Induction of histone acetylation in mouse erythroleukemia cells by some organosulfur compounds including allyl isothiocyanate

Citation
Ma. Lea et al., Induction of histone acetylation in mouse erythroleukemia cells by some organosulfur compounds including allyl isothiocyanate, INT J CANC, 92(6), 2001, pp. 784-789
Citations number
27
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
INTERNATIONAL JOURNAL OF CANCER
ISSN journal
00207136 → ACNP
Volume
92
Issue
6
Year of publication
2001
Pages
784 - 789
Database
ISI
SICI code
0020-7136(20010615)92:6<784:IOHAIM>2.0.ZU;2-T
Abstract
In previous studies we observed that some allyl sulfides can cause increase d acetylation of histones and differentiation in DSIP mouse erythroleukemia cells. In the present work we observed increased acetylation of histones w ith allyl isothiocyanate and butanethiol but not with butyl sulfide or buty l disulfide, Increased acetylation of histones was established by change in electrophoretic mobility, incorporation of [H-3]acetate or immunoblotting, Histone deacetylase in nuclei of DS19 cells was inhibited 74% by 0.5 mM al lyl mercaptan and 43% by 0.5 mM butanethiol but was not significantly affec ted by 0.5 mM allyl isothiocyanate. There was some degree of reversibility in the effect of allyl isothiocyanate when the cells were incubated for 15 hr in fresh medium. The data suggested that allyl isothiocyanate may stimul ate histone acetylation rather than inhibit histone deacetylation. Addition of allyl isothiocyanate, however, had very little or no additional effect on the induction of histone acetylation caused by trichostatin A. Histone a cetyltransferase activity determined in cell homogenates was not increased by preincubation of cells with allyl isothiocyanate or inclusion of allyl i sothiocyanate in the assay medium, It was concluded that treatment of mouse erythroleukemia cells with allyl isothiocyanate can cause increased acetyl ation of histones but the mechanism for this effect requires further elucid ation, (C) 2001 Wiley-Liss. Inc.