The linking chain length in bridged aldehyde-substituted pyridinium dimers modulates a slow reversible binding that affects supercoiling of plasmid DNA.

Bridged aldehyde substituted pyridinium dimers bind to DNA. Binding induces retardation of the electrophoretic migration of circular plasmid due to relaxation of supercoiling. Binding to DNA is slow and reversible and depends on the length of linking chain, pH, ionic strength and temperature. It is postulated that release of topological stress results from the disruption of hydrogen bonding between complementary bases, a hypothesis consistent with facilitated attack of DNA by formaldehyde promoted by the bridged compounds.