The absorption and steady-state emission properties of a series of N-alkyl- and N-aryl-9-aminoacridizinium derivatives and two 9-sulfanyl-substituted acridizinium derivatives were investigated. The N-alkyl derivatives and the 9-methylsulfanylacridizinium have an intense intrinsic fluorescence (phi(f) = 0.2-0.6), whereas the N-aryl-substituted compounds are virtually nonfluorescent in liquid solutions (phi(f) <= 0.01). The emission intensity of the latter compounds significantly increases with increasing viscosity of the medium. It is demonstrated that the excited-state deactivation of the N-aryl-9-aminoacridizinium derivatives is due to two nonradiative processes: (i) torsional relaxation by rotation about the N-aryl bond and (ii) an electron-transfer process from an electron-donor substituted phenyl ring to the photoexcited acridizinium chromophore. The binding of several representative acridizinium derivatives to double-stranded DNA was studied by the spectrophotometric titrations and linear dichroism spectroscopy. The results give evidence that the prevailing binding mode is intercalation with binding constants in the range (0.5-5.0) x 10(5) M-1 (in base pairs). Notably, the binding of most of the N-aryl-9-aminoacridizinium derivatives leads to a fluorescence enhancement by a factor of up to 50 upon binding to the biomacromolecules. Moreover, the addition of selected proteins, namely albumins, to N-(halogenophenyl)-9-aminoacridizinium ions in the presence of an anionic surfactant (sodium dodecyl sulfate) results in a 20-fold fluorescence enhancement. In each case, the emission enhancement is supposed to result from the hindrance of the torsional relaxation in the corresponding binding site of the biomacromolecule, which in turn suppresses the excited-state deactivation pathway.