The Pyrabactin resistance 1-like proteins (PYR/PYL/RCAR) protein plays a critical regulatory role in the ABA signal transduction pathway as a direct receptor of abscisic acid (ABA). Although PYL genes have been identified in a variety of plants, the evolution and structural characteristics of these genes in alfalfa (Medicago sativa) are largely unknown. Therefore, a comprehensive bioinformatics analysis of the PYL gene family was performed in this research.

Recurrence after oxaliplatin chemotherapy is a major challenge in the treatment of advanced hepatocellular carcinoma patients. Differential expression gene analysis and Kaplan-Meier curves were screened biomarkers associated with OXA-treated recurrence in GSE51951, TCGA-LIHC, and Chinese Liver Cancer Atlas databases. We retrospectively collected 39 cases of HCC treated with platinum based drugs at the First Hospital of Shanxi Medical University. Immunohistochemistry was used to analyze the relationship between PDZK1 expression and patient recurrence of HCC. Cell model and subcutaneous transplant tumor model of HCC were established to detect the cell growth ability treated with OXA. Gene Set Enrichment Analysis analysis identified signaling pathways associated with high PDZK1. Co-Immunoprecipitation and immunofluorescence experiments were used to explore the potential interaction between PDZK1 and MRP2. We identified that high expression of PDZK1 was associated with OXA resistance and poor prognosis in HCC. PDZK1 promoted the cell viability, migration, and invasion of HCC after OXA treatment in vitro and vivo. MRP2-mediated ABC transporters pathway and bile acid metabolism were significantly activated in the PDZK1 overexpression group of HCC. PDZK1 interacted and co-localized with the carboxyl terminal PDZ binding motif of MRP2. Clinical specimen analysis have shown a positive correlation between the protein levels of PDZK1 and MRP2. Our study identified PDZK1 as a novel biomarker significantly associated with OXA chemosensitivity in HCC. Mechanistically, PDZK1 promoted the OXA sensitivity of HCC by activating the MRP2-mediated signaling pathway.

Previous studies conducted by the same group of researchers found that Traditional Chinese Medicine Astragalus mongholicus Bunge and Hedyotis diffusa Willd (A-H) significantly suppressed the cell proliferation of lung adenocarcinoma (LUAD). MicroRNAs are considered promising candidates for cancer diagnosis and treatment. This study focused on miR-582-3p as the primary subject of investigation to explore the mechanism by which A-H inhibits cell proliferation through miR-582-3p. The overexpressing and silencing miR-582-3p cell models were established by using lentiviral transfection technology. CCK-8 assay (24 h, 48 h, 72 h) and clone formation assay (1 w) were employed to detect the proliferation of A549 cells. Moreover, flow cytometry analysis (24 h) was performed to detect the cell cycle. Western blotting (WB) and a luciferase reporter assay were also used to measure the expression of cell cycle-related proteins and verify the direct interaction between miR-582-3p and p27, respectively. The LV-miR-582-3p inhibitor + shRNA-p27 stable A549 cells were constructed in the same manner to repeat the above-mentioned procedure. The CCK-8 assay was conducted to assess the effects of various concentrations of A-H on the proliferation of A549 cells. A-H-containing serum was prepared to intervene in LV-miR-582-3p and mimic A549 cells. Subsequently, the same procedure was repeated, as described earlier. Results indicated a direct interaction between miR-582-3p and p27. Furthermore, miR-582-3p was found to enhance the proliferation of A549 cells by regulating cell cycle-related proteins, specifically p27. It was also observed that A-H-containing serum inhibited the proliferation of A549 cells through the miR-582-3p-p27 signaling pathway. The study findings revealed the underlying molecular mechanisms of miR-582-3p in the development and prognosis of A549 LUAD cells. In addition, A-H inhibited LUAD proliferation through the miR-582-3p-p27 signaling pathway. These findings may provide a new understanding of the use of Chinese medicine in treating lung cancer.

Grade IV astrocytoma, also referred to as glioblastoma (GBM), is the most common type of glioma, accounting for over 60% of all brain tumors. It is still a fatal illness in spite of years of investigation and does not currently have a treatment. Thus, scientists and medical professionals are constantly trying to understand the molecular processes and heterogeneity of GBM as well as looking for new ways to improve treatment results. Numerous studies have indicated that nanomaterials, and more especially nanoparticles, offer a great deal of potential for killing cancer cells; as a result, they are being considered as a potential alternative cancer treatment. Several studies have demonstrated that ZnO NPs have shown specific cytotoxicity against cancer cells while leaving normal cells unharmed. In this study we aim to synthesize sodium doped zinc oxide NPs using zingerone in an environmentally friendly manner to evaluate their cytotoxic effects on U87 GBM cell line and normal HEK cell line and investigate the occurrence of apoptosis via apoptosis assay by flowcytometry and gene expression study of TP53 and related genes to apoptosis and cell cycle regulation pathways. It was demonstrated that Na-doped ZnO NPs had a significant cytotoxic effect on U87 cells while having significantly less effect on normal HEK cells. Na-doped ZnO NPs eliminated cancerous cells through apoptosis induction and possibly cell cycle regulation via up-regulation of TP53, PTEN, BAX, P21 and down-regulation of Bcl2. The unique physicochemical properties of nanoparticles turn them into fascinating agents to treat GBM. Hence, the necessity of exploring the vast, yet unknown field of nanoparticles potentials cannot be over looked.

Elevated hexosamine biosynthesis fuels tumor growth by facilitating protein and lipid glycosylation. But which enzyme in this pathway is better to serve as an antitumor target remains unclear. Here, we revealed that targeting GFAT1, the rate-limiting enzyme in hexosamine synthesis, exhibits limited inhibitory effects on glioblastoma (GBM), the most lethal brain tumor. This outcome is due to the compensation of NAGK-mediated hexosamine salvage pathway. Unexpectedly, inhibiting PGM3, which controls the flux of both de novo hexosamine synthesis and salvage pathways, down-regulates the expression of other enzymes in this pathway and suppresses SREBP-1, a critical lipogenic transcription factor, effectively inhibiting GBM growth. Unexpectedly, SREBP-1 transcriptionally up-regulates the expression of hexosamine synthesis enzymes, while inhibition of these enzymes in turn down-regulates SREBP-1 activation via reducing N-glycosylation of its transporter, SCAP. Our study identified PGM3 as a promising target for treating GBM. Its inhibition disrupts the SREBP-1 activation-hexosamine synthesis positive feedback regulation to effectively eliminate GBM cells.

Anoxygenic phototrophic sulfur bacteria flourish in contemporary and ancient euxinic environments, driving the biogeochemical cycles of carbon and sulfur. However, it is unclear how these strict anaerobes meet their high demand for iron in iron-depleted environments. Here, we report that pyrite, a widespread and highly stable iron sulfide mineral in anoxic, low-temperature environments, can support the growth and metabolic activity of anoxygenic phototrophic sulfur bacteria by serving as the sole iron source under iron-depleted conditions. Transcriptomic and proteomic analyses revealed that pyrite addition substantially up-regulated genes and protein expression involved in photosynthesis, sulfur metabolism, and biosynthesis of organics. Anoxic microbial oxidation of pyritic sulfur and consequent destabilization of the pyrite structure were postulated to facilitate microbial iron acquisition. These findings advance our understanding of the survival strategies of anaerobes in iron-depleted environments and are important for revealing the previously underappreciated bioavailability of pyritic iron in anoxic environments and anoxic weathering of pyrite.

Eukaryotic cells contain the endoplasmic reticulum (ER), a prevalent and intricate membranous structural system. During the development of inflammatory bowel disease (IBD), the stress on the ER and the start of the unfolded protein response are very important. Some chemicals, including 4μ8C, small molecule agonists of X-box binding protein 1, and ISRIB, work on the inositol-requiring enzyme 1, turn on transcription factor 6, and activate protein kinase RNA-like ER kinase pathways. This may help ease the symptoms of IBD. Researchers investigating the gut microbiota have discovered a correlation between ER stress and it. This suggests that changing the gut microbiota could help make new medicines for IBD. This study looks at how ER stress works and how it contributes to the emergence of IBD. It also talks about its possible clinical importance as a therapeutic target and looks into new ways to treat this condition.

Enhanced glycolytic levels in cancer cells are a common characteristic of many cancer types. Modulation of glycolytic metabolism is crucial for enhancing the efficacy of cancer therapy. The specific role of 6-methoxyflavone in regulating glycolytic metabolism in cancer cells remains unclear. This study aimed to elucidate the impact of 6-methoxyflavone on glycolytic metabolism in cervical cancer cells and its clinical relevance.

Paclitaxel combination therapy is the main chemotherapy regimen for endometrial cancer (EC); however, subsequent drug resistance is a bottleneck limiting its widespread clinical application. We found that human insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) was abnormally elevated in paclitaxel-resistant EC cells and confirmed that the reduction of IGF2BP3 can effectively improve the sensitivity of EC cells to paclitaxel in vitro and in vivo. Mechanistically, elevated IGF2BP3 promotes the half-life of c-Myc by competitively inhibiting Speckle-type POZ protein (SPOP)-mediated ubiquitination and degradation of c-Myc. As a transcription factor, c-Myc can bind to the promoter of IGF2BP3, thus contributing to the increased transcription of IGF2BP3 via positive feedback and forming a signaling loop that ultimately causes the accumulation of c-Myc-induced paclitaxel resistance. Based on these findings, the application of c-Myc inhibitors (10058-F4) combined with paclitaxel helped paclitaxel-resistant EC cells regain paclitaxel sensitivity in vitro and in vivo. Together, we reveal the underlying mechanism of paclitaxel resistance in endometrial cancer cells and provide insights into treatment strategies for paclitaxel-resistant EC patients.

Trichophyton mentagrophytes (T. mentagrophytes) is a prevalent pathogen that causes human and animal dermatophytosis. The clinical treatment of the infections is challenging due to the prolonged treatment duration, limited efficacy, antifungal resistance and side effects of existing drugs. Modern research has reported that the classic Traditional Chinese medicine (TCM) prescription Huangqin decoction (HQD) along with its principal ingredients could exhibit antifungal properties. Given the valued advantages of TCM such as broad-spectrum antifungal activity, low incidence of drug resistance and low toxicity, this study investigated the antifungal activity of HQD against T. mentagrophytes and explored the potential inhibitory mechanism, aimed to provide new clues for the treatment of dermatophytosis. By detecting minimal inhibitory concentration (MIC) using the broth microdilution method, the results showed that HQD could significantly inhibit the growth of T. mentagrophytes, with a minimal inhibitory concentration (MIC) of 3.13 mg/mL. The transcriptome sequencing and quantitative real-time PCR (qRT-PCR) technology were combined to shed light on the complicated adaptive responses of T. mentagrophytes upon HQD. The results demonstrated that at MIC, compared with the control group, a total of 730 differentially expressed genes (DEGs) were detected in T. mentagrophytes after HQD exposure (FDR adjusted p-value < 0.05), of which 547 were up-regulated and 183 were down-regulated. These DEGs were abundant in "single-organism metabolic process", "catalytic activity" and "oxidoreductase activity", and were significantly enriched in seven signaling pathways including glutathione metabolism, DNA replication, glyoxylate and dicarboxylate metabolism, taurine and hypotaurine metabolism, carotenoid biosynthesis, ubiquitin-mediated proteolysis, and cyanoamino acid metabolism. The results of transcriptome profiling were verified using qRT-PCR for a subset of 10 DEGs. The overall evidence indicated that HQD had a significant anti-dermatophyte activity and the adaptive responses of T. mentagrophytes upon HQD might be related to targeting glutathione S-transferase (GST) gene that could conjugate with toxic xenobiotics to defense oxidative stress, the inhibition of DNA replication pathway by downgrading the DNA replication licensing factors MCM3, MCM5 and ribonuclease H1 (RNaseH1) genes, and the repressed expression of phosphatidylserine decarboxylase (PSD) gene related to phospholipid synthesis which was indispensable for hyphal morphology, hyphal differentiation and cell wall integrity. Our study showed a new theoretical basis for the effective control of T. mentagrophytes infection and the effect of HQD on fungi, which are expected to offer aids for discovering new antifungal agents upon dermatophytosis.

Elevated brain levels of the essential metals manganese (Mn), copper, or iron induce motor disease. However, mechanisms of metal-induced motor disease are unclear and treatments are lacking. Elucidating the mechanisms of Mn-induced motor disease is particularly important because occupational and environmental Mn overexposure is a global public health problem. To address this, here we combined unbiased transcriptomics and metabolomics with functional studies in a mouse model of human environmental Mn exposure. Transcriptomics unexpectedly revealed that Mn exposure up-regulated expression of metabolic pathways in the brain and liver. Notably, genes in the kynurenine pathway of tryptophan metabolism, which produces neuroactive metabolites that impact neurological function, were up-regulated by Mn. Subsequent unbiased metabolomics revealed that Mn treatment altered kynurenine pathway metabolites in the brain and liver. Functional experiments then demonstrated that pharmacological inhibition of the first and rate-limiting step of the kynurenine pathway fully rescued Mn-induced motor deficits. Finally, elevated Mn directly activates hypoxia-inducible factor (HIF) transcription factors, and additional mechanistic assays identified a role for HIF1, but not HIF2, in regulating expression of hepatic kynurenine pathway genes under physiological or Mn exposure conditions, suggesting that Mn-induced HIF1 activation may contribute to the dysregulation of the kynurenine pathway in Mn toxicity. These findings (1) identify the upregulation of the kynurenine pathway by elevated Mn as a fundamental mechanism of Mn-induced motor deficits; (2) provide a pharmacological approach to treat Mn-induced motor disease; and (3) should broadly advance understanding of the general principles underlying neuromotor deficits caused by metal toxicity.

The regulation of downstream responsive genes by transcription factors (TFs) is a critical step in the stress response system of plants. While bZIP transcription factors are known to play important roles in stress reactions, their functional characterization in soybeans remains limited. Here, we identified a soybean bZIP gene, GmbZIP60, which encodes a protein containing a typical bZIP domain with a basic region and a leucine zipper region. Subcellular localization studies confirmed that GmbZIP60 is localized in the nucleus. Expression analysis demonstrated that GmbZIP60 is induced by salt stress, drought stress, and various plant hormone treatments, including abscisic acid (ABA), ethylene (ETH), and methyl jasmonate acid (MeJA). Overexpressing GmbZIP60 (OE-GmbZIP60) in transgenic soybean and rice enhanced tolerance to both salt and drought stresses. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis indicated that the expression levels of abiotic stress-responsive genes were significantly higher in transgenic plants than in wild-type (WT) plants under stress conditions. Chromatin immunoprecipitation-qPCR (ChIP-qPCR) analysis further confirmed that GmbZIP60 directly binds to the promoters of abiotic stress-related genes induced by ABA, ETH, JA, and salicylic acid (SA). Overall, these findings revealed GmbZIP60 as a positive regulator of salt and drought stress tolerance.

The diverse hormonal treatments applied to hemp (Cannabis sativa L.) carry significant implications for cultivation, and yield optimization across a range of applications, including fiber, seed, oil production, and the enhancement of medicinal compounds. However, there is no evidence concerning the long-term consequences of hormonal treatment. To determine the connection between the effects of hormonal treatment and cannabinoid accumulation, hemp plants were treated with γ-aminobutyric acid (GABA), abscisic acid (ABA), and salicylic acid (SA) to investigate their effects on gene expression and cannabinoid content levels in female inflorescences at 3 days and 4 weeks after treatment. The treatments influenced the transcript levels of five key cannabinoid biosynthesis genes, with 1.0 mM GABA significantly increasing OAC, THCAS, and CBCAS transcripts within 48 to 72 h. Additionally, 1.0 mM GABA led to a significant increase in tetrahydrocannabinol content by day three and significant increases in total cannabidiol and cannabinoid by week four. In addition, both ABA and SA induced transient, dose-dependent increases or decreases in gene expressions, but cannabinoid accumulation at 4 weeks showed no significant changes compared to the control. These results provide valuable insights for hormonal application in cultivation and the development of traits that enhance cannabinoid production in cannabis cultivation, which could significantly contribute to optimizing industrial applications.

This study explores the dual effects of selenium (Se) supplementation on silkworm development by analyzing miRNA expression profiles of fat bodies in silkworms under different Se concentrations (50 µM and 200 µM). Compared to the control, 84 miRNAs displayed different expression levels in the F_50 µM group, with 72 miRNAs up-regulated and 12 down-regulated; 152 miRNAs were differentially expressed in the F_200 µM group, with 124 up-regulated and 28 down-regulated. In the F_50 µM group, the target genes of differentially expressed miRNAs were mainly enriched in Toll and Imd signaling pathways, oxidative phosphorylation, and ribosome biogenesis in eukaryotes; however, mainly oxidative phosphorylation, ribosome biogenesis in eukaryotes, and the spliceosome were enriched in the F_200 µM group. Based on the results of the protein-protein interaction network and miRNA-target network, bmo-miR-2a-1-5p and bmo-miR-317-3p_L-2R+2 were screened as key miRNAs in the F_50 µM group and the F_200 µM group, respectively. The bmo-miR-2a-1-5p mainly targeted 10014128 (DREDD), 100862750 (ATF2), and 101744000 (Tak1) genes, which were enriched in Toll and Imd signaling pathways. The bmo-miR-317-3p_L-2R+2 primarily regulated 101738508 (SF3b) and 101746688 (Prp19) genes, which were in the spliceosome pathway. Thus, our results demonstrated that Se supplementation improved the silkworm development via bmo-miR-2a-1-5p miRNA regulation of the Toll and Imd signaling pathways and inhibited it via bmo-miR-317-3p_L-2R+2 miRNA targeting the spliceosome pathway. Our data revealed that 50 µM Se supplementation could improve silkworm productivity; meanwhile, a 200 µM Se treatment displayed toxic effects, leading to impaired development.

Air pollution is a major global health threat, responsible for over 8 million deaths in 2021, including 700,000 fatalities among children under the age of five. It is currently the second leading risk factor for mortality worldwide. Key pollutants, such as particulate matter (PM2.5, PM10), ozone, sulfur dioxide, nitrogen oxides, and carbon monoxide, have significant adverse effects on human health, contributing to respiratory and cardiovascular diseases, as well as neurodevelopmental and neurodegenerative disorders. Among these, particulate matter poses the most significant threat due to its highly complex mixture of organic and inorganic compounds with diverse sizes, compositions, and origins. Additionally, it can penetrate deeply into tissues and cross the blood-brain barrier, causing neurotoxicity which contributes to the development of neurodegenerative diseases. Although the link between air pollution and neurological disorders is well documented, the precise mechanisms and their sequence remain unclear. Beyond causing oxidative stress, inflammation, and excitotoxicity, studies suggest that air pollution induces epigenetic changes. These epigenetic alterations may affect the expression of genes involved in stress responses, neuroprotection, and synaptic plasticity. Understanding the relationship between neurological disorders and epigenetic changes induced by specific air pollutants could aid in the early detection and monitoring of central nervous system diseases.

Exogenous abscisic acid (ABA) and brassinosteroid (BR) play important roles in alleviating cold stress in maize. In this study, two maize inbred lines with differing cold tolerance were treated with exogenous ABA, BR, and their combined solution under cold stress conditions at 10 °C to investigate the effects of these treatments on the physiological characteristics of maize seedlings. The results indicated that cold stress significantly inhibited the growth of maize seedlings. Exogenous hormone treatments enhanced antioxidant enzyme activities and promoted the synthesis of osmolytes, thereby alleviating cold stress; however, the combined treatment (AR) did not significantly improve maize cold tolerance. Transcriptomic analysis revealed that pathways including plant hormone signal transduction, fatty acid elongation, and phenylpropanoid biosynthesis were involved in the interaction between ABA and BR. Weighted gene co-expression network analysis (WGCNA) identified four key candidate genes responsive to exogenous ABA and BR under cold stress, namely Zm00001eb343270, Zm00001eb401890, Zm00001eb206790, and Zm00001eb199820. Based on the gene annotation results, we speculate that ubiquitin-conjugating enzyme E2 O, tubulin-tyrosine ligase-like protein 12, the negative regulator of systemic acquired resistance SNI1, and mRNA stability regulators in response to DNA damage may be involved in regulating maize cold tolerance. These findings provide further evidence for the regulatory mechanisms by which exogenous ABA and BR affect maize cold tolerance and elucidate their interaction under cold stress.

Heavy metal pollution and soil salinization harm human health and the environment. Phytoremediation is a widely accepted soil decontamination method, with woody plants being particularly effective due to their large biomass and extensive root systems. In this study, we identified and cloned PsnMLP328 from Populus simonii × P. nigra and demonstrated its role in mitigating salt and cadmium stress. PsnMLP328 expression was up-regulated under both stress conditions, and its overexpression in tobacco enhanced resistance to these stresses, albeit through distinct mechanisms. Transgenic plants exhibited increased Cd2+ uptake and a higher biomass, alleviating Cd2+-induced growth inhibition. Additionally, PsnMLP328 boosted proline content, chlorophyll levels, and antioxidative enzyme activities (POD, SOD) under Cd2+ stress, likely by protecting cells from oxidative damage. Expression analysis revealed that PsnMLP328 down-regulated the cadmium transporter Nramp2 while up-regulating YSL2 (another cadmium transporter) and potassium channels (AKT1 and AKT2/3), suggesting its role in modulating K+ and Cd2+ homeostasis. These findings indicate that PsnMLP328 enhances tobacco resistance to salt and cadmium stress, particularly the latter. This study is the first to elucidate the function of poplar MLP family genes under salt and cadmium stress, advancing our understanding of MLP gene roles in heavy metal stress and offering new insights for remediating salinized and heavy metal-contaminated soils.

Medical treatment of glioblastoma presents a significant challenge. A conventional medication has limited effectiveness, and a single-target therapy is usually effective only in the early stage of the treatment. Recently, there has been increasing focus on multi-target therapies, but the vast range of possible combinations makes clinical experimentation and implementation difficult. From the perspective of systems biology, this study conducted simulations for multi-target glioblastoma therapy based on dynamic analysis of previously established endogenous networks, validated with glioblastoma single-cell RNA sequencing data. Several potentially effective target combinations were identified. The findings also highlight the necessity of multi-target rather than single-target intervention strategies in cancer treatment, as well as the promise in clinical applications and personalized therapies.

As a unique class of plant-specific transcription factors, the GROWTH-REGULATING FACTORs (GRFs) play pivotal roles in regulating plant growth, development, and stress responses. In this study, the woody plant Populus ussuriensis was taken as the research object. Nineteen PuGRFs were identified and classified into six clades, and their potential evolutionary relationships were analyzed. The possible biological functions of PuGRFs were speculated through bioinformatics analysis. Combining real-time fluorescence quantitative PCR, PuGRFs were determined to be actively expressed in young tissues, and there are distinct tissue-specific expressions in the mature tissues of woody plants. We also conducted RT-qPCR of PuGRFs under different abiotic stresses and phytohormone treatments, most of the family members were induced under the treatments of methyl jasmonate (MEJA) and salicylic acid (SA), and we also found that 4 of 19 PuGRFs might participate in abscisic acid (ABA)-mediated osmotic stress in roots. Protein-protein interaction prediction analysis showed that six PuGRFs can interact with two types of growth-regulating interaction factors (GIFs). Further prediction and verification revealed that PuGRF1/2c and PuGRF1/2d, which belong to the same clade and have highly similar sequences, exhibited divergent interaction capabilities with GIFs, indicating evolutionary fine-tuning and functional redundancy within the GRF family. These findings lay a foundation for studying the molecular mechanisms of PuGRFs in P. ussuriensis, suggest that PuGRFs play important roles in responding to hormones and environmental changes, and the potential interaction relationships are worthy of exploration.

Gaseous chlorine dioxide (ClO2) is a potent antimicrobial agent used to control microbial contamination in food and water. This study evaluates the bactericidal activity of gaseous ClO2 released from a sodium chlorite (NaClO2) pad against Campylobacter jejuni. Exposure to a low concentration (0.4 mg/L) of dissolved ClO2 for 2 h resulted in a >93% reduction of C. jejuni, highlighting the bacterium's extreme sensitivity to gaseous ClO2. To elucidate the molecular mechanism of ClO2-induced bactericidal action, transcriptomic analysis was conducted using RNA sequencing (RNA-seq). The results indicate that C. jejuni responds to ClO2-induced oxidative stress by upregulating genes involved in reactive oxygen species (ROS) detoxification (sodB, ahpC, katA, msrP, and trxB), iron transport (ceuBCD, cfbpABC, and chuBCD), phosphate transport (pstSCAB), and DNA repair (rdgB and mutY). Reverse transcription-quantitative PCR (RT-qPCR) validated the increased expression of oxidative stress response genes but not general stress response genes (spoT, dnaK, and groES). These findings provide insights into the antimicrobial mechanism of ClO2, demonstrating that oxidative damage to essential cellular components results in bacterial cell death.