involves the thiol redox state of ANT-1 and the Aβ1-42-induced ROS increase. This result represents an important innovation because it suggests the possibility of using various strategies to protect cells at the mitochondrial level, by stabilizing or restoring mitochondrial function or by interfering with the energy metabolism providing a promising tool for treating or preventing AD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Bioenergetics - Volume 1827, Issue 7, July 2013, Pages 848-860
Journal: Biochimica et Biophysica Acta (BBA) - Bioenergetics - Volume 1827, Issue 7, July 2013, Pages 848-860
نویسندگان
A. Bobba, G. Amadoro, V.A. Petragallo, P. Calissano, A. Atlante,