کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9028636 | 1561662 | 2005 | 4 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Benzene metabolites block gap junction intercellular communication
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
A metabolite of benzene, trans,trans-muconaldehyde (MUC) was found to be a strong inhibitor of gap junction intercellular communication (GJIC) with potency similar to that of chlordane. Hydroquinone and the MUC metabolite OH-M-CHO were also strong inhibitors of GJIC. The other MUC metabolites tested, CHO-M-COOH and OH-M-COOH had weak effects on GJIC, while COOH-M-COOH had no effect. Benzene showed no effect on GJIC. The relative potency of the metabolites on GJIC is similar to what is observed with regard to hematotoxic effects. The effect of MUC on GJIC took place in parallel with a strong cellular loss of connexin 43. Substances found to inhibit connexin 43 dependent GJIC have been shown to disrupt normal hematopoietic development. The finding that benzene metabolites interfere with gap junction functionality, and especially the loss of connexin 43 induced by MUC, should be considered concerning the mechanism of benzene-induced hematotoxicity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Chemico-Biological Interactions - Volumes 153â154, 30 May 2005, Pages 257-260
Journal: Chemico-Biological Interactions - Volumes 153â154, 30 May 2005, Pages 257-260
نویسندگان
Edgar Rivedal, Gisela Witz,