کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2598947 1133173 2014 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Effect of hexavalent chromium on histone biotinylation in human bronchial epithelial cells
ترجمه فارسی عنوان
اثر کروم شش ظرفیتی بر بیوتینیلینگ هیستون در سلولهای اپیتلیال انسانی
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی


• Cr(VI) (≥2.5 μM) induced histone deacetylation in 16HBE cells.
• Cr(VI) (≤0.6 μM) increased histone biotinylation in 16HBE cells.
• Cr(VI) (≥0.6 μM) affected the distribution of biotinidase in 16HBE cells.
• Cr(VI)-induced histone deacetylation takes part in adjusting histone biotinylation.

Chromium is a potent human mutagen and carcinogen. The capability of chromium to cause cancers has been known for more than a century, and numerous epidemiological studies have been performed to determine its carcinogenicity. In the post-genome era, cancer has been found to relate to epigenetic mutations. However, very few researches have focused on hexavalent chromium (Cr(VI))-induced epigenetic alterations. The present study was designed to investigate whether Cr(VI) would affect the level of a newfound epigenetic modification: histone biotinylation. Histone acetylation and histone biotinylation were studied in detail using human bronchial epithelial (16HBE) cells as an in vitro model after Cr(VI) treatment. Our study showed that Cr(VI) treatment decreased histone acetylation level in 16HBE cells. In addition, low doses of Cr(VI) (≤0.6 μM) elevated the level of histone biotinylation. Furthermore, immunoblot analysis of biotinidase (BTD), a major protein which maintains homeostasis of histone biotinylation, showed that the distribution of BTD became less even and more concentrated at the nuclear periphery in cells exposed to Cr(VI). Moreover, Cr(VI)-induced histone deacetylation may take part in the regulation of histone biotinylation. Together, our study provides new insight into the mechanisms of Cr(VI)-induced epigenetic regulation that may contribute to the chemoprevention of Cr(VI)-induced cancers and may have important implications for epigenetic therapy.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology Letters - Volume 228, Issue 3, 4 August 2014, Pages 241–247
نویسندگان
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