کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5861422 | 1133760 | 2015 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Global histone modifications in Fumonisin B1 exposure in rat kidney epithelial cells
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کلمات کلیدی
PBSH3K9acNRK-52EH3K9me2NOELHistone H3 lysine 9 trimethylationJECFAhMTH3K4me3PMTDIhistone H3 lysine 9 acetylationNRK-52E cellsH4K20me3FB1PICTSAH3K9me3International Agency for Research on Cancer - آژانس بین المللی تحقیقات سرطانIARC یا International Agency for Research on Cancer - آژانس بین المللی تحقیقات سرطانTrichostatin A - تریکوستاتین AHistone modifications - تغییرات هیستونprovisional maximum tolerable daily intake - حداکثر مصرف روزانه قابل تحمل روزانهstandard error - خطای استانداردphosphate buffer saline - فسفات بافر شورFumonisin B1 - فومونیزین B1Joint FAO/WHO Expert Committee on Food Additives - مجمع متخصص FAO / WHO در مورد مواد افزودنی مواد غذاییhistone H3 lysine 4 trimethylation - هیستون H3 لیزین 4 trimethylationHistone acetyltransferase - هیستون استیل ترانسفرازHistone Methyltransferase - هیستون متیل ترانسفرازNo observed effect level - هیچ سطح اثر مشاهده شدهHAT - کلاهprotease inhibitor cocktail - کوکتل مهار کننده پروتئاز
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
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چکیده انگلیسی
Fumonisin B1 (FB1) is a Fusarium mycotoxin frequently occurring in maize-based food and feed. Although the effects of FB1 on sphingolipid metabolism are clear, little is known about early molecular changes associated with FB1 carcinogenicity. It has been shown that FB1 disrupts DNA methylation and chromatin modifications in HepG2 cells. We investigated dose- and time-dependent effects of FB1 in global histone modifications such as histone H3 lysine 9 di-, trimethylation (H3K9me2/me3), histone H3 lysine 4 trimethylation (H3K4me3), histone H4 lysine 20 trimethylation (H4K20me3), histone H3 lysine 9 acetylation (H3K9ac) and the enzymes involved in these mechanisms in rat kidney epithelial cells (NRK-52E). The increased levels of global H3K9me2/me3 were observed in FB1 treated cells, while the global levels of H4K20me3 and H3K9ac were decreased. FB1 caused some changes on the activities of H3K9 histone methyltransferase (HMT) and histone acetyltransferase (HAT) at high concentrations in NRK-52E cells. Further, the effects of trichostatin A (TSA), a histone deacetylase inhibitor, were investigated in NRK-52E cells. TSA was found to cause an increase on H3K9ac levels as expected. In this study we suggest that FB1 may disrupt epigenetic events by altering global histone modifications, introducing a novel aspect on the potential mechanism of FB1 carcinogenesis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology in Vitro - Volume 29, Issue 7, October 2015, Pages 1809-1815
Journal: Toxicology in Vitro - Volume 29, Issue 7, October 2015, Pages 1809-1815
نویسندگان
Duygu Sancak, Sibel Ozden,