کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
7638683 | 1494806 | 2018 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Respiratory complex II in mitochondrial dysfunction-mediated cytotoxicity: Insight from cadmium
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کلمات کلیدی
SQRMPTFCCPDNPIPCDCFH2-DACCCPDCFH2antimycin ACyclophilin DoligomycinRHMdithiotreitolPBSCyP-DRLMDUBdecylubiquinoneTTFAStigmatellinTMPDSuccinate:ubiquinone oxidoreductaseAnt AMYXSTIGNACEGTAANTMCUSDHDTTDcf2′,7′-dichlorodihydrofluorescein - 2 '، 7'-dichlorodihydrofluorescein2′,7′-dichlorodihydrofluorescein diacetate - 2 '، 7'-dichlorodihydrofluorescein diacetate2′,7′-dichlorofluorescein - 2 '، 7'-dichlorofluorescein2,4-Dinitrophenol - 2،4-دینیتروفنلBSA - BSACd2+ - Cd2 +I/R - I / RN-acetylcysteine - N-استیل سیستئینischemic preconditioning - preconditioning ایسکمیکROS - ROSbovine serum albumin - آلبومین سرم گاوoligo - الیگوmitochondrial permeability transition - انتقال نفوذپذیری میتوکندریimm - انحصارCSA - ایالات مؤتلفهٔ آمریکاischemia-reperfusion - ایسکمی-رپرفیوژنadenine nucleotide translocase - ترانسکوز نوکلئوتید آدنینtrypan blue - تریپان آبیthenoyltrifluoroacetone - تیتویلتروفلوآرآستونMalonate - خوشحالیinner mitochondrial membrane - درونی غشای میتوکندریDiazo - دیازوdiazoxide - دیازوکسیدRot - روتRotenone - روتنونmitochondrial electron transport chain - زنجیره حمل و نقل الکترون الکترونیک میتوکندریsuccinate dehydrogenase - سوکسیناد دهیدروژنازCyclosporine A - سیکلوسپورینAPhosphate buffered saline - فسفات بافر شورinorganic phosphate - فسفات معدنیlactate dehydrogenase - لاکتات دهیدروژناز LDH - لاکتات دهیدروژناز به صورت مختصر شده LDH Mitochondrial Ca2+ uniporter - متقاطع کلسیم + mitochondrial uniporterRat heart mitochondria - میتوکندری قلب موشRat liver mitochondria - میتوکندری کبدی موشMyxothiazol - میکسوتیازولPropidium iodide - پروتئین یدیدCarbonyl cyanide 3-chlorophenylhydrazone - کربنیل سیانید 3-کلروفنیل هیدرازونcarbonyl cyanide p-trifluoromethoxyphenylhydrazone - کربونیل سیانید p-trifluoromethoxyphenylhydrazoneReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
مهندسی و علوم پایه
شیمی
شیمی آنالیزی یا شیمی تجزیه
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
In the present work we studied action of several inhibitors of respiratory complex II (CII) of mitochondrial electron transport chain, namely malonate and thenoyltrifluoroacetone (TTFA) on Cd2+-induced toxicity and cell mortality, using two rat cell lines, pheochromocytoma PC12 and ascites hepatoma AS-30D and isolated rat liver mitochondria (RLM). It was shown that malonate, an endogenous competitive inhibitor of dicarboxylate-binding site of CII, restored in part RLM respiratory function disturbed by Cd2+. In particular, malonate increased both phosphorylating and maximally uncoupled respiration rates in KCl medium in the presence of CI substrates as well as palliated changes in basal and resting state respiration rates produced by the heavy metal on the mitochondria energized by CI or CII substrates. Notably, malonate enhanced Cd2+-induced swelling of the mitochondria energized by CI substrates in KCl and, in a much lesser extent and at higher [Cd2+], in sucrose media but did not influence on the Cd2+ effects in NaCl medium. Besides, malonate did not affect swelling in sucrose media of RLM energized by CIV substrates under using of Cd2+ or Ca2+ whereas it strongly increased the mitochondrial swelling produced by selenite. In addition, malonate produced some protection against Cd2+-promoted necrotic death of AS-30D and PC12 cells and reduced intracellular reactive oxygen species (ROS) formation evoked by Cd2+ in PC12 cells. Importantly, TTFA, an irreversible competitive inhibitor of Q-binding site of CII, per se induced apoptosis of AS-30D cells which was inhibited by co-treatment with Cd2+ as well as decreased the Cd2+-enhanced intracellular ROS formation. In turn, decylubiquinone (dUb) at low μM concentrations did not protect AS-30D cells against the Cd2+-induced necrosis and enhanced the Cd2+-induced apoptosis of the cells. High μM concentrations of dUb were highly toxic for the cells. As consequence, the findings give new evidence indicative of critical involvement of CII in mechanism(s) of Cd2+-produced cytotoxicity and support the notion on CII as a perspective pharmacological target in mitochondria dysfunction-mediated conditions and diseases.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Trace Elements in Medicine and Biology - Volume 50, December 2018, Pages 80-92
Journal: Journal of Trace Elements in Medicine and Biology - Volume 50, December 2018, Pages 80-92
نویسندگان
Elena A. Belyaeva,