کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9890128 | 1540002 | 2005 | 20 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
β-Phenylethyl isothiocyanate mediated apoptosis; contribution of Bax and the mitochondrial death pathway
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کلمات کلیدی
MPTTFZPEITCmBClGSLTMRMMMPGSHITCMitochondrial dysfunction - اختلال در عملکرد میتوکندریBongkrekic acid - اسید بونکروکیکmitochondrial permeability transition pore - انتقال نفوذی میتوکندری منفی استCSA - ایالات مؤتلفهٔ آمریکاIsothiocyanate - ایزوتیوسیاناتBax - باکسTrifluoperazine - تریفلوپرازینApoptosis - خزان یاختهایRh-123 - ر-123Rhodamine-123 - رودامین 123cytochrome c - سیتوکروم سیCyclosporine A - سیکلوسپورینAMonochlorobimane - مونوکلروبیمانMitochondrial membrane potential - پتانسیل غشای میتوکندریCaspases - کاسپازGlutathione - گلوتاتیونGlucosinolate - گلوکوزینولات
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: β-Phenylethyl isothiocyanate mediated apoptosis; contribution of Bax and the mitochondrial death pathway β-Phenylethyl isothiocyanate mediated apoptosis; contribution of Bax and the mitochondrial death pathway](/preview/png/9890128.png)
چکیده انگلیسی
The initiating events that lead to the induction of apoptosis mediated by the chemopreventative agent β-phenyethyl isothiocyanate (PEITC) have yet to be elucidated. In the present investigation, we examined the effects of PEITC on mitochondrial function and apoptotic signaling in hepatoma HepG2 cells and isolated rat hepatocyte mitochondria. PEITC induced a conformational change in Bax leading to its translocation to mitochondria in HepG2 cells. Bax accumulation was associated with a rapid loss of mitochondrial membrane potential (ÎÏm), impaired respiratory chain enzymatic activity, release of mitochondrial cytochrome c and the activation of caspase-dependent cell death. Caspase inhibition did not prevent Bax translocation, the release of cytochrome c or the loss of ÎÏm, but blocked caspase-mediated DNA fragmentation and cell death. To determine whether PEITC dependent Bax translocation caused loss of ÎÏm by the activation of the mitochondrial permeability transition (MPT), we examined the effects of PEITC in isolated rat hepatocyte mitochondria. Interestingly, PEITC did not induce MPT in isolated rat mitochondria. Accordingly, using pharmacological inhibitors of MPT namely cyclosporine A, trifluoperazine and Bongkrekic acid we were unable to block PEITC mediated apoptosis in HepG2 cells, this suggesting that mitochondrial permeablisation is a likely consequence of Bax dependent pore formation. Taken together, our data suggest that mitochondria are a key target in PEITC induced apoptosis in HepG2 cells via the pore forming ability of pro-apoptotic Bax.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The International Journal of Biochemistry & Cell Biology - Volume 37, Issue 1, January 2005, Pages 100-119
Journal: The International Journal of Biochemistry & Cell Biology - Volume 37, Issue 1, January 2005, Pages 100-119
نویسندگان
Peter Rose, Jeffery S. Armstrong, Yee Liu Chua, Choon Nam Ong, Matthew Whiteman,