Alterations In DNA Structure Research Articles

Entropy Driven Binding of 2-(4-Aminophenyl)benzothiazole with DNA: An Experimental and Theoretical Insights

Molecular recognition driven by molecular interactions is an intricate part of drug discovery and targeted drug delivery systems due to the dependence of thetherapeutic properties of drugs on interaction with desired target biomolecules as receptors. 2-(4-Aminophenyl) benzothiazole (APB), a heterocyclic molecule containing a benzothiazole nucleus, is known to induce apoptosis besides inhibiting cancer cell development and has been found effective against different microorganisms. This study highlights the spectroscopic and theoretical investigation of binding interactions of APB and ct-DNA. The UV-vis experiments indicate a binding constant of 9.73 ± 0.4 × 105 M-1. The measured binding constants of 1.0 ± 0.2 × 105, 2.4 ± 0.3 × 105 and 3.5 ± 0.3 × 105 at 298, 303 and 308 K, respectively, from fluorescence experiments indicated a dynamic quenching type. The binding was driven by hydrophobic forces with positive ΔHº (64.8467 ± 2 KJ mol–1) and ΔSº (317.12 ± 2 J mol–1 K–1) values besides spontaneity of the process with negative ΔGº values. The binding of APB molecule in the minor groove of ct-DNA was demonstrated by DNA melting tests, viscosity measurements and site marker displacement using ethidium bromide and Hoechst. Additional studies conducted by KI provided support for minor groove binding and NaCl has no impact on the binding electrostatic interactions, while the CD investigations showed no DNA structural alterations. Molecular docking studies also confirmed the experimental findings placing APB in the ct-DNA minor groove.

Deciphering HMGB1: Across a spectrum of DNA and nucleosome dynamics

AbstractHMGB1 is the most abundant nonhistone nuclear protein, which has been widely studied for its roles in the cytoplasm as an autophagy mediator and in the extracellular matrix as an inflammatory molecule. Studies concerning HMGB1's actual role and its binding within the nucleus are inadequate. Through this in vitro study, we aimed to discern the binding parameters of HMGB1 with various types of DNA, nucleosomes, and chromatin. HMGB1 binds differentially to different DNA, with a high affinity for altered DNA structures such as triplex and bulge DNA. Remodelling of nucleosome by CHD7 remodeller was negatively impacted by the binding of HMGB1. We also found that HMGB1 binds to the linker DNA of chromatin. Findings from this study shed light on the diverse roles HMGB1 may play in transcription, gene expression, viral replication, CHARGE syndrome and so forth.

Canonical and Non-Canonical Roles of Human DNA Polymerase η.

DNA damage tolerance pathways that allow for the completion of replication following fork arrest are critical in maintaining genome stability during cell division. The main DNA damage tolerance pathways include strand switching, replication fork reversal and translesion synthesis (TLS). The TLS pathway is mediated by specialised DNA polymerases that can accommodate altered DNA structures during DNA synthesis, and are important in allowing replication to proceed after fork arrest, preventing fork collapse that can generate more deleterious double-strand breaks in the genome. TLS may occur directly at the fork, or at gaps remaining behind the fork, in the process of post-replication repair. Inactivating mutations in the human POLH gene encoding the Y-family DNA polymerase Pol η causes the skin cancer-prone genetic disease xeroderma pigmentosum variant (XPV). Pol η also contributes to chemoresistance during cancer treatment by bypassing DNA lesions induced by anti-cancer drugs including cisplatin. We review the current understanding of the canonical role of Pol η in translesion synthesis following replication arrest, as well as a number of emerging non-canonical roles of the protein in other aspects of DNA metabolism.

Advancing Epigenetic and Antioxidant Strategies in Natural Therapeutics Against SARS-CoV-2: A Mini Review of Current Innovations and Future Directions

Abstract: This review explores the potential of natural products, particularly curcumin and gingerol, as immune regulators and anti-inflammatory agents in combating SARS-CoV-2 infections via epigenetic and antioxidant mechanisms. Oxidative stress induced by coronavirus infections can trigger severe immune responses, such as cytokine storms, often leading to therapy failure. This oxidative stress is exacerbated by depleted antioxidant defenses. The review examines how natural ingredients activate endogenous antioxidants through pathways like nuclear factor erythroid 2-related factor 2 (Nrf-2) activation, leading to gene expression changes without altering DNA structure. These changes enhance cellular defenses against oxidative stress and reduce inflammation, potentially mitigating the virus's effects. The methodology involved a literature review of scientific articles from databases such as Google Scholar, Elsevier, Science Direct, Scopus, and Wiley Online Library, focusing on publications from 2010 to 2023. Data were analyzed using deductive qualitative descriptive techniques, emphasizing the role of natural compounds in activating antioxidant responses to prevent or minimize cellular damage caused by COVID-19. The review underscores the significant role of diet and nutritional intake in supporting the body's antioxidant capacity by activating specific receptors that influence gene expression related to immune responses and cellular repair mechanisms. Flavonoids and anthocyanins are highlighted as key compounds in natural products with therapeutic potential against COVID-19. Overall, this research advocates for further exploration of natural products as viable options for preventing and treating COVID-19, suggesting that these compounds offer dual benefits of antiviral activity and immune modulation through epigenetic regulation and antioxidant support.

Mutations in tyrosyl-DNA phosphodiesterase 2 suppress top-2 induced chromosome segregation defects during Caenorhabditis elegans spermatogenesis

Meiosis reduces ploidy through two rounds of chromosome segregation preceded by one round of DNA replication. In meiosis I, homologous chromosomes segregate, while in meiosis II, sister chromatids separate from each other. Topoisomerase II (Topo II) is a conserved enzyme that alters DNA structure by introducing transient double-strand breaks. During mitosis, Topo II relieves topological stress associated with unwinding DNA during replication, recombination, and sister chromatid segregation. Topo II also plays a role in maintaining mitotic chromosome structure. However, the role and regulation of Topo II during meiosis is not well-defined. Previously, we found an allele of Topo II, top-2(it7), disrupts homologous chromosome segregation during meiosis I of Caenorhabditis elegans spermatogenesis. In a genetic screen, we identified different point mutations in 5'-tyrosyl-DNA phosphodiesterase two (Tdp2, C.elegans tdpt-1) that suppress top-2(it7) embryonic lethality. Tdp2 removes trapped Top-2-DNA complexes. The tdpt-1 suppressing mutations rescue embryonic lethality, ameliorate chromosome segregation defects, and restore TOP-2 protein levels of top-2(it7). Here, we show that both TOP-2 and TDPT-1 are expressed in germ line nuclei but occupy different compartments until late meiotic prophase. We also demonstrate that tdpt-1 suppression is due to loss of function of the protein and that the tdpt-1 mutations do not have a phenotype independent of top-2(it7) in meiosis. Lastly, we found that the tdpt-1 suppressing mutations either impair the phosphodiesterase activity, affect the stability of TDPT-1, or disrupt protein interactions. This suggests that the WT TDPT-1 protein is inhibiting chromosome biological functions of an impaired TOP-2 during meiosis.

Mono-quinoxaline-induced DNA structural alteration leads to ZBP1/RIP3/MLKL-driven necroptosis in cancer cells

Evading the cellular apoptosis mechanism by modulating multiple pathways poses a sturdy barrier to effective chemotherapy. Cancer cell adeptly resists the apoptosis signaling pathway by regulating anti and pro-apoptotic proteins to escape cell death. Nevertheless, bypassing the apoptotic pathway through necroptosis, an alternative programmed cell death process, maybe a potential therapeutic modality for apoptosis-resistant cells. However, synthetic mono-quinoxaline-based intercalator-induced cellular necroptosis as an anti-cancer perspective remains under-explored. To address this concern, we undertook the design and synthesis of quinoxaline-based small molecules (3a-3l). Our approach involved enhancing the π-surface of the mandatory benzyl moiety to augment its ability to induce DNA structural alteration via intercalation, thereby promoting cytotoxicity across various cancer cell lines (HCT116, HT-29, and HeLa). Notably, the potent compound 3a demonstrated the capacity to induce DNA damage in cancer cells, leading to the induction of ZBP1-mediated necroptosis in the RIP3-expressed cell line (HT-29), where Z-VAD effectively blocked apoptosis-mediated cell death. Interestingly, we observed that 3a induced RIP3-driven necroptosis in combination with DNA hypomethylating agents, even in the RIP3-silenced cell lines (HeLa and HCT116). Overall, our synthesized compound 3a emerged as a promising candidate against various cancers, particularly in apoptosis-compromised cells, through the induction of necroptosis.

Bleomycin-induced modulations of PARP 1 activity, NAD+ and PARG content in rat lung nuclei

Bleomycin-induced lung pathology in rodents is a well recognized animal model widely used for evaluation of new therapeutic approaches in treatment of lung inflammation and fibrotic diseases. It is documented that poly(ADP-ribose)polymerase 1 activity has a significant role in development of inflammatory processes in the heart, liver and brain. Herein, we used biochemical and immunochemical methods for estimation of poly(ADP-ribose)polymerase 1 (PARP 1) activity, NAD+ and poly(ADP-ribose)glycohydrolase (PARG) protein content in rat lung nuclei during the inflammatory phase in a bleomycin-induced one-hit rat model. To evaluate the influence of bleomycin – induced alterations in DNA structure on regulation of poly(ADP-ribose)polymerase 1 activation pathways, we isolated DNA from nuclei of lung tissues in the phase of acute lung inflammation induced by bleomycin, and DNA melting profiles were investigated. In the present study we investigated whether naturally occurring water-soluble polyphenol tannic acid with widely accepted anti-fibrotic and anti-inflammatory effects can influence poly(ADP-ribose)polymerase 1 activity, NAD+ and poly(ADP-ribose)glycohydrolase protein content in nuclear fraction isolated from rat lung tissues in a bleomycin-induced acute lung injury model. It was demonstrated that NAD+ level and poly(ADP-ribose)glycohydrolase protein content decreased in rat lung nuclei during the inflammatory phase in the bleomycin-induced acute lung injury model. Treatment of rats with tannic acid enhanced the effects displayed by bleomycin in lung nuclei, thus indicating synergistic interaction with the drug in the field covering PARP 1 activity, poly(ADP-ribose)glycohydrolase (PARG) protein and NAD+ content in lung nuclei. We observed PARP 1 inhibition in nuclei of lung tissue during the inflammatory phase in the bleomycin-induced acute lung injury rat model, which could be coupled with the drop of NAD+ level in nuclei. In the present study we highlighted that bleomycin (BLM) can induce DNA destabilization in lung nuclei. It was proposed that bleomycin-induced modulations in DNA structure could hamper PARP 1 binding with DNA and down-regulate the enzyme activating pathway in lung nuclei. The role of poly(ADP-ribose)glycohydrolase depletion in lung nuclei and sequential accumulation of poly(ADP-ribose)polymers in lung cells, which triggers their destruction and tissues damage, was proposed. It is suggested that in the light of synergistic interaction between bleomycin and tannic acid (TA) the anti-inflammatory role of tannic acid should be repurposed.

Evaluation of the toxicity of clozapine on the freshwater diatom Navicula sp. using the FTIR spectroscopy

Clozapine is an often prescribed neuroactive pharmaceutical and frequently detected in the aquatic environments. However, its toxicity on low trophic level species (i.e., diatoms) and associated mechanisms are seldom reported. In this study, the toxicity of clozapine on a widely distributed freshwater diatom Navicula sp. was evaluated using the FTIR spectroscopy along with biochemical analyses. The diatoms were exposed to various concentrations of clozapine (0, 0.01, 0.05, 0.10, 0.50, 1.00, 2.00, 5.00 mg/L) for 96 h. The results revealed that clozapine reached up to 392.8 μg/g in the cell wall and 550.4 μg/g within the cells at 5.00 mg/L, suggesting that clozapine could be adsorbed extracellularly and accumulated intracellularly in diatoms. In addition, hormetic effects were displayed on the growth and photosynthetic pigments (chlorophyll a and carotenoid) of Navicula sp., with a promotive effect at concentrations less than 1.00 mg/L while an inhibited effect at concentrations over 2 mg/L. Clozapine induced oxidative stress in Navicula sp., accompanied by decreased levels of total antioxidant capacity (T-AOC) (>0.05 mg/L), in which, the activity of superoxide dismutase (SOD) (at 5.00 mg/L) was increased whereas the activity of catalase (CAT) (>0.05 mg/L) was decreased. Furthermore, FTIR spectroscopic analysis showed that exposure to clozapine resulted in accumulation of lipid peroxidation products, increased sparse β-sheet structures, and altered DNA structures in Navicula sp. This study can facilitate the ecological risk assessment of clozapine in the aquatic ecosystems.

Di-aryl-aldimines synthesis, crystal structure, anticancer efficacy, and molecular docking with active proteins

The di-aryl-aldimines 3a and 3b have been synthesized, respectively, by reaction of 2‑hydroxy-1-naphthaldehyde 1a or 9-phenanthrenecarboxaldehyde 1b with 1-aminonaphthalene 2. Careful analysis of molecular packing at both qualitative and quantitative levels has been performed using Hirshfeld calculations. In both compounds, the CH…π and π-π stacking interactions are the most important. In case of 3a, the H…H, H…C and C…C contacts contributed significantly by 46.2, 36.0 and 7.0%, respectively. The corresponding values in case of 3b, are 44.4–47.7, 43.8–50.1 and 3.0–6.2%, respectively. The electronic aspects and NMR chemical shifts have been calculated using DFT. In both compounds, high correlation coefficients between the calculated and experimental chemical shifts have been obtained. Compounds 3a and 3b anticancer qualities prevent the development of cancer cells in the HepG2 liver cell line and the MCF-7 breast cell line, respectively. The development of molecular docking modules used components 3a and 3b against topoisomerase in liver cancer and aromatase cytochrome P450 in breast cancer receptor protein. Compounds 3a and 3b were found to have the largest influence on DNA structural alterations and inhibit the production of estrogen and progesterone in molecular docking studies.

Biophysical characterization of the DNA binding motif of human phospholipid scramblase 1.

Human phospholipid scramblase 1 (hPLSCR1) is a 37kDa multi-compartmental protein, which was initially identified as a Ca2+-dependent phospholipid translocator upon localizing to the plasma membrane. However, under certain physiological conditions, hPLSCR1 is localized to the nucleus where it interacts with the IP3R1 promoter (IP3R1P) and regulates its expression. In this study, the DNA binding properties of hPLSCR1 and ∆100-hPLSCR1 (N-terminal 100 amino acids deleted from hPLSCR1) were investigated by using a synthetic IP3R1P oligonucleotide and nonspecific scrambled-sequence oligonucleotides. Our results revealed that hPLSCR1 and ∆100-hPLSCR1 were bound to IP3R1P oligos in a 1:1 stoichiometry. In addition, ∆160-hPLSCR1 could not bind to IP3R1P oligonucleotide suggesting that the proposed DNA binding motif is the actual DNA binding motif. Specific binding of hPLSCR1 and ∆100-hPLSCR1 to IP3R1P oligos was demonstrated by fluorescence anisotropy assay. ITC analysis revealed that hPLSCR1 binds to IP3R1P oligos with Kd = 42.91 ± 0.23nM. Binding of IP3R1P oligos induces β-sheet formation in hPLSCR1 and increases the thermal stability of hPLSCR1 and ∆100-hPLSCR1. Binding of IP3R1P oligos to hPLSCR1 altered the B-form of the DNA, which was not observed with ∆100-hPLSCR1. Results from this study suggest that (i) ∆100-hPLSCR1 possesses a minimal DNA binding region and (ii) structural alterations of IP3R1P oligo by hPLSCR1 require proline-rich N-terminal region.

Multi-Faceted Roles of ERCC1-XPF Nuclease in Processing Non-B DNA Structures

Genetic instability can result from increases in DNA damage and/or alterations in DNA repair proteins and can contribute to disease development. Both exogenous and endogenous sources of DNA damage and/or alterations in DNA structure (e.g., non-B DNA) can impact genome stability. Multiple repair mechanisms exist to counteract DNA damage. One key DNA repair protein complex is ERCC1-XPF, a structure-specific endonuclease that participates in a variety of DNA repair processes. ERCC1-XPF is involved in nucleotide excision repair (NER), repair of DNA interstrand crosslinks (ICLs), and DNA double-strand break (DSB) repair via homologous recombination. In addition, ERCC1-XPF contributes to the processing of various alternative (i.e., non-B) DNA structures. This review will focus on the processing of alternative DNA structures by ERCC1-XPF.

Diastereomeric Separation of Chiral fac-Tricarbonyl(iminopyridine) Rhenium(I) Complexes and Their Cytotoxicity Studies: Approach toward an Action Mechanism against Glioblastoma.

A series of new (tricarbonyl)rhenium(I) complexes were synthesized using chiral bidentate ligands (+)/(-)-iminopyridines (LR/LS). The reaction yielded a mixture of mononuclear Re(I) diastereoisomers, formulated as fac-[Br(CO)3Re(S/R)L(S/R)]. Each single diastereoisomer was isolated and fully characterized. X-ray crystallography and circular dichroism spectra verified their enantiomeric nature. The cytotoxicity of each complex was evaluated against six cancer cell lines. The effect of the two complexes on viability, proliferation, and migration was analyzed on glioblastoma cell lines (U251 and LN229). Changes in the expression of histones, apoptotic, and key signaling proteins, as well as alterations in DNA structure, were also observed. These experiments showed that the chirality associated with both metal and ligand has a strong influence on cytotoxicity.

Homologues of epigenetic pyrimidines: 5-alkyl-, 5-hydroxyalkyl and 5-acyluracil and -cytosine nucleotides: synthesis, enzymatic incorporation into DNA and effect on transcription with bacterial RNA polymerase.

Homologues of natural epigenetic pyrimidine nucleosides and nucleotides were designed and synthesized. They included 5-ethyl-, 5-propyl-, 5-(1-hydroxyethyl)-, 5-(1-hydroxypropyl)- and 5-acetyl- and 5-propionylcytosine and -uracil 2′-deoxyribonucleosides and their corresponding 5′-O-triphosphates (dNXTPs). The epimers of 5-(1-hydroxyethyl)- and 5-(1-hydroxypropyl)pyrimidine nucleosides were separated and their absolute configuration was determined by a combination of X-ray and NMR analysis. The modified dNXTPs were used as substrates for PCR synthesis of modified DNA templates used for the study of transcription with bacterial RNA polymerase. Fundamental differences in transcription efficiency were observed, depending on the various modifications. The most notable effects included pronounced stimulation of transcription from 5-ethyluracil-bearing templates (200% transcription yield compared to natural thymine) and an enhancing effect of 5-acetylcytosine versus inhibiting effect of 5-acetyluracil. In summary, these results reveal that RNA polymerase copes with dramatically altered DNA structure and suggest that these nucleobases could potentially play roles as artificial epigenetic DNA nucleobases.

Analysis of nucleoid-associated protein-binding regions reveals DNA structural features influencing genome organization in Mycobacteriumtuberculosis.

Nucleoid-associated proteins (NAPs) maintain bacterial nucleoid configuration through their architectural properties of DNA bending, wrapping, and bridging. However, the contribution of DNA structural alterations to DNA-NAP recognition at the genomic scale remains unresolved. Present work dissects the DNA sequence, shape and altered structural preferences at a genomic scale for six NAPs in Mycobacteriumtuberculosis. Results suggest narrower minor groove width (MGW) and higher DNA rigidity are marked for the binding sites of EspR and Lsr2, while mIHF, MtHU and NapM haveheterogeneous DNA structural predilections. In contrast, WhiB4-DNA-binding sites were characterized by wider MGW, highly deformable and less curved DNA. This work provides systematic insight into NAP-mediated genome organization as a function of DNA structural features.

G-quadruplexes in the mitochondrial genome - a cause for instability.

Accumulation of mutations such as deletions in mitochondrial DNA is associated with ageing, cancer and human genetic disorders. These deletions are often flanked by GC-skewed sequence motifs that can potentially fold into secondary non-B DNA conformations. G-quadruplexes are emerging as key initiators of mitochondrial genomic instability. In this issue, Dahal etal provide an insilico analysis of sequence motifs that can fold into altered DNA structures in mitochondrial genomic regions that contain frequent deletions. They show the formation of five G-quadruplexes near such frequent breakpoints using biochemical and biophysical approaches invitro and more importantly inside mammalian cells. Comment on: https://doi.org/10.1111/febs.16113.

C-terminal truncation of [formula omitted]-synuclein alters DNA structure from extension to compaction

Parkinson's disease (PD) is linked to aggregation of the protein α-synuclein (aS) into amyloid fibers. aS is proposed to regulate synaptic activity and may also play a role in gene regulation via interaction with DNA in the cell nucleus. Here, we address the role of the negatively-charged C-terminus in the interaction between aS and DNA using single-molecule techniques. Using nanofluidic channels, we demonstrate that truncation of the C-terminus of aS induces differential effects on DNA depending on the extent of the truncation. The DNA extension increases for full-length aS and the (1–119)aS variant, but decreases about 25% upon binding to the (1–97)aS variant. Atomic force microscopy imaging showed full protein coverage of the DNA at high aS concentration. The characterization of biophysical properties of DNA when in complex with aS variants may provide important insights into the role of such interactions in PD, especially since C-terminal aS truncations have been found in clinical samples from PD patients.

The Role of Epigenomics in Osteoporosis and Osteoporotic Vertebral Fracture.

Osteoporosis is a complex multifactorial condition of the musculoskeletal system. Osteoporosis and osteoporotic vertebral fracture (OVF) are associated with high medical costs and can lead to poor quality of life. Genetic factors are important in determining bone mass and structure, as well as any predisposition for bone degradation and OVF. However, genetic factors are not enough to explain osteoporosis development and OVF occurrence. Epigenetics describes a mechanism for controlling gene expression and cellular processes without altering DNA sequences. The main mechanisms in epigenetics are DNA methylation, histone modifications, and non-coding RNAs (ncRNAs). Recently, alterations in epigenetic mechanisms and their activity have been associated with osteoporosis and OVF. Here, we review emerging evidence that epigenetics contributes to the machinery that can alter DNA structure, gene expression, and cellular differentiation during physiological and pathological bone remodeling. A progressive understanding of normal bone metabolism and the role of epigenetic mechanisms in multifactorial osteopathy can help us better understand the etiology of the disease and convert this information into clinical practice. A deep understanding of these mechanisms will help in properly coordinating future individual treatments of osteoporosis and OVF.

Systematic investigation of promoter substitutions resulting from somatic intrachromosomal structural alterations in diverse human cancers

One of the ways in which genes can become activated in tumors is by somatic structural genomic rearrangements leading to promoter swapping events, typically in the context of gene fusions that cause a weak promoter to be substituted for a strong promoter. While identifiable by whole genome sequencing, limited availability of this type of data has prohibited comprehensive study of the phenomenon. Here, we leveraged the fact that copy number alterations (CNAs) arise as a result of structural alterations in DNA, and that they may therefore be informative of gene rearrangements, to pinpoint recurrent promoter swapping at a previously intractable scale. CNA data from nearly 9500 human tumors was combined with transcriptomic sequencing data to identify several cases of recurrent activating intrachromosomal promoter substitution events, either involving proper gene fusions or juxtaposition of strong promoters to gene upstream regions. Our computational screen demonstrates that a combination of CNA and expression data can be useful for identifying novel fusion events with potential driver roles in large cancer cohorts.

Roles of Histone Deacetylases and Inhibitors in Anticancer Therapy.

Histones are the main structural proteins of eukaryotic chromatin. Histone acetylation/ deacetylation are the epigenetic mechanisms of the regulation of gene expression and are catalyzed by histone acetyltransferases (HAT) and histone deacetylases (HDAC). These epigenetic alterations of DNA structure influence the action of transcription factors which can induce or repress gene transcription. The HATs catalyze acetylation and the events related to gene transcription and are also responsible for transporting newly synthesized histones from the cytoplasm to the nucleus. The activity of HDACs is mainly involved in silencing gene expression and according to their specialized functions are divided into classes I, II, III and IV. The disturbance of the expression and mutations of HDAC genes causes the aberrant transcription of key genes regulating important cancer pathways such as cell proliferation, cell-cycle regulation and apoptosis. In view of their role in cancer pathways, HDACs are considered promising therapeutic targets and the development of HDAC inhibitors is a hot topic in the search for new anticancer drugs. The present review will focus on HDACs I, II and IV, the best known inhibitors and potential alternative inhibitors derived from natural and synthetic products which can be used to influence HDAC activity and the development of new cancer therapies.

The Genoprotective Role of Naringin.

Since ancient times, fruits and edible plants have played a special role in the human diet for enhancing health and maintaining youthfulness. The aim of our work was to determine the interactions between naringin, a natural ingredient of grapefruits, and DNA using an electrochemical biosensor. Electrochemical methods allow analyzing the damages occurring in the structure of nucleic acids and their interactions with xenobiotics. Our study showed that the changes in the location of electrochemical signals and their intensity resulted from the structural alterations in DNA. The signal of adenine was affected at lower concentrations of naringin, but the signal of guanine was unaffected in the same condition. The dynamics of changes occurring in the peak height and surface of adenine related to naringin concentration was also significantly lower. The complete binding of all adenine bases present in the tested double-stranded DNA solution was observed at naringin concentrations ranging from 8.5 to 10.0 µM. At larger concentrations, this active compound exerted an oxidizing effect on DNA. However, the critical concentrations of naringin were found to be more than twice as high as the dose absorbable in an average human (4 µM). The results of our work might be helpful in the construction of electrochemical sensors for testing the content of polyphenols and would allow determining their genoprotective functionality.