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Photochemical reactions in cell DNA are induced in various organisms by solar UV radiation and may lead to a series of biological responses to DNA damage, including apoptosis, mutagenesis, and carcinogenesis. The chemical nature and the amount of DNA lesions depend on the wavelength of UV radiation. UV type B (UVB, 290-320 nm) causes two main lesions, cyclobutane pyrimidine dimers (CPDs) and, with a lower yield, pyrimidine (6-4) pyrimidone photoproducts (6-4PPs). Their formation is a result of direct UVB photon absorption by DNA bases. UV type A (UVA, 320-400 nm) induces only cyclobutane dimers, which most likely arise via triplet-triplet energy transfer (TTET) from cell chromophores to DNA thymine bases. UVA is much more effective than UVB in inducing sensitized oxidative DNA lesions, such as single-strand breaks and oxidized bases. Of the latter, 8-oxo-dihydroguanine (8-oxodG) is the most frequent, being produced in several oxidation processes. Many recent studies reported novel, more detailed information about the molecular mechanisms of the photochemical reactions that underlie the formation of various DNA lesions. The information is mostly summarized and analyzed in the review. Special attention is paid to the oxidation reactions that are initiated by reactive oxygen species (ROS) and radicals generated by potential endogenous photosensitizers, such as pterins, riboflavin, protoporphyrin IX, NADH, and melanin. The review discusses the role that specific DNA photoproducts play in genotoxic processes induced in living systems by UV radiation of various wavelengths, including human skin carcinogenesis.

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High-linear energy transfer (LET) radiation is a promising alternative to conventional low-LET radiation for therapeutic gain against cancer owing to its ability to induce complex and clustered DNA lesions. However, the development of radiation resistance poses a significant barrier. The potential molecular mechanisms that could confer resistance development are translesion synthesis (TLS), replication gap suppression (RGS) mechanisms, autophagy, epithelial-mesenchymal transition (EMT) activation, release of exosomes, and epigenetic changes. This article will discuss various types of complex clustered DNA damage, their repair mechanisms, mutagenic potential, and the development of radiation resistance strategies. Furthermore, it highlights the importance of careful consideration and patient selection when employing high-LET radiotherapy in clinical settings.

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Urbanization has numerous benefits to human society, but some aspects of urban environments, such as air pollution, can negatively affect human health. Two major air pollutants, particulate matter (PM) and polycyclic aromatic hydrocarbons (PAH), have been classified as carcinogens by the International Agency for Research on Cancer. Here, we answer two questions: (1) What are the carcinogenic effects of PM and PAH exposure? (2) How does carcinogenic risk vary across geographical regions? We performed a comprehensive literature search of peer-reviewed published studies examining the link between air pollution and human cancer rates. Focusing on studies published since 2014 when the last IARC monograph on air pollution was published, we converted the extracted data into relative risks and performed subgroup analyses. Exposure to PM2.5 (per 10 µg/m3) resulted in an 8.5% increase in cancer incidence when all cancer types were combined, and risk for individual cancer types (i.e. lung cancer and adenocarcinoma) was also elevated. PM2.5 was also associated with 2.5% higher mortality due to cancer when all types of cancer were combined, and for individual cancer types (i.e., lung and breast cancer). Exposure to PM2.5 and PM10 posed the greatest risk to lung cancer incidence and mortality in Europe (PM2.5 RR 2.15; PM10 RR 1.26); the risk in Asia and the Americas was also elevated. Exposure to PAH and benzo[a]pyrene significantly increased the pooled risk of cancer incidence (10.8% and 8.0% respectively) at the highest percentile of exposure concentration. Our meta-analyses of studies over the past decade shows that urban air pollution in the form of PM2.5, PM10, and PAH all elevate the incidence and mortality of cancer. We discuss the possible mechanisms of carcinogenesis of PM and PAH. These results support World Health Organization's conclusion that air pollution poses among the greatest health risks to humans living in cities.

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Purified translesion synthesis (TLS) DNA polymerases (Pols) replicate through DNA lesions with a low fidelity; however, TLS operates in a predominantly error-free manner in normal human cells. To explain this incongruity, here we determine whether Y family Pols, which play an eminent role in replication through a diversity of DNA lesions, are incorporated into a multiprotein ensemble and whether the intrinsically high error rate of the TLS Pol is ameliorated by the components in the ensemble. To this end, we provide evidence for an indispensable role of Werner syndrome protein (WRN) and WRN-interacting protein 1 (WRNIP1) in Rev1-dependent TLS by Y family Polη, Polι, or Polκ and show that WRN, WRNIP1, and Rev1 assemble together with Y family Pols in response to DNA damage. Importantly, we identify a crucial role of WRN's 3' → 5' exonuclease activity in imparting high fidelity on TLS by Y family Pols in human cells, as the Y family Pols that accomplish TLS in an error-free manner manifest high mutagenicity in the absence of WRN's exonuclease function. Thus, by enforcing high fidelity on TLS Pols, TLS mechanisms have been adapted to safeguard against genome instability and tumorigenesis.

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The T7 gene 3 product, T7 endonuclease I, acts on various substrates with DNA structures, including Holliday junctions, heteroduplex DNAs and single-mismatch DNAs. Genetic analyses have suggested the occurrence of DNA recombination, replication and repair in Escherichia coli. In this study, T7 endonuclease I digested UV-irradiated covalently closed circular plasmid DNA into linear and nicked plasmid DNA, suggesting that the enzyme generates single- and double-strand breaks (SSB and DSB). To further investigate the biochemical functions of T7 endonuclease I, we have analysed endonuclease activity in UV-induced DNA substrates containing a single lesion, cyclobutane pyrimidine dimers (CPD) and 6-4 photoproducts (6-4PP). Interestingly, the leading cleavage site for CPD by T7 endonuclease I is at the second and fifth phosphodiester bonds that are 5' to the lesion of CPD on the lesion strand. However, in the case of 6-4PP, the cleavage pattern on the lesion strand resembled that of CPD, and T7 endonuclease I could also cleave the second phosphodiester bond that is 5' to the adenine-adenine residues opposite the lesion, indicating that the enzyme produces DSB in DNA containing 6-4PP. These findings suggest that T7endonuclease I accomplished successful UV damage repair by SSB in CPD and DSB in 6-4PP.

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Attaching/effacing (A/E) pathogens induce DNA damage and colorectal cancer by injecting effector proteins into host cells via the type III secretion system (T3SS). EspF is one of the T3SS-dependent effector proteins exclusive to A/E pathogens, which include enterohemorrhagic Escherichia coli. The role of EspF in the induction of double-strand breaks (DSBs) and the phosphorylation of the repair protein SMC1 has been demonstrated previously. However, the process of damage accumulation and DSB formation has remained enigmatic, and the damage response is not well understood. Here, we first showed a compensatory increase in the mismatch repair proteins MutS homolog 2 (MSH2) and MSH6, as well as poly(ADP-ribose) polymerase 1, followed by a dramatic decrease, threatening cell survival in the presence of EspF. Flow cytometry revealed that EspF arrested the cell cycle at the G2/M phase to facilitate DNA repair. Subsequently, 8-oxoguanine (8-oxoG) lesions, a marker of oxidative damage, were assayed by ELISA and immunofluorescence, which revealed the accumulation of 8-oxoG from the cytosol to the nucleus. Furthermore, the status of single-stranded DNA (ssDNA) and DSBs was confirmed. We observed that EspF accelerated the course of DNA lesions, including 8-oxoG and unrepaired ssDNA, which were converted into DSBs; this was accompanied by the phosphorylation of replication protein A 32 in repair-defective cells. Collectively, these findings reveal that EspF triggers various types of oxidative DNA lesions with impairment of the DNA damage response and may result in genomic instability and cell death, offering novel insight into the tumorigenic potential of EspF.IMPORTANCEOxidative DNA lesions play causative roles in colitis-associated colon cancer. Accumulating evidence shows strong links between attaching/effacing (A/E) pathogens and colorectal cancer (CRC). EspF is one of many effector proteins exclusive to A/E pathogens with defined roles in the induction of oxidative stress, double-strand breaks (DSBs), and repair dysregulation. Here, we found that EspF promotes reactive oxygen species generation and 8-oxoguanine (8-oxoG) lesions when the repair system is activated, contributing to sustained cell survival. However, infected cells exposed to EspF presented 8-oxoG, which results in DSBs and ssDNA accumulation when the cell cycle is arrested at the G2/M phase and the repair system is defective or saturated by DNA lesions. In addition, we found that EspF could intensify the accumulation of nuclear DNA lesions through oxidative and replication stress. Overall, our work highlights the involvement of EspF in DNA lesions and DNA damage response, providing a novel avenue by which A/E pathogens may contribute to CRC.

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Since DNA damage is of great importance in various biological processes, its rate is frequently assessed both in research studies and in medical diagnostics. The most precise methods of quantifying DNA damage are based on real-time PCR. However, in the conventional version, they require a large amount of genetic material and therefore their usefulness is limited to multicellular samples. Here, we present a novel approach to long-run real-time PCR-based DNA-damage quantification (L1-LORD-Q), which consists in amplification of long interspersed nuclear elements (L1) and allows for analysis of single-cell genomes. The L1-LORD-Q was compared with alternative methods of measuring DNA breaks (Bioanalyzer system, γ-H2AX foci staining), which confirmed its accuracy. Furthermore, it was demonstrated that the L1-LORD-Q is sensitive enough to distinguish between different levels of UV-induced DNA damage. The method was validated on mouse oocytes and fibroblasts, but the general idea is universal and can be applied to various types of cells and species.

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5-Methyl-2'-deoxycytidine (mC) at CpG sites plays a key role in the epigenetic gene regulation, cell differentiation, and carcinogenesis. Despite the importance of mC for normal cell function, CpG dinucleotides are known as mutagenesis hotspots. Deamination of mC yields T, causing C→T transitions. However, several recent studies demonstrated the effect of epigenetic modifications of C on the fidelity and efficiency of DNA polymerases and excision repair enzymes. The review summarizes the available data that indicate the existence of deamination-independent mechanisms of mutagenesis at CpG sites.

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Spontaneous or induced DNA lesions can result in stable gene mutations and chromosomal aberrations due to their inaccurate repair, ultimately resulting in phenotype changes. Some DNA lesions per se may interfere with transcription, leading to temporary phenocopies of mutations. The direct impact of primary DNA lesions on phenotype before their removal by repair is not well understood. To address this question, we used the alpha-test, which allows for detecting various genetic events leading to temporary or hereditary changes in mating type α→a in heterothallic strains of yeast Saccharomyces cerevisiae. Here, we compared yeast strains carrying mutations in DNA repair genes, mismatch repair (pms1), base excision repair (ogg1), and homologous recombination repair (rad52), as well as mutagens causing specific DNA lesions (UV light and camptothecin). We found that double-strand breaks and UV-induced lesions have a stronger effect on the phenotype than mismatches and 8-oxoguanine. Moreover, the loss of the entire chromosome III leads to an immediate mating type switch α→a and does not prevent hybridization. We also evaluated the ability of primary DNA lesions to persist through the cell cycle by assessing the frequency of UV-induced inherited and non-inherited genetic changes in asynchronous cultures of a wild-type (wt) strain and in a cdc28-4 mutant arrested in the G1 phase. Our findings suggest that the phenotypic manifestation of primary DNA lesions depends on their type and the stage of the cell cycle in which it occurred.

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Modified nucleotides often hinder and/or decrease the fidelity of DNA polymerases. Tandem lesions, which are comprised of DNA modifications at two contiguous nucleotide positions, can be even more detrimental to genome stability. Recently, tandem lesions containing 5-formyl-2'-deoxyuridine (5fdU) flanked at the 5'-position by 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-OxodGuo) or N-(2-deoxy-α,ß-D-erythropentofuranosyl)-N-(2,6-diamino-4-hydroxy-5-formamidopyrimidine (Fapy•dG) were discovered. We examined the replication of 5'- 8-OxodGuo-5fdU and 5'-Fapy•dG-5fdU tandem lesions in HEK 293T cells and several polymerase deficient variants by transfecting single-stranded vectors containing them. The local sequence of the tandem lesions encompasses the 273 codon of the p53 gene, a mutational hot-spot. The bypass efficiency and mutation spectra of the tandem lesions were compared to those of the isolated lesions. Replication of weakly mutagenic 5-fdU is little changed when part of the 5'- 8-OxodGuo-5fdU tandem lesion. G → T transversions attributable to 8-OxodGuo increase > 10-fold when the tandem lesion is bypassed. 5'-Fapy•dG-5fdU has a synergistic effect on the error-prone bypass of both lesions. The mutation frequency (MF) of 5'-Fapy•dG-5fdU increases 3-fold compared to isolated Fapy•dG. In addition, a 5'-adjacent Fapy•dG significantly increases the MF of 5fdU. The major mutation, G → T transversions, decrease by almost a third in hPol κ- cells, which is the opposite effect when isolated Fapy•dG in the same sequence context is replicated in HEK 293T cells in the same sequence. Steady-state kinetics indicate that hPol κ contributes to greater G → T transversions by decreasing the specificity constant for dCTP compared to an isolated Fapy•dG. The greater conformational freedom of Fapy•dG compared to 8-OxodGuo and its unusual ability to epimerize at the anomeric center is believed to be the source of the complex effects of 5'-Fapy•dG-5fdU on replication.

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The genome must be monitored to ensure its duplication is completed accurately to prevent genome instability. In Saccharomyces cerevisiae, the 5' to 3' DNA helicase Rrm3, a member of the conserved PIF1 family, facilitates replication fork progression through an unknown mechanism. Disruption of Rrm3 helicase activity leads to increased replication fork pausing throughout the yeast genome. Here, we show that Rrm3 contributes to replication stress tolerance in the absence of the fork reversal activity of Rad5, defined by its HIRAN domain and DNA helicase activity, but not in the absence of Rad5's ubiquitin ligase activity. The Rrm3 and Rad5 helicase activities also interact in the prevention of recombinogenic DNA lesions, and DNA lesions that accumulate in their absence need to be salvaged by a Rad59-dependent recombination pathway. Disruption of the structure-specific endonuclease Mus81 leads to accumulation of recombinogenic DNA lesions and chromosomal rearrangements in the absence of Rrm3, but not Rad5. Thus, at least two mechanisms exist to overcome fork stalling at replication barriers, defined by Rad5-mediated fork reversal and Mus81-mediated cleavage, and contribute to the maintenance of chromosome stability in the absence of Rrm3.

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Boron neutron capture therapy (BNCT) is an approach to the radiotherapy of solid tumors that was first outlined in the 1930s but has attracted considerable attention recently with the advent of a new generation of neutron sources. In BNCT, tumor cells accumulate 10B atoms that react with epithermal neutrons, producing energetic α particles and 7Li atoms that damage the cell's genome. The damage inflicted by BNCT appears not to be easily repairable and is thus lethal for the cell; however, the molecular events underlying the action of BNCT remain largely unaddressed. In this review, the chemistry of DNA damage during BNCT is outlined, the major mechanisms of DNA break sensing and repair are summarized, and the specifics of the repair of BNCT-induced DNA lesions are discussed.

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PURPOSE: To demonstrate how the search by the Molecular Radiobiologists for enzymes that could recognize and remove DNA damage produced by ionizing radiation was intertwined with the development of the Base Excision Repair pathway. CONCLUSION: The Base Excision Repair pathway repairs the vast majority of radiation-induced DNA damages including base damages, alkali labile lesions, and single strand breaks. It turns out that Base Excision Repair actually evolved to repair some thirty to forty thousand endogenous lesions formed in each of our cells every day. Thus, this process is extremely efficient and accordingly, at relatively low doses of radiation, the single lesions repaired by base excision repair result in few lethal or mutagenic events. This efficiency is a double-edged sword since ionizing radiation-induced hydroxyl radicals produced along the radiation track form both bistranded and tandem clustered lesions in DNA. These damages are recognized by the efficient Base Excision Repair enzymes, which, during attempted repair, lead to double strand breaks and/or multiple lesions that can collapse replication forks. Double strand breaks and other complex or clustered lesions formed by ionizing radiation present distinct challenges to DNA repair systems compared to the relative ease and efficiency by which isolated lesions are repaired.

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Environmental pollution increases due to anthropogenic activities. Toxic chemicals in the environment affect the health of aquatic organisms. Tributyltin (TBT) is a toxic chemical widely used as an antifouling paint on boats, hulls, and ships. The toxic effect of TBT is well documented in aquatic organisms; however, little is known about the effects of TBT on DNA lesions in shellfish. The American oyster (Crassostrea virginica, an edible and commercially important species) is an ideal marine mollusk to examine the effects of TBT exposure on DNA lesions and oxidative/nitrative stress. In this study, we investigated the effects of TBT on 8'-hydroxy-2'-deoxyguanosine (8-OHdG, a biomarker of pro-mutagenic DNA lesion), double-stranded DNA (dsDNA), dinitrophenyl protein (DNP, a biomarker on reactive oxygen species, ROS), 3-nitrotyrosine protein (NTP, a biomarker of reactive nitrogen species, RNS), catalase (CAT, an antioxidant), and acetylcholinesterase (AChE, a cholinergic enzyme) expressions in the gills and digestive glands of oysters. We also analyzed extrapallial (EF) fluid conditions. Immunohistochemical and qRT-PCR results showed that TBT exposure significantly increased 8-OHdG, dsDNA, DNP, NTP, and CAT mRNA and/or protein expressions in the gills and digestive glands. However, AChE mRNA and protein expressions, and EP fluid pH and protein concentrations were decreased in TBT-exposed oysters. Taken together, these results suggest that antifouling biocide-induced production of ROS/RNS results in DNA damage, which may lead to decreased cellular functions in oysters. To the best of our knowledge, the present study provides the first molecular/biochemical evidence that TBT exposure results in oxidative/nitrative stress and DNA lesions in oysters.

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Mitoxantrone (MTO) is clinically utilized for treating hormone-refractory prostate cancer (PCa), however, the therapeutic outcome is far from optimal due to the lack of proper drug carrier as well as the inherent MTO detoxification mechanisms of DNA lesion repair and anti-oxidation. Herein, a bombesin-installed nanoplatform combining the chemotherapeutic MTO and the chemotherapeutic sensitizer of nitric oxide (NO) is developed based on MTO-loaded macromolecular NO-donor-containing polymeric micelles (BN-NMMTO ) for targeted NO-sensitized chemotherapy against PCa. BN-NMMTO actively target and accumulates in PCa sites and are internalized into the tumor cells. The macromolecular NO-donor of BN-NMMTO undergoes a reductive reaction to unleash NO upon intracellular glutathione (GSH), accompanying by micelle swelling and MTO release. The targeted intracellular MTO release induces DNA lesion and reactive oxygen species (ROS) generation in tumor cells without damage to the normal cells, and MTO's cytotoxicity is further augmented by NO release via the inhibition of both DNA repair and anti-oxidation pathways as compared with traditional MTO therapies.

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Bioactive glasses (BGs), also known as bioglasses, are very attractive and versatile materials that are increasingly being used in dentistry. For this study, two new bioglasses-one with boron (BG1) and another with boron and vanadium (BG2)-were synthesized, characterized, and tested on human dysplastic keratinocytes. The in vitro biological properties were evaluated through pH and zeta potential measurement, weight loss, Ca2+ ions released after immersion in phosphate-buffered saline (PBS), and scanning electron microscopy (SEM) coupled with energy dispersive spectroscopy (EDS) analysis. Furthermore, biocompatibility was evaluated through quantification of lactate dehydrogenase activity, oxidative stress, transcription factors, and DNA lesions. The results indicate that both BGs presented the same behavior in simulated fluids, characterized by high degradation, fast release of calcium and boron in the environment (especially from BG1), and increased pH and zeta potential. Both BGs reacted with the fluid, particularly BG2, with irregular deposits covering the glass surface. In vitro studies demonstrated that normal doses of the BGs were not cytotoxic to DOK, while high doses reduced cell viability. Both BGs induced oxidative stress and cell membrane damage and enhanced NFkB activation, especially BG1. The BGs down-regulated the expression of NFkB and diminished the DNA damage, suggesting the protective effects of the BGs on cell death and efficacy of DNA repair mechanisms.

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The consequences of aging and disease conditions in tissues involve reactive oxygen species (ROS) and related molecular alterations of different cellular compartments. We compared a murine model of immunodeficient (SCID) xenografted young (4 weeks old) and old (17 weeks old) mice with corresponding controls without tumor implantation and carried out a compositional evaluation of brain tissue for changes in parallel DNA and lipids compartments. DNA damage was measured by four purine 5',8-cyclo-2'-deoxynucleosides, 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxo-dG), and 8-oxo-7,8-dihydro-2'-deoxyadenosine (8-oxo-dA). In brain lipids, the twelve most representative fatty acid levels, which were mostly obtained from the transformation of glycerophospholipids, were followed up during the aging and disease progressions. The progressive DNA damage due to age and tumoral conditions was confirmed by raised levels of 5'S-cdG and 5'S-cdA. In the brain, the remodeling involved a diminution of palmitic acid accompanied by an increase in arachidonic acid, along both age and tumor progressions, causing increases in the unsaturation index, the peroxidation index, and total TFA as indicators of increased oxidative and free radical reactivity. Our results contribute to the ongoing debate on the central role of DNA and genome instability in the aging process, and on the need for a holistic vision, which implies choosing the best biomarkers for such monitoring. Furthermore, our data highlight brain tissue for its lipid remodeling response and inflammatory signaling, which seem to prevail over the effects of DNA damage.

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Alicyclobacillus acidoterrestris causes the spoilage of pasteurized acidic fruit juice, seriouslydecreasing quality and posing a significant safety concern. We previously discovered that acid adaptation could induce stress adaptive responses of A. acidoterrestris, however, the underlying mechanisms of this induction have not been fully elucidated. In this work, the effects of acid adaptation (pH = 3.0, 1 h) on intracellular pH (pHi) and the morphophysiological properties of A. acidoterrestris under lethal heat and acid stresses were investigated, and gene expression profiles after acid adaptation were measured by transcriptomic analysis. The results showed that acid adaptation increased the pHi of A. acidoterrestris cells in response to lethal stresses, enhanced membrane integrity, decreased surface shrinkage and roughness, and altered the Fourier transform infrared spectra profiles. After acid adaptation of A. acidoterrestris, 517 differentially expressed genes (DEGs) were detected. Consistent with resistance phenotypes, DEGs included genes related to cell surface modification and pHi homeostasis. Specifically, the barrier function of cell membrane was strengthened during acid adaptation by increasing fatty acid (FA) chain length, promoting unsaturated FA biosynthesis, and maintaining balanced synthesis of zwitterionic and acidic phospholipids. To reduce excessive intracellular protons, cells upregulated glutamate decarboxylation, urease system, and branched-chain amino acid synthesis. Additionally, the nucleotide salvage pathway was activated, and homologous recombination, UvrD-mediated transcription-coupled, and ribonucleotide excision repair pathways were applied to repair DNA lesions. Sporulation metabolism was also induced. The findings of this study provide insight into the multiple layers of acid adaptive response strategies of A. acidoterrestris, with implications for the formulation of improved control measures in the fruit juice industry.

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AIMS: The aim of the current study was to investigate the effect of plasma-mediated oxidative stress on the post-treatment viability of Listeria monocytogenes at the physiological and molecular levels. METHODS AND RESULTS: 107  CFU/ml L. monocytogenes in 10 ml phosphate-buffered saline (PBS) was treated with atmospheric non-thermal plasma for 0, 30, 60, 90 and 120 s respectively. Optical diagnostics using optical emission spectroscopy (OES) confirmed that dielectric barrier discharge (DBD) plasma was a significant source of ample exogenous reactive oxygen and nitrogen species (RONS). The development of extracellular main long-lived species was associated with plasma exposure time, accompanied by a massive accumulation of intracellular ROS in L. monocytogenes (p < 0.01). With the exception of virulence genes (hly), most oxidation resistance genes (e.g. sigB, perR, lmo2344, lmo2770 and trxA) and DNA repair gene (recA) were upregulated significantly (p < 0.05). A visible fragmentation in genomic DNA and a decline in the secretion of extracellular proteins and haemolytic activity (p < 0.01) were noticed. The quantitate oxygen consumption rates (OCRs) and extracellular acidification rates (ECARs) confirmed the viability attenuation from the aspect of energy metabolism. Survival assay in a real food system (raw milk) further suggested not only the viability attenuation, but also the resuscitation potential and safety risk of mild plasma-treated cells during post-treatment storage. CONCLUSION: DBD plasma had the potential to inactivate and attenuate the virulence of L. monocytogenes, and it was recommended that plasma exposure time longer than 120 s was more suitable for attenuating viability and avoiding the recovery possibility of L. monocytogenes in raw milk within 7 days. SIGNIFICANCE AND IMPACT OF THE STUDY: The current results presented a strategy to inactivate and attenuate the viability of L. monocytogenes, which could serve as a theoretical basis for better application of non-thermal plasma in food in an effort to effectively combat foodborne pathogens.

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