کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5510664 | 1539268 | 2017 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Apoptotic death in erythrocytes of lamprey Lampetra fluviatilis induced by ionomycin and tert-butyl hydroperoxide
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کلمات کلیدی
MMPFCCPRBCsionomycinTMRMtBHPtetramethyl rhodamine methyl esterRed blood cells - سلولهای قرمز خونApoptosis - خزان یاختهایPhosphatidylserine - فسفاتیدیلسرینMitochondrial pathway - مسیر میتوکندریاییtert-butyl hydroperoxide - هیدروپراکسید تری بوتیلMitochondrial membrane potential - پتانسیل غشای میتوکندریPropidium iodide - پروتئین یدیدcarbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone - کربونیل سیانید 4- (trifluoromethoxy) phenylhydrazone
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The work examined the effects of Ca2+ overload and oxidative damage on erythrocytes of river lamprey Lampetra fluvialtilis. The cells were incubated for 3 h with 0.1-5 μM Ca2+ ionophore ionomycin in combination with 2.5 mM Ca2+ and 10-100 μM pro-oxidant agent tert-butyl hydroperoxide (tBHP). The sensitivity of lamprey RBCs to studied compounds was evaluated by the kinetics of their death. Both toxicants induced dose- and time dependent phosphatidylserine (PS) externalization (annexin V-FITC labeling) and loss of membrane integrity (propidium iodide uptake). Highest doses of ionomycin (1-2 μM) increased the number of PS-exposed erythrocytes to 7-9% within 3 h, while 100 μM tBHP produced up to 50% of annexin V-FITC-positive cells. Caspase inhibitor Boc-D-FMK (50 μM), calpain inhibitor PD150606 (10 μM) and broad protease inhibitor leupeptin (200 μM) did not prevent ionomycin-induced PS externalization, whereas tBHP-triggered apoptosis was blunted by Boc-D-FMK. tBHP-dependent death of lamprey erythrocytes was accompanied by the decrease in relative cell size, loss of cell viability, activation of caspases 9 and 3/7, and loss of mitochondrial membrane potential, but all these processes were partially attenuated by Boc-D-FMK. None of examined death-associated events were observed in ionomycin-treated erythrocytes except activation of caspase-9. Incubation with ionomycin did not alter intracellular K+ and Na+ content, while exposure to tBHP resulted in 80% loss of K+ and 2.8-fold accumulation of Na+. Thus, lamprey erythrocytes appear to be more susceptible to oxidative damage. Ca2+ overload does not activate the cytosolic death pathways in these cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology - Volume 194, April 2017, Pages 48-60
Journal: Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology - Volume 194, April 2017, Pages 48-60
نویسندگان
Natalia I. Agalakova, Tatiana I. Ivanova, Gennadii P. Gusev, Anna V. Nazarenkova, Dina A. Sufiyeva,