The effect of phenobarbital on the methylation level of the p16 promoter region in rat liver.

It has been suggested that non-genotoxic carcinogens (NGCs) may cause modification of the DNA methylation status. We studied the effects of phenobarbital (PB) -- a non-genotoxic rodent liver carcinogen -- on the methylation level of the promoter region of the p16 suppressor gene, as well as on hepatomegaly, DNA synthesis, and DNA-methyltransferase (DNMTs) activity in the rat liver. Male Wistar rats received PB in 1, 3 or 14 daily oral doses (at 24-h intervals), each equivalent to 1/10 of the LD(50) value.

[DNA methylation--alternative mechanism of chemical carcinogenesis].

It is increasingly accepted that the initiation of chemical carcinogenesis should be considered as a transformation process of a normal cell caused by genetic changes, i.e. mutational DNA damage and/or epigenetic changes, which render normal gene expression impossible with the preservation of the DNA sequence intact.

Tetra-amino-acid tandem repeats are involved in HsdS complementation in type IC restriction-modification systems.

All known type I restriction and modification (R-M) systems of Escherichia coli and Salmonella enterica belong to one of four discrete families: type IA, IB, IC or ID. The classification of type I systems from a wide range of other genera is mainly based on complementation and molecular evidence derived from the comparison of the amino acid similarity of the corresponding subunits. This affiliation was seldom based on the strictest requirement for membership of a family, which depends on relatedness as demonstrated by complementation tests.