کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5561929 | 1562300 | 2016 | 42 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
3-Monochloro-1,2-propanediol (3-MCPD) induces apoptosis via mitochondrial oxidative phosphorylation system impairment and the caspase cascade pathway
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کلمات کلیدی
MMPQ-VD-OPH3-MCPDGSTP1sdhANADPHTCABcl2pKacAMP - cAMPROS - ROSCyclic adenosine monophosphate - آدنوزین مونوفسفات CyclicBax - باکسApoptosis - خزان یاختهایHuman embryonic kidney cell - سلول انسانی جنین انسانATP synthesis - سنتز ATPActb - عملMitochondrial oxidative phosphorylation - فسفوریلاسیون اکسیداتیو MitohondrialB-cell lymphoma-2 - لنفوم سلول B-2nicotinamide adenine dinucleotide phosphate - نیکوتین آمید adenine dinucleotide phosphateMitochondrial membrane potential - پتانسیل غشای میتوکندریBCL2-associated X protein - پروتئین X مرتبط با BCL2protein kinase A - پروتئین کیناز Atricarboxylic acid cycle - چرخه اسید تریکاربوکیلیکcaspase - کسپاز یا کاسپازReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: 3-Monochloro-1,2-propanediol (3-MCPD) induces apoptosis via mitochondrial oxidative phosphorylation system impairment and the caspase cascade pathway 3-Monochloro-1,2-propanediol (3-MCPD) induces apoptosis via mitochondrial oxidative phosphorylation system impairment and the caspase cascade pathway](/preview/png/5561929.png)
چکیده انگلیسی
3-Monochloro-1,2-propanediol (3-MCPD) is the most toxic chloropropanols compounds in foodstuff which mainly generated during thermal processing. Kidney is one of the primary target organs for 3-MCPD. Using human embryonic kidney cell (HEK293FT) as an in vitro model, we found that 3-MCPD caused concentration-dependent increase in cytoxicity as assessed by dye uptake, lactatedehydrogenase (LDH) leakage and MTT assays. HEK293FT cell treated with 3-MCPD suffered the decrease of mitochondrial membrane potential and the impairment of mitochondrial oxidative phosphorylation system, especially the reduced amount of mRNA expression and protein synthesis of electron transport chain complex II, complex IV, and complex III. More importantly, energy release (ATP synthesis) was significantly inhibited by 3-MCPD resulting from the down regulation expressions of ATP synthase (ATP6 and ATP8), as well as the loss of transmembrane potential required for synthesis of ATP. The decreased ratio of mitochondrial apoptogenic factors Bax/Bcl-2 and the cytochrome-c release from mitochondria to cytosol followed by the activation of apoptotic initiators caspase 9 and apoptotic executioners (caspase 3, caspase 6 and caspase 7) leading to apoptosis. The activation of caspase 8 and caspase 2 implied that there were probably other factors to induce the caspase-dependent apoptosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology - Volume 372, 30 November 2016, Pages 1-11
Journal: Toxicology - Volume 372, 30 November 2016, Pages 1-11
نویسندگان
Xiaoli Peng, Jing Gan, Qian Wang, Zhenqiang Shi, Xiaodong Xia,