Peroxide Research Articles (Page 1)

We resolved that SlMYC2 positively regulated tomato leaf senescence by inhibiting ROS scavenging capacity and exacerbating oxidative damage and PSII functional decline using a darkness-induced senescence model. Tomato leaf senescence seriously affects its yield and quality. Jasmonic acid (JA) signaling can promote tomato leaf senescence, but the mechanism is unclear. SlMYC2, as a core transcription factor in JA signaling, may play a role in regulating leaf senescence. Therefore, this study used SlMYC2 overexpression and silencing lines to systematically analyze the mechanism of SlMYC2 regulation of leaf senescence through a darkness-induced senescence model. The results showed SlMYC2 accelerated the leaf senescence process in tomato by increased chlorophyll degradation and malondialdehyde accumulation in SlMYC2-OE lines after dark treatment, and the expressions of senescence-related genes SlSGR1, SlSAG12, and SlSAG15 were significantly upregulated. At the photosynthetic physiological level, SlMYC2-OE caused damage to photosystem II (PSII) function, with a significant decrease in maximum photochemical efficiency (Fv/Fm) and performance index (PIABS), and exacerbated damage to the donor side (Wk). Further studies found SlMYC2 accelerated programmed cell death (PCD) by promoting the accumulation of reactive oxygen species (ROS). The contents of superoxide anion (O₂⁻·) and hydrogen peroxide (H₂O₂) significantly increased in the SlMYC2-OE lines, while the contents of ascorbic acid (AsA) and glutathione (GSH), as well as the activities and gene expressions of key antioxidant enzymes such as SOD, POD, CAT, APX, and GR were all inhibited. In summary, SlMYC2 has been shown to inhibit the removal of reactive oxygen species (ROS), exacerbate oxidative damage and photosystem II (PSII) function decline, and positively regulate the process of leaf senescence in tomato. This study will provide a theoretical foundation for targeting the JA signaling pathway to regulate tomato senescence.

Root colonization by the endophytic fungus Serendipita indica (Si) effectively inhibited Sclerotium rolfsii (Sr) and controlled peanut stem rot. In vitro and microscopic analyses confirmed the strong antifungal activity of S. indica against S. rolfsii. Pot experiments revealed that Si markedly reduced the disease index to 5.12 ± 0.49% in resistant 'Luhua11' (L) and 8.65 ± 0.53% in susceptible 'Huayu6103' (H), indicating > 90% protection. Furthermore, Si colonization increased the biomass and health of the two peanut cultivars. Antioxidant enzyme activities were significantly increased: peroxidase (POD) activity in roots increased by 39.28-110.8% (24-96h), superoxide dismutase (SOD) activity was increased in 'LSi-Sr' and 'HSi-Sr' at 48-96h, ascorbate peroxidase (APX) activity was increased in 'LSi-Sr' (≥ 48h) and 'HSi-Sr' (≥ 72h), phenylalanine ammonia-lyase (PAL) activity peaked at 72h, and catalase (CAT) activity under 'Si-Sr' exceeded that under 'Sr'. Similarly, hydrogen peroxide (H2O2) was detected within 96h after Sr infection, whereas the malondialdehyde (MDA) content decreased. Si significantly increased jasmonic acid (JA) (500-600 pmol L⁻¹) and salicylic acid (SA) (900-1100 pmol L⁻¹) accumulation in peanut roots, with stronger induction in the Huayu103 cultivar under Si + Sr and Si + Sr treatments, peaking at 72-96h, whereas leaf levels remained comparatively low and less variable. Defense gene expression was activated, with greater induction of AhPAL, AhNPR1, and AhPR10 in the 'Luhua11' cultivar than in 'Huayu6103' at 96h; AhCSD1 increased in 'LSi-Sr' at 24h and 96h and in 'HSi-Sr' at 96h; AhAPX was upregulated in 'LSi-Sr' at 96h; and AhCAT was greater in 'LSi-Sr' (72h) and 'HSi-Sr' (96h). This study highlights S. indica as a potent biocontrol agent for managing peanut stem rot caused by S. rolfsii.

The protective properties of argon-oxygen mixture were studied in the culture of M-22 human fibroblasts, piglet thymus cells, and rat brain cells. To induce damage to cell membranes, 200 μM H2O2 and 500 μM acetic acid were used. The cells were exposed in the presence of a gas mixture containing 70% argon and 30% oxygen (ArgOx 70/30) at 37°C for 6 h. The ArgOx 70/30 mixture produced no toxic effect on the cells of all studied cultures. In culture of M-22 fibroblasts, acetic acid-induced cell death decreased by 1.5-1.9 times under the influence of ArgOx 70/30 and the cell membranes remained better preserved. In none cultures, ArgOx 70/30 mixture significantly protected cells from hydrogen peroxide-induced damage. Piglet thymus culture cells demonstrated very high resistance to high concentrations of hydrogen peroxide and acetic acid, while rat brain cells, on the contrast, had low resistance.

Alzheimer's disease is the most common form of dementia; however, its molecular mechanisms are not fully understood. We recently identified polymericglycine-arginine-containing (polyGR+) aggregates as a novel type of proteinopathy in AD autopsy brains. Here, we performed a comprehensive analysis to study if polyGR+ aggregates are associated with AD neuropathological changes (ADNC) and clinical features of AD cases. We show polyGR+ aggregates are detected in ~ 60% of AD postmortem brains from three AD cohorts but not age-similar controls or disease controls with primary age-related tauopathy (PART). A subtype of polyGR+ aggregates with a clustered-punctate morphology that is positive for the markers of dystrophic neurites is associated with earlier onset and shortened survival in AD cases. Increased levels of Aβ plaques and phosphorylatedtau (pTau)tangles are detected in the hippocampus of AD autopsy brains with high levels of polyGR+ aggregates compared to AD autopsy brains with minimal polyGR+ staining. In addition to ADNC, a subset of polyGR+ aggregates coexists with limbic-predominant age-related TDP-43 encephalopathy neuropathological changes (LATE-NC) or Lewy body pathology (LBP). Hippocampal polyGR+ aggregate levels are ~ 3.8- and ~ 3.71-fold higher in late-onset AD cases who experienced stroke or high blood pressure, respectively. In SH-SY5Y cells, hydrogen peroxide treatment which mimics oxidative stress leads to increased levels of polyGR+ proteins produced by the CASP8GGGAGA repeat expansion, which was recently shown to associate with increased AD risk. In addition, we show the accumulation of pTau induced by CASP8 polyGR+ protein aggregates is elevated upon hydrogen peroxide treatment. In summary, our results demonstrate polyGR+ aggregates are a frequent and understudied type of proteinopathy in AD autopsy brains and that polyGR proteinopathy is associated with ADNC.

While promising for photocatalytic hydrogen peroxide (H2O2) production, the performance of graphitic carbon nitride (g-C3N4) is curtailed by a central synthesis paradox: the mutually exclusive conditions required to simultaneously create its most effective dual active sites-nitrogen vacancies and cyano groups. Herein, this paradox is resolved with a molecular assembly-molten salt coupling strategy, a precise bottom-up approach enabling the one-step, synergistic creation of K-doped g-C3N4 with both defect types. This photocatalyst achieves an exceptional H2O2 production activity of 2.65 mmol·g-1·h-1, which is 6.2 and 3.0 times higher than that of pristine and physically-ground K-doped g-C3N4, respectively. Characterization and theoretical calculations reveal that molecular assembly promotes K+ interlayer embedding to facilitate charge migration, while the dual defects exhibit functional complementarity: nitrogen vacancies enhance O2 adsorption, and cyano groups facilitate proton coupling. In situ analysis also confirms an easier O2 activation effect and a lowered energy barrier for *OOH formation, ensuring high selectivity via a two-step, single-electron pathway. This study not only offers a route to rationally engineer dual-defect sites in carbon nitride but also provides a generalizable strategy for designing other advanced photocatalysts.

Cellular insights into reactive oxidative species (ROS) and bacterial stress responses induced by antimicrobial blue light (aBL) for inactivating antibiotic resistant bacteria (ARB) in wastewater.

Graphitic carbon nitride (g-C3N4) assisted photocatalytic hydrogen peroxide (H2O2) production has garnered significant interest due to its environmental sustainability. This study successfully synthesizes the crystalline material NaLi-CN via a simple molten salt-assisted method, simultaneously introducing Na+ dopant alongside nitrogen vacancies and cyanide groups. The obtained photocatalyst exhibits exceptional H2O2 production capacity, reaching 25.65mmol g-1 h-1, representing a 113-fold enhancement over pristine g-C3N4. This performance enhancement stems from its highly crystalline structure, which effectively reduces the interlayer spacing and significantly promotes in-plane and interlayer electron migration. Moreover, a synergistic effect between Na+ dopant and defect structures not only broadens the light absorption range but also significantly enhances charge separation efficiency. Interestingly, NaLi-CN enables simultaneous activation of multiple reaction pathways in the presence of a sacrificial agent, collectively suppressing competing reactions and dramatically enhancing two-electron oxygen reduction reaction selectivity. This study elucidates the synergic role of doping and defects in crystalline carbon nitride and provides valuable insights for designing efficient photocatalytic systems by optimizing the H2O2 production reaction pathways.

This study assesses the potential of supercritical water (SCW) technology for the degradation of antibiotics in aqueous systems, addressing the limitations of conventional methods, including low efficiency and prolonged reaction times. The antibiotics analyzed in this investigation include amoxicillin, ciprofloxacin, clindamycin, levofloxacin, sulfamethoxazole, and trimethoprim. Key treatment parameters-temperature, feed flow rate, and hydrogen peroxide (H2O2) concentration-were optimized to enhance degradation efficiency. Under optimal conditions (692.8°C, 6.6mLmin-1 feed flow rate, and an oxidation coefficient of 0.36), clindamycin, sulfamethoxazole, and trimethoprim were effectively degraded within a reaction time of four minutes. Furthermore, reductions in total organic carbon (TOC), chemical oxygen demand (COD), and biochemical oxygen demand (BOD) were observed at 64.1%, 64.8%, and 72.4%, respectively. Gaseous-phase analysis revealed the generation of hydrogen-rich syngas (12 N mLmin-1). These findings underscore the efficacy of SCW technology in mitigating pharmaceutical pollutants and its broader applicability in environmental remediation.

Titanium dioxide (TiO2) has been extensively investigated in photocatalysis due to its high stability, low toxicity, and biocompatibility. However, its application in hydrogen peroxide (H2O2) production is hindered by the rapid recombination of photogenerated charge carriers and the poor selectivity of the two-electron oxygen reduction reaction (2e- ORR). Here, a CuO/TiO2 photocatalyst is reported, in which CuO nanoparticles are anchored on the TiO2 surface as cocatalysts to provide additional active sites and promote efficient separation of photogenerated electrons and holes. The optimized CuO/TiO2 exhibits a remarkable photocatalytic H2O2 production rate of 19.48mmol g-1 h-1, which is 162 times higher than that of pristine TiO2, with excellent stability sustained over 7 h' continuous irradiation. The apparent quantum yield (AQY) of CuO/TiO2 reaches 7.30% at 365nm. Notably, the CuO/TiO2 demonstrated the promising H2O2 production in pure water (182.31 µmol g-1 h-1). Femtosecond transient absorption spectra (Fs-TAS) reveal that the average lifetime of photogenerated electrons in CuO/TiO2 is 5.8 times longer than in TiO2, confirming the enhanced charge separation and transfer. In situ spectroscopic analyses further demonstrate that CuO/TiO2 facilitates both oxygen reduction and water oxidation pathways. These results highlight CuO/TiO2 as a cost-effective and efficient photocatalyst for sustainable H2O2 production.

Abstract The generation of discharges from a DC voltage source for treating large polluted areas, such as soil, air, and water, has been investigated using an innovative approach. In this study, the device's effectiveness was assessed using deionized water as a target by analyzing geometric, electrical, and physicochemical parameters, as well as the production of hydrogen peroxide, nitrite, and nitrate. Electrical characterization of the discharge indicates that, under the tested conditions, the discharge remains stable throughout the treatment, maintaining consistent production of species for 30 minutes. A voltage of 10 kV maximizes the generation of reactive oxygen and nitrogen species (RONS) while ensuring system stability. Treatments lasting 15 minutes at an inter-electrode distance of 5 mm produced significant concentrations of hydrogen peroxide, nitrite, and nitrate (1.41 mg/L for H₂O₂, 1.23 mg/L for NO₂⁻, and 2.39 mg/L for NO₃⁻).

Methicillin-resistant Staphylococcus aureus (MRSA) is a Gram-positive bacterium found in hospital-acquired infections, particularly in immunosuppressed individuals. Brazilian red propolis is a beekeeping product with antimicrobial and immunomodulatory properties. Its composition includes flavonoids and benzophenones, such as oblongifolin B (OBLB). This study investigated the antibacterial activity of OBLB isolated from Brazilian red propolis against MRSA in vitro and its modulatory effects on macrophages. The activity of OBLB was assessed both alone and in combination with antimicrobials. The minimum inhibitory and minimum bactericidal concentrations were determined for the USA300 MRSA strain and for a clinical isolate. The interaction between OBLB and the antimicrobials against MRSA was analysed using the checkerboard method. The effects of OBLB on THP-1 cells differentiated into macrophages were analysed regarding cytokine and eicosanoid production, cell surface marker expression, bactericidal activity, and hydrogen peroxide production. OBLB exhibited anti-MRSA activity and had no synergistic effects with antimicrobials or cytotoxic effects on macrophages. It stimulated tumor necrosis factor-α and interleukin-1β production, CD80 expression, and increased the bactericidal activity of macrophages suppressed or not by dexamethasone against MRSA. OBLB exerted anti-MRSA properties and modulated macrophage activity, suggesting it is a potential candidate in new therapeutic approaches for MRSA infections.

Brucellosis, a globally significant zoonotic disease caused byBrucellainfection, relies on the pathogen's ability to invade and replicate within host cells. This intracellular replication is tightly regulated by transcriptional networks, including the LysR-family regulator VtlR, which is critical forB. abortusvirulence but whose role in B. melitensis remains unclear. Here, we constructedvtlRmutant and complemented strains in B. melitensis M5 and demonstrated that VtlR is essential for virulence. Phenotypic assays revealed that vtlR deletion impaired bacterial growth on L-fucose, D-glucose, and meso-erythritol, increased sensitivity to hydrogen peroxide and sodium nitroprusside, and reduced intracellular survival in RAW264.7 macrophages while triggering reactive oxygen species (ROS) production. RNA-seq and RT-qPCR analysis indicated that VtlR positively regulates small RNA AbcR2 and three DUF1127-domain proteins (RS13565, RS04310, RS13280), mirroring its regulatory role inB. abortus. However, overexpression of these targets failed to restore virulence in thevtlRmutant. Notably, the mutant strain elicited protective immunity in mice, suggesting its potential as a live-attenuated vaccine candidate. Collectively, this study elucidates the VtlR regulon inB. melitensis, advancing our understanding ofBrucellapathogenesis and vaccine development.

Management of Intraoperative Air Embolism into the Spinal Cord due to Hydrogen Peroxide Irrigation: 2-Dimensional Operative Video.

Intervertebral disc degeneration (IVDD) is a complex and multifactorial condition characterized by the progressive deterioration of the intervertebral discs. Ginsenoside Rg1, a bioactive compound isolated from Panax ginseng C.A.Mey., that has demonstrated promising therapeutic potential in the treatment of IVDD. This study employed a multi-faceted approach to investigate the therapeutic effects of ginsenoside Rg1 on IVDD. Initially, histopathology, magnetic resonance imaging (MRI) were performed in clinical IVDD patients. Subsequently, histopathology, safranin green staining, X-ray, and MRI were utilized to evaluate the efficacy of ginsenoside Rg1 in alleviating in a rat model in vivo. Transcriptomics and gene set enrichment analysis (GESA) were conducted, and a network pharmacology visualization of ginsenoside Rg1-ferroptosis key targets-pathways-IVDD was constructed, along with molecular docking of ginsenoside Rg1 and targets, to identify the signaling pathways and proteins associated with the therapeutic effects of ginsenoside Rg1 on alleviating IVDD. Additionally, an Hydrogen peroxide (H2O2)-induced degeneration model of nucleus pulposus cells (NP cells) was used to evaluate the efficacy of ginsenoside Rg1 in alleviating IVDD in vitro. Methods including lipid-reactive oxygen species (ROS) detection, enzyme-linked immunosorbent assay (ELISA), FerroOrange staining, and transmission electron microscopy were employed to validate the effect and mechanism of ginsenoside Rg1 on alleviating IVDD in vivo and in vitro. ML385, a nuclear factor erythroid 2-related factor 2 (NRF2) inhibitor, was used to reverse the effect of ginsenoside Rg1 in mitophagy and ferroptosis, respectively. The expression of proteins was assessed on immunochemical, immunofluorescence, and western blotting techniques. Significant ferroptosis was observed in the NP tissue of IVDD patients, with more effects in patients with higher imaging grades. Ginsenoside Rg1 significantly mitigated IVDD in rats and promoted intervertebral disc repair. Network pharmacology and transcriptomics analyses indicated the key targets of ginsenoside Rg1 for the treatment of IVDD, including NRF2, glutathione peroxidase 4 (GPX4), solute carrier family 7a member 11 (SLC7A11), and ferritin light chain 1 (FTL1). Molecular docking exhibited that ginsenoside Rg1 had good binding ability between ginsenoside Rg1 and these ferroptosis key targets. Ginsenoside Rg1 reduced the expression of ROS and malondialdehyde (MDA), decreased Fe2+ content, increased the expression of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), and upregulated the expression of ferroptosis key proteins NRF2, GPX4, FTL1, and SLC7A11 in intervertebral disc tissues and NP cells. Treatment with ML385 attenuated the ginsenoside Rg1-induced upregulation of these proteins in NP cells, thereby promoting ferroptosis and reversing the protective effects of ginsenoside Rg1. Ginsenoside Rg1 can mitigate IVDD by inhibiting ferroptosis in NP cells. The NRF2/GPX4 pathway was validated as the key ferroptosis pathway through which ginsenoside Rg1 exerts its therapeutic effects on IVDD.

Citral is an active compound of lemongrass oil which has been reported to have anti-inflammatory effects. This study investigates, for the first time, the simultaneous protective effects of citral on both liver and kidney in a rat model of lipopolysaccharide (LPS)-induced oxidative stress and metabolic dysfunction, a condition relevant to sepsis-associated multi-organ injury. Male rats were divided into six groups of six animals each pretreated orally with citral (10, 20, and 40 mg kg-1, body weight (b.w.)) for 7 days before LPS intoxication (8 mg kg-1, intraperitoneal (i.p.)). Citral significantly prevented oxidative damage induced by LPS. This was evidenced by the decrease in elevated levels of malondialdehyde (MDA) and hydrogen peroxide (H2O2), restoration of the enzymatic antioxidant (catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx)), and non-enzymatic defenses (glutathione (GSH) and thiol groups). In addition, citral improved liver and kidney function markers, as shown by decrease levels of aspartate transaminase (AST), alanine transaminase (ALT), bilirubin, urea, creatinine, and uric acid levels, and also stabilized lipid profiles. Inflammatory markers such as C-reactive protein (CRP) and alkaline phosphatase (ALP) were similarly mitigated. Citral gives strong protection against LPS-induced hepatorenal injuries, likely mediated through its antioxidant, lipid regulatory and anti-inflammatory actions. These results highlight citral's translational potential as a natural therapeutic agent for preventing or treating endotoxin-mediated organ damage, suggesting promise for future clinical applications in sepsis or systemic inflammatory disorders. © 2025 Society of Chemical Industry.

Microcystis spp. blooms in fish ponds can lead to fluctuations in water parameters, and the microcystin-LR (MC-LR) toxin they produce may pose health risks for fish, as well as consumers. Hydrogen peroxide (H2O2) treatment has been demonstrated to reduce populations of Microcystis spp. in aquaculture ponds. This study conducted 2 trials to investigate whether these treatments result in the release of MC-LR under laboratory conditions. We applied 7 mg l-1 of H2O2 to a Microcystis sp. culture and assessed the MC-LR level post-treatment. In the first trial, no MC-LR was detected in the H2O2 treatment group nor the negative control group, while 0.933 ± 0.381 ppb of MC-LR was extracted from 2344230 Microcystis sp. cells in 5 ml of media stock in our positive control group (where all cells were destroyed). In our second trial, where we added almost 30 times more Microcystis sp. to the culture media (i.e. 64125000 cells in 5 ml of stock), 19.333 ± 0.742 ppb of MC-LR were detected in the positive control on average. At this concentration of algae, our negative control (no treatment) and our H2O2 treatment group had 16.933 ± 0.303 ppb and 16.933 ± 0.109 ppb of MC-LR, respectively. The toxin levels were similar between the treated and untreated groups, but significantly less than the positive control group (p = 0.003). The results suggest that 7 mg l-1 H2O2 treatment to Microcystis sp. did not increase the level of MC-LR in the solution, but MC-LR was also not removed by the treatment. The low-dose 7 mg l-1 H2O2 treatment against Microcystis sp. bloom is unlikely to cause extra toxin (MC-LR) release to the medium.

Background Eimeria infection in pigeons induces severe oxidative stress in intestinal tissues, disrupting the balance between oxidant and antioxidant systems and leading to cellular and physiological damage. The resin of Commiphora myrrha has long been recognized in traditional medicine for its therapeutic potential. Purpose This study evaluated the protective effect of methanolic C. myrrha resin extract (MYE) against oxidative stress and cellular injury induced by Eimeria labbeana -like infection in pigeons. Methods Twenty-five pigeons (300–380 g) were divided into five groups (G1–G5). Following infection, birds were treated daily with MYE. On day 8 post-infection, intestinal tissues were collected to assess oxidative stress markers, antioxidant enzyme activities, and inducible nitric oxide synthase (iNOS) expression via immunohistochemistry. Results Infection with E. labbeana -like markedly elevated intestinal levels of nitric oxide (NO), malondialdehyde (MDA), and hydrogen peroxide (H 2 O 2 ), indicating enhanced oxidative stress. MYE administration significantly reduced these markers compared to infected controls. Concurrently, MYE enhanced antioxidant defense by increasing catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) activities. Moreover, MYE modulated iNOS expression, suggesting regulation of inflammation-associated oxidative pathways. Conclusion Methanolic extract of C. myrrha resin effectively mitigated oxidative and related intestinal issues induced by E. labbeana -like infection in pigeon intestines. These findings highlight its potential as a natural source of antioxidant and anticoccidial agents for managing avian coccidiosis.

Salinity stress severely hampers wheat productivity by impairing growth, photosynthesis, and metabolic balance. Potassium nutrition, however, can mitigate these effects by supporting physiological and biochemical stability. This study assessed the impact of foliar potassium application (0, 200 and 400 ppm) on two wheat cultivars, Galaxy-13 and Uqab-2000, exposed to normal (0 mM NaCl) and saline conditions (100 and 150 mM NaCl, respectively). Salinity significantly reduced root and shoot growth, biomass, chlorophyll content, photosynthetic rate, and stomatal conductance. Potassium supplementation, particularly at 400 ppm, alleviated these reductions, with Galaxy-13 showing a 32.01% increase in shoot length and a 45.11% increase in shoot dry weight compared to Uqab-2000. Biochemical analyses revealed that Galaxy-13 sustained higher nitrate and nitrite reductase activities (6.23 and 3.63 μmol NO2 g-1 FW h-1, respectively) and total soluble proteins (10.1 mg g-1 FW), whereas Uqab-2000 accumulated more soluble sugars and free amino acids under stress (9.8 and 19.8 mg g-1 FW, respectively). Oxidative stress indicators (malondialdehyde and hydrogen peroxide) rose under salinity, but potassium reduced their levels, with Galaxy-13 exhibiting stronger antioxidant regulation. Nutrient profiling further demonstrated that Galaxy-13 maintained higher N, P, and K contents and minimized Na uptake, unlike Uqab-2000, which showed severe ionic imbalance. Multivariate analyses (PCA, heatmap, and correlation) highlighted strong positive associations of potassium, especially K400, with biomass accumulation, photosynthetic efficiency, and nutrient homeostasis. The findings establish that Galaxy-13 possesses superior salinity tolerance and responds more favorably to potassium nutrition. This study provides novel evidence that cultivar-specific potassium management can enhance wheat resilience in saline environments, offering a practical strategy for sustaining yield under stress.

Colletotrichum tropicale is an endophyte that has been reported as a pathogen in ripe mango fruits (Mangifera indica L. cv. Azúcar) in Magdalena, Colombia, causing anthracnose. However, gene expression in the host that promotes its lifestyle transition remains unknown. This study aimed to analyze gene expression during the interaction between ripe mango fruit cv. Azúcar and C. tropicale to identify differentially expressed host genes that facilitate the pathogen’s infection process. RNA sequencing (RNA-seq) analysis was conducted at 0 and 12 h post inoculation (hpi), including de novo assembly and bioinformatic functional annotation using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). A total of 5,435 differentially expressed genes (DEGs) were identified in the interaction, of which only 421 DEGs were detected in ripe mango fruits. Among these, 379 were upregulated and 42 were downregulated (T0 vs. T12 hpi). GO functional annotation of downregulated fruit genes revealed that the molecular functions affected at 12 hpi were related to the plant’s defensive oxidative burst mediated by reactive oxygen species (ROS)—including NADPH oxidase activity, hydrogen peroxide formation, and the action of peroxidases and oxidoreductase enzymes—whereas upregulated genes were associated with stress response, defense, transferase activity, and kinase activity. KEGG analysis identified pathways related to mitogen-activated protein kinase (MAPK) signaling, pathogen-associated molecular pattern (PAMP)-triggered immunity, and phenylalanine metabolism. In conclusion, ripe mango fruit cv. Azúcar activates a defense response against C. tropicale at 12 hpi that does not overcome the pathogen’s initial quiescent phase but instead facilitates conditions for its establishment by suppressing oxidative burst pathways, which may later contribute to oxidative stress during the necrotrophic phase.

Skin aging is associated with fibroblast senescence, impaired wound healing, and dysregulation of markers such as sirtuin 1 (SIRT1) and fibroblast activation protein-α (FAP-α). It is known that proliferation and migration decrease in aging fibroblasts, which delays the repair process. Metformin, a widely used anti-diabetic drug, can regulate cellular senescence pathways. This study evaluated the effects of metformin on wound healing and SIRT1 and FAP-α expression in senescent fibroblasts. Cellular senescence was induced in primary human dermal fibroblasts using 100µM hydrogen peroxide (H2O2), as validated by a WST-8 assay and SA-β-gal staining. Wound healing assay and immunocytochemistry were performed on control, senescent, and metformin-treated groups (2.5, 5, and 10mM). Wound closure was significantly impaired in senescent fibroblasts (38% at 72h versus 89% in the control group). Metformin restored wound healing in a dose-dependent manner; the 10mM group achieved 94% closure at 72h, which was comparable to the control group. SIRT1 expression decreased in senescent fibroblasts (90.17 ± 4.67 vs. 124.83 ± 4.31 in controls, p < 0.001) and increased progressively with metformin treatment, reaching control levels at 10mM. FAP-α expression increased in senescent fibroblasts (91.83 ± 4.36 vs. 78.17 ± 2.56 in controls, p < 0.05) and declined towards baseline with metformin treatment, being significantly reduced at 5 and 10mM. Metformin improved wound healing capacity and normalized age-related alterations in SIRT1 and FAP-α expression in senescent fibroblasts. These results imply that metformin alleviates senescence-associated dysfunction, suggesting its potential as a therapeutic agent to enhance wound repair in aging skin.