کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6276861 | 1295745 | 2010 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Pathways involved in the generation of reactive oxygen and nitrogen species during glucose deprivation and its role on the death of cultured hippocampal neurons
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کلمات کلیدی
XaoRFU2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione7-NINBQXcPLA2MK-801RNSNOSNDGAXanthine oxidase - زانتین اکسیداز3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide - 3- (4،5-Dimethylthiazol-2-yl) -2،5-diphenyltetrazoliumbromide7-nitroindazole - 7-نیتریدازولMTT - MTTROS - ROSOxidative damage - آسیب اکسیداتیوphospholipase A2 - آنزیم فسفولیپاز A2 Ethidium - اتیدیمnordihydroguaiaretic acid - اسید نوردی هیدروگالیارتیexcitotoxicity - اکسید سمیتNADPH oxidase - اکسیداز NADPH LOX - اکسیژن مایعdihydroethidium - دی هیدروتیدیمDIV - دیوdays in vitro - روز in vitrolactate dehydrogenase - لاکتات دهیدروژناز LDH - لاکتات دهیدروژناز به صورت مختصر شده LDH lipoxygenase - لیپواکسیژنازglucose deprivation - محرومیت گلوکزnitric oxide synthase - نیتریک اکسید سنتازhypoglycemia - هیپوگلایسمی DHE - وRelative Fluorescence Units - واحد فلورسانس نسبیreactive nitrogen species - گونه های واکنش پذیر نیتروژنReactive species - گونه های واکنشیReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
Oxidative stress has been suggested as a mechanism contributing to neuronal death induced by hypoglycemia, and an early production of reactive species (RS) during the hypoglycemic episode has been observed. However, the sources of reactive oxygen (ROS) and nitrogen (RNS) species have not been fully identified. In the present study we have examined the contribution of various enzymatic pathways to RS production and neuronal death induced by glucose deprivation (GD) in hippocampal cultures. We have observed a rapid increase in RS during GD, which depends on the activation of NMDA and non-NMDA receptors and on the influx of calcium from the extracellular space. Accordingly, intracellular calcium concentration [Ca2+]i progressively increases more than 30-fold during the GD period. It was observed that superoxide production through the activation of the calcium-dependent enzymes, phospholipase A2 (cPLA2) and xanthine oxidase (XaO), contributes to neuronal damage, while nitric oxide synthase (NOS) is apparently not involved. Inhibition of cPLA2 decreased RS at early times of GD whereas inhibition of XaO diminished RS at more delayed times. The antioxidants trolox and ebselen also showed a protective effect against neuronal death and diminished RS generation. Inhibition of NADPH oxidase also contributed to the early generation of superoxide. Taking together, the present results suggest that the early activation of calcium-dependent ROS producing pathways is involved in neuronal death associated with glucose deprivation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 167, Issue 4, 2 June 2010, Pages 1057-1069
Journal: Neuroscience - Volume 167, Issue 4, 2 June 2010, Pages 1057-1069
نویسندگان
B. Páramo, K. Hernández-Fonseca, A.M. Estrada-Sánchez, N. Jiménez, A. Hernández-Cruz, L. Massieu,