ABSTRACT
The discovery that butyrate at millimolar concentrations causes hyperacetylation of eukaryotic chromatin (Riggs et al., 1977) by inhibiting histone deacetylases (Cousens et al., 1979) triggered a large number of investigations on the biological role of histone acetylation, in which butyrate was used as a tool for achieving a higher acetylated state of core histones. The previous observations, that butyrate treatment leads to the induction of the globin gene in Friend erythroleukemia cells (Leder and Leder, 1975) and increases the activity of various enzymes in other cell lines (Prasad and Sinha, 1976), were consistent with a positive regulatory role of histone acetylation in eukaryotic gene expression (Allfrey et al., 1964). In addition it was noted that butyrate is an inhibitor of cell growth (Wright, 1973) and an inducer of differentiation (Prasad, 1980; Kruh, 1982). Moreover, butyratetreated cells exhibited drastic changes in cell morphology and a large number of other pleiotropic effects. Generally, the effects of butyrate appeared to be reversible. The manifold effects of butyrate observed in studies with cell lines derived from a great variety of species and tissues were the subject of previous reviews (Prasad, 1980; Kruh, 1982; Kruh et al., 1992).
