کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5861704 | 1133764 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
CYP2E1 induction leads to oxidative stress and cytotoxicity in glutathione-depleted cerebellar granule neurons
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کلمات کلیدی
CGNsL-buthionine sulfoximine8-oxo-7,8-dihydro-2-deoxyguanosine8-oxodGCYP2E1BSO8-oxo-dGGSHDASINHROS - ROSisoniazid - ایزونیازیدOxidative stress - تنش اکسیداتیوdiallyl sulfide - دیالیل سولفیدDIV - دیوdays in vitro - روز in vitrocerebellar granule cells - سلول های گرانول مخچهcytochrome P450 2E1 - سیتوکروم P450 2E1cerebellar granule neurons - نورونهای گرانشی مخچهGlutathione - گلوتاتیونReactive 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
چکیده انگلیسی
Increasing evidence suggests that brain cytochrome P450 (CYP) can contribute to the in situ metabolism of xenobiotics. In the liver, some xenobiotics can be metabolized by CYPs into more reactive products that can damage hepatocytes and induce cell death. In addition, normal CYP activity may produce reactive oxygen species (ROS) that contribute to cell damage through oxidative mechanisms. CYP2E1 is a CYP isoform that can generate ROS leading to cytotoxicity in multiple tissue types. The aim of this study was to determine whether CYP2E1 induction may lead to significant brain cell impairment. Immunological analysis revealed that exposure of primary cerebellar granule neuronal cultures to the CYP inducer isoniazid, increased CYP2E1 expression. In the presence of buthionine sulfoximine, an agent that reduces glutathione levels, isoniazid treatment also resulted in reactive oxygen species (ROS) production, DNA oxidation and cell death. These effects were attenuated by simultaneous exposure to diallyl sulfide, a CYP2E1 inhibitor, or to a mimetic of superoxide dismutase/catalase, (Euka). These results suggest that in cases of reduced antioxidant levels, the induction of brain CYP2E1 could represent a risk of in situ neuronal damage.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology in Vitro - Volume 28, Issue 7, October 2014, Pages 1206-1214
Journal: Toxicology in Vitro - Volume 28, Issue 7, October 2014, Pages 1206-1214
نویسندگان
Valencia-Olvera Ana Carolina, Morán Julio, Camacho-Carranza Rafael, Prospéro-GarcÃa Oscar, Espinosa-Aguirre Jesús Javier,