N-Nitrosopiperidine (NP) and various derivatives were fed to Drosophila melanogaster males over a wide concentration range in order to assess their mutagenic potency in the induction of X-linked recessive lethals and chromosome loss. NP was effective in inducing lethals, as were its halogen and methylsubstituted derivatives, with the exception of 2,6-dimethyl NP. (Methyl substitutions at the alpha carbon atoms reduce or eliminate mutagenic activity.) Substitutions of halogen groups on the piperidine ring enhanced the mutagenic activity, with the 3-chloro compound being the most mutagenic. In contrast, substitutions with a hydroxyl, carboxyl, or keto group resulted in a loss of mutagenicity. None of the compounds tested increased the frequency of chromosome loss or breakage in mature sperm.

Hindered amines such as 2,2,6,6-tetramethyl piperidines and N-methyl-2,2,6,6-tetramethyl piperidines and hindered amino ethers such as N-methoxy-2,2,6,6-tetramethyl piperidines were examined with respect to their reactivity towards triplet-excited benzophenone (3BP∗) in Ar-saturated acetonitrile solution at room temperature. Upon measuring phosphorescence decay rates in the absence and presence of quencher it was found that the amines are two to three orders of magnitude more reactive than the amino ethers. For all amine/BP systems examined the generation of free ions was inferred from an increase in the electrical conductivity. This indicates that a charge transfer (CT) mechanism is operative in these cases. Notably, tertiary amines were found to be more reactive towards 3BP∗ and give higher free ion yields than secondary amines. In the case of amino ether/BP systems evidence for a CT mechanism was not obtained in spite of an increase in the electrical conductivity indicating the generation of free ions. The latter are formed much faster than the phosphorescence decays and very likely originate from triplet–triplet annihilation (3BP∗+3BP∗→BP++BP−).