Preliminary electrochemical study of Ap3A and Ap4A potential role in enhancing allicin-induced DNA denaturization and susceptibility to structure damage

Thiopolysulfides (TPS) are a group of organic sulphur compounds and are a part of secondary metabolites produced by plants of the Alliaceae family. A key representative compound of TPS is allicin, which has documented bacteriostatic properties by damaging bacterial DNA. However, in eukaryotic organisms, it exhibits no genotoxic effects, except for cancer cells, for which the IC 50 is significantly higher than that of non-cancerous cells. Diadenosine tetraphosphate (Ap 4 A) is recognized as a stress-responsive signaling nucleotide whose intracellular levels rise under environmental and genotoxic stresses. Current evidence suggests that Ap 4 A may participate in cellular pathways associated with response to DNA damage-including the regulation of gene expression, DNA replication, and possibly immune signaling, although these roles remain incompletely characterised and require further experimental validation. To determine whether cell cycle regulators such as Ap 4 A and Ap 3 A may be responsible for regulating and limiting the DNA structure and damage induced by allicin, we applied dsDNA to a carbon paste electrode (CPE) in the set of three-electrodes. After electrostatic deposition of dsDNA, the CPE was transferred to a well containing different concentrations of Ap 4 A or Ap 3 A aliquots for kinematic association with bonded DNA strands. Changes in adenine and guanine signals showed that Ap 3 A may, at a certain dose, trigger the allicin ability to interact with dsDNA, disrupting A-T base pairs in DNA. In opposition, Ap 4 A interactswith allicin limiting the susceptibility of G-C bonds to dissolve and thus limiting guanosine tendency to oxidation.