دانلود رایگان مقاله لاتین حساسیت دیفرانسیل کمپلکس میتوکندری از سایت الزویر
عنوان فارسی مقاله:
حساسیت دیفرانسیل کمپلکس میتوکندری دوم به بازداری توسط اگزالواستات در مغز و قلب
عنوان انگلیسی مقاله:
Differential susceptibility of mitochondrial complex II to inhibition by oxaloacetate in brain and heart
سال انتشار : 2016
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مقدمه انگلیسی مقاله:
1. Introduction
Mitochondrial complex II (EC 1.3.5.1, succinate:quinone reductase (SQR), succinate dehydrogenase (SDH)) catalyzes oxidation of matrix succinate to fumarate by membrane bound ubiquinone, thereby feeding electrons to the cytochrome bc1 complex. Complex II is composed of four nuclear encoded subunits. The structure of complex II resolved at 2.4 Å resolution [1] revealed that the hydrophobic subunits SDHC and SDHD are anchored to the inner mitochondrial membrane with a short segment extended into the intermembrane space, while the catalytic subunits SDHA and SDHB project into the matrix. Electrons are transferred from succinate to ubiquinone through the covalently bound flavin-adenine dinucleotide (FAD) and three iron-sulphur clusters [2]. SDHA is the largest subunit and contains a covalently attached flavin in the dicarboxylate-binding site, where succinate is oxidized to fumarate. The regulation of complex II activity is not well understood, which is surprising since this enzyme integrates the tricarboxylic acid (TCA) cycle metabolism with the mitochondrial respiratory chain. As found in pioneering work of Singer [3], preparations of the enzyme isolated from tissues show a spontaneous increase in the rate of catalytic reaction. It was found that preparations of isolated SDH or enzyme in the membrane of submitochondrial particles (SMP) could be significantly activated by succinate and its analogues [4–7]. This activation was attributed to a slow dissociation of the competitive inhibitor oxaloacetate (OAA) from the active centre of the enzyme. However, whether the observed inhibition of SDH by OAA is significant for physiological regulation of the enzyme in vivo, or just an artefact caused by the isolation procedure is still a matter of controversy [6,8,9]. Matrix OAA might be a potent physiological effector of SDH with a very high af- finity to the dicarboxylate binding site of the enzyme (Kd ~ 10−8 M) [7] or, it may bind to SDH during the isolation procedure due to the very fast rate of binding, and stay in a bound state even after repetitive washing or gel filtration [5,10]. Studies of mitochondrial complex II are clinically important [11], since this enzyme has recently emerged as focal point of investigation in cell signalling [12–15], cancer biology [16–19], immunology [20], neurodegeneration [21] and cardiovascular conditions [22,23]. Acute tissue ischemia is known to be associated with blockade of respiration, accumulation of reduced equivalents in the matrix (NAD(P)H), depletion of cellular ATP/phosphocreatine pool, and, eventually, impairment of mitochondrial function [24]. Hypoxia-dependent inhibition of complex I and II would have a strong effect on TCA cycle reactions [25]. In turn, this would result in significant alterations in the concentration of intermediates of the TCA cycle [22,26,27], including OAA and succinate. Therefore, it is crucial to know whether binding of OAA to SDH is a physiologically relevant process
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کلمات کلیدی:
Differential susceptibility of mitochondrial complex II to inhibition by ... https://www.researchgate.net/.../303847220_Differential_susceptibility_of_mitochondria... Differential susceptibility of mitochondrial complex II to inhibition by oxaloacetate in brain and heart on ResearchGate, the professional network for scientists. Studies on succinate dehydrogenase. V. Inhibition by oxaloacetate https://www.researchgate.net/.../17815448_Studies_on_succinate_dehydrogenase_V_In... V. Inhibition by oxaloacetate on ResearchGate, the professional network for ... of mitochondrial complex II to inhibition by oxaloacetate in brain and heart. [PDF]Differential susceptibility of mitochondrial complex II to inhibition by ... iranarze.ir/wp-content/uploads/2016/10/E405.pdf Jun 7, 2016 - We found that complex II from mouse heart and brain tissue has similar affinity to ... oxaloacetate (OAA) from the active centre of the enzyme. The Neuromediator Glutamate, through Specific Substrate Interactions ... www.jbc.org/content/284/21/14448.abstract by A Panov - 2009 - Cited by 39 - Related articles May 22, 2009 - With the non-bovine serum albumin brain and heart mitochondria ... pyruvate and glutamate abrogated inhibition of Complex II by oxaloacetate. Comprehensive Toxicology - Page 439 - Google Books Result https://books.google.com/books?isbn=0080468845 2010 - Medical 1.19.5.4 Inhibitors of Complex II (Succinate:Ubiquinone Reductase) X-ray ... the structure of complex II with oxaloacetate, a classical competitive inhibitor, bound ... in rat brain or heart and improves long-term neurological outcome after brain or ... FastRef | FastFormat https://fastformat.co/b/fastref?ww=&ep=&alw=&a=&w... ... of mitochondrial complex II to inhibition by oxaloacetate in brain and heart ... Mitochondrial Complex II is a key mitochondrial enzyme connecting the ... Biomarkers for Traumatic Brain Injury - Page 110 - Google Books Result https://books.google.com/books?isbn=1849733899 Svetlana A. Dambinova, Ronald L. Hayes, Kevin K. W. Wang - 2012 - Science Thus, the neuromediator glutamate controls energy metabolism in the brain not only ... (Complex II) in the postsynaptic mitochondria is inhibited by oxaloacetate ... Complex II - Bioblast www.bioblast.at/index.php/Complex_II May 17, 2016 - Complex II or succinate dehydrogenase or succinate-coenzyme Q reductase is .... complex II to inhibition by oxaloacetate in brain and heart.
