کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5858941 | 1562316 | 2016 | 37 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Repeated exposure to neurotoxic levels of chlorpyrifos alters hippocampal expression of neurotrophins and neuropeptides
ترجمه فارسی عنوان
قرار گرفتن در معرض سطوح عصبی تنفسی کلروپیریفوس تکرار می شود و بیان هیپوکامپ نوروپروتئین ها و نوروپروتئین ها را تغییر می دهد
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کلمات کلیدی
GABRG2DYRK1As.c.mitogen-activated protein kinase kinase 4ADCYAP1R1MDKMADDMAP2K4acyl-CoA oxidase 1aRNAMAPK1CDH13MAP1BSEQNPTX2Corticotropin-releasing factor-binding proteinADORA1Syt1PNOCSlit3CRHBPsynaptotagmin-1gamma-aminobutyric acid receptorpituitary adenylate cyclase-activating polypeptide receptorPrepronociceptinFDRNPYb.w.ACOX1CPFMidkineBDNF - BDNF یا فاکتور نورونزایی مشتقشده از مغز Antisense RNA - RNA آنتیسنسAdenosine A1 receptor - آدنوزین A1 گیرندهOrganophosphorus - ارگانوفسفورSpectrin - اسپکترونیGene expression - بیان ژنsequencing - توالییابیMicroarray - ریزآرایهsubcutaneous - زیر جلدیSerglycin - سروگلیسینOrganophosphorus pesticide - سموم دفع آفات فسفرDEG - شماphosphatase and tensin homolog - فسفاتاز و تنسین همولوگLong Evans - لوی اوانسCholinesterase inhibition - مهار کولین استرازfalse discovery rate - میزان کشف کاذبMiRNA - میکروRNA، ریزآرانای، miRNAGene ontology - هستیشناسی ژنیbody weight - وزن بدنMicrotubule-associated protein 1B - پروتئین وابسته به میکروتوبول 1Bmitogen-activated protein kinase 1 - پروتئین کیناز فعال با mitogen-1Pten - ژن PTENDifferentially expressed gene - ژن بیان شده متفاوت استChlorpyrifos - کلرپیریفوسMultiple acyl-CoA dehydrogenase deficiency - کمبود کمبود آسیل-کئوآآدیدروژنازCHE - کهCORT - کورتCortistatin - کورتیستاتینCholinesterase - کولین استرازNeuropeptide Y - یوروپروتئین Y
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی
Chlorpyrifos (CPF), an organophosphorus pesticide (OP), is one of the most widely used pesticides in the world. Subchronic exposures to CPF that do not cause cholinergic crisis are associated with problems in cognitive function (i.e., learning and memory deficits), but the biological mechanism(s) underlying this association remain speculative. To identify potential mechanisms of subchronic CPF neurotoxicity, adult male Long Evans (LE) rats were administered CPF at 3 or 10Â mg/kg/d (s.c.) for 21 days. We quantified mRNA and non-coding RNA (ncRNA) expression profiles by RNA-seq, microarray analysis and small ncRNA sequencing technology in the CA1 region of the hippocampus. Hippocampal slice immunohistochemistry was used to determine CPF-induced changes in protein expression and localization patterns. Neither dose of CPF caused overt clinical signs of cholinergic toxicity, although after 21 days of exposure, cholinesterase activity was decreased to 58% or 13% of control levels in the hippocampus of rats in the 3 or 10Â mg/kg/d groups, respectively. Differential gene expression in the CA1 region of the hippocampus was observed only in the 10Â mg/kg/d dose group relative to controls. Of the 1382 differentially expressed genes identified by RNA-seq and microarray analysis, 67 were common to both approaches. Differential expression of six of these genes (Bdnf, Cort, Crhbp, Nptx2, Npy and Pnoc) was verified in an independent CPF exposure study; immunohistochemistry demonstrated that CRHBP and NPY were elevated in the CA1 region of the hippocampus at 10Â mg/kg/d CPF. Gene ontology enrichment analysis suggested association of these genes with receptor-mediated cell survival signaling pathways. miR132/212 was also elevated in the CA1 hippocampal region, which may play a role in the disruption of neurotrophin-mediated cognitive processes after CPF administration. These findings identify potential mediators of CPF-induced neurobehavioral deficits following subchronic exposure to CPF at a level that inhibits hippocampal cholinesterase to less than 20% of control. An equally significant finding is that subchronic exposure to CPF at a level that produces more moderate inhibition of hippocampal cholinesterase (approximately 50% of control) does not produce a discernable change in gene expression.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology - Volume 340, 18 January 2016, Pages 53-62
Journal: Toxicology - Volume 340, 18 January 2016, Pages 53-62
نویسندگان
Young S. Lee, John A. Lewis, Danielle L. Ippolito, Naissan Hussainzada, Pamela J. Lein, David A. Jackson, Jonathan D. Stallings,