کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2010415 1066973 2016 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Ethylene glycol ethers induce apoptosis and disturb glucose metabolism in the rat brain
ترجمه فارسی عنوان
اتر اتیلن گلیکول باعث ایجاد آپوپتوز و متابولیسم گلوکز در مغز موش صحرایی می شود
کلمات کلیدی
اتر اتیلن گلیکول، آپوپتوز متابولیسم گلوکز، سموم زیست محیطی
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
چکیده انگلیسی

BackgroundEthylene glycol ethers (EGEs) are compounds widely used in industry and household products, but their potential, adverse effect on brain is poorly understood, so far. The aim of the present study was to determine whether 4-week administration of 2-buthoxyethanol (BE), 2-phenoxyethanol (PHE), and 2-ethoxyethanol (EE) induces apoptotic process in the rat hippocampus and frontal cortex, and whether their adverse effect on the brain cells can result from disturbances in the glucose metabolism.MethodsExperiments were conducted on 40 rats, exposed to BE, PHE, EE, saline or sunflower oil for 4 weeks. Markers of apoptosis and glucose metabolism were determined in frontal cortex and hippocampus by western blot, ELISA, and fluorescent-based assays.ResultsBE and PHE, but not EE, increased expression of the active form of caspase-3 in the examined brain regions. BE and PHE increased caspase-9 level in the cortex and PHE also in the hippocampus. BE and PHE increased the level of pro-apoptotic proteins (Bax, Bak) and/or reduced the concentration of anti-apoptotic proteins (Bcl-2, Bcl-xL); whereas, the effect of BE was observed mainly in the cortex and that of PHE in the hippocampus. It has also been found that PHE increased brain glucose level, and both BE and PHE elevated pyruvate and lactate concentration.ConclusionsIt can be concluded that chronic treatment with BE and PHE induced mitochondrial pathway of apoptosis, and disturbed glucose metabolism in the rat brain.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Pharmacological Reports - Volume 68, Issue 1, February 2016, Pages 162–171
نویسندگان
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