کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2146874 | 1548378 | 2010 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
3-Nitrobenzanthrone and 3-aminobenzanthrone induce DNA damage and cell signalling in Hepa1c1c7 cells
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کلمات کلیدی
3-NBANF-κBPFT-α3-aminobenzanthrone3-ABAATRATM- and Rad3-relatedNOSPifithrin-alphaα-NF3-Nitrobenzanthrone - 3-نیترو بنزنترونونDMSO - DMSOMAPKs - MAPK هاROS - ROSα-Naphthoflavone - α-نفتوفلوانDNA damage - آسیبDNAATM - خودپردازDimethyl sulfoxide - دیمتیل سولفواکسیدCarcinogenesis - سرطانزاییCytokines - سیتوکین هاNuclear factor-kappa B - فاکتور هسته ای-کاپا BCell death - مرگ سلولی Nitro-PAHs - نیترو-PAH هاNitro-polycyclic aromatic hydrocarbons - هیدروکربن های آروماتیک نیترو-چند حلقه ایPropidium iodide - پروتئین یدیدmitogen-activated protein kinases - کیناز پروتئین فعال Mitogenreactive nitrogen species - گونه های واکنش پذیر نیتروژنReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
3-Nitrobenzanthrone (3-NBA) is a mutagenic and carcinogenic environmental pollutant found in diesel exhaust and urban air pollution. In the present work we have characterised the effects of 3-NBA and its metabolite 3-aminobenzanthrone (3-ABA) on cell death and cytokine release in mouse hepatoma Hepa1c1c7 cells. These effects were related to induced DNA damage and changes in cell signalling pathways. 3-NBA resulted in cell death and caused most DNA damage as judged by the amount of DNA adducts (32P-postlabelling assay), single strand (ss)DNA breaks and oxidative DNA lesions (comet assay) detected. An increased phosphorylation of H2AX, chk1, chk2 and partly ATM was observed using flow cytometry and/or Western blotting. Both compounds increased phosphorylation of p53 and MAPKs (ERK, p38 and JNK). However, only 3-NBA caused an accumulation of p53 in the nucleus and a translocation of Bax to the mitochondria. The p53 inhibitor pifithrin-alpha inhibited 3-NBA-induced apoptosis, indicating that cell death was a result of the triggering of DNA signalling pathways. The highest phosphorylation of Akt and degradation of IκB-α (suggesting activation of NF-κB) were also seen after treatment with 3-NBA. In contrast 3-ABA increased IL-6 release, but caused little or no toxicity. Cytokine release was inhibited by PD98059 and curcumin, suggesting that ERK and NF-κB play a role in this process. In conclusion, 3-NBA seems to have a higher potency to induce DNA damage compatible with its cytotoxic effects, while 3-ABA seems to have a greater effect on the immune system.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 684, Issues 1â2, 3 February 2010, Pages 11-23
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 684, Issues 1â2, 3 February 2010, Pages 11-23
نویسندگان
N.E. Landvik, V.M. Arlt, E. Nagy, A. Solhaug, X. Tekpli, H.H. Schmeiser, M. Refsnes, D.H. Phillips, D. Lagadic-Gossmann, J.A. Holme,