Search Results (562)

Diabetic cardiomyopathy (DCM) under glucolipotoxic stress is sustained by a reactive oxygen species (ROS)-driven circuit in which oxidative DNA damage and nitrosative injury prime NLR family pyrin domain containing 3 (NLRP3) inflammasome assembly, triggering caspase-1 activation, gasdermin D (GSDMD) cleavage, and pyroptotic cardiomyocyte death that propagates apoptosis and fibrotic remodeling. Whether melatonin can disrupt this oxidative-pyroptotic axis when both hyperglycemia and dyslipidemia coexist, the metabolic context most refractory to current therapy has not been established. Apolipoprotein E-deficient (ApoE⁻/⁻) mice were subjected to streptozotocin-induced hyperglycemia and high-fat diet-induced dyslipidemia, then treated with oral melatonin (20 mg/kg/day) for 8 weeks. Despite unchanged fasting glycemia, melatonin attenuated cardiac oxidative stress, reducing 8-OHdG and inducible nitric oxide synthase while restoring Nrf2. Suppression of nuclear factor-κB and NLRP3 was accompanied by lowered interleukin-1β, caspase-1, and GSDMD, indicating disrupted inflammasome priming and pyroptotic execution. Downstream pathology was concurrently attenuated, with reduced TUNEL-positive cardiomyocytes, normalized Bax/Bcl-2 ratio, lower natriuretic peptide expression, diminished interstitial fibrosis, and improved electrocardiographic parameters. These findings position melatonin as a cardioprotective agent that operates despite persistent fasting hyperglycemia, acting through combined attenuation of lipid burden, cumulative glycemic stress, oxidative stress, and inflammatory signaling to arrest downstream apoptotic and fibrotic remodeling under glucolipotoxic conditions, providing a mechanistic rationale for adjunctive melatonin therapy in DCM. Full article

Background: Data on the nutritional adequacy of unsupplemented vegetarians in Northeast China are limited. Methods: We compared dietary intake, body composition, and serum biomarkers among vegans, lacto-ovo-vegetarians, and omnivores. This cross-sectional study included 356 adults (all diet ≥ 2 years, no supplements). Dietary intake was assessed using a validated semi-quantitative FFQ, body composition by BIA, and serum biomarkers. Kruskal–Wallis tests with Bonferroni correction were used. Results: Vegans had lower BMI (22.0 vs. 24.6 kg/m²), body fat (24.5% vs. 28.0%), and visceral fat (0.65 vs. 1.05 L) than omnivores (all p < 0.002). Vegans consumed more fiber (38.5 vs. 18.0 g/d) and vitamin C (180 vs. 85 mg/d), but less vitamin B₁₂ (0.3 vs. 4.2 μg/d), vitamin D (0.5 vs. 3.2 μg/d), calcium (520 vs. 720 mg/d), iodine (65 vs. 130 μg/d), and selenium (45 vs. 85 μg/d). Serum vitamin B₁₂, 25-(OH)D, ferritin, and selenium were significantly lower in vegans, while homocysteine was higher. The proportion of vegans with dietary intake below the recommendation reached 100% for vitamin B₁₂ and 97% for vitamin D, whereas omnivores showed excessive sodium (75%) and SFA (70%) intake. Conclusions: In this Northeast China cohort, unsupplemented vegetarian diets offered favorable macronutrient profiles and body composition but were associated with a high prevalence of dietary intakes below recommendations for vitamin B₁₂, vitamin D, iodine, selenium, zinc, and calcium. These findings underscore the need for targeted supplementation and food fortification strategies for individuals adhering to plant-based diets without supplement use in this region. Full article

Plant-derived compounds have recently attracted considerable scientific attention due to their potential therapeutic applications, which are largely attributed to their antioxidant properties. Tert-butyl hydroperoxide (t-BHP) is a potent inducer of intracellular oxidative stress, generating reactive free radicals, which significantly contribute to hepatic and renal damage. Micromeria frivaldszkyana (M. frivaldszkyana), a Bulgarian endemic species, contains high levels of phenolic compounds, including linarin, rosmarinic acid (RA), chlorogenic acid, rutin, quercetin, naringenin, and apigenin. In this study, male Wistar rats received oral treatment for 5 days comprising saline, 250, 400, or 500 mg/kg of M. frivaldszkyana methanolic extract, 100 mg/kg RA, or 125 mg/kg silymarin. On the final day, 0.5 mmol/kg of t-BHP was injected intraperitoneally, and blood and liver tissue samples were collected 18 h later for biochemical and histological analysis. Liver and kidney function was evaluated using biochemical markers (alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea, creatinine (Cr), uric acid (UA)), indicators of oxidative stress (malondialdehyde (MDA), 8-hydroxy-2′-deoxyguanosine (8-OHdG), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT)), and histopathology. Exposure to t-BHP resulted in significant hepatic and renal damage, including elevated serum markers, increased lipid peroxidation, and deoxyribonucleic acid (DNA) damage. Administration of 500 mg/kg M. frivaldszkyana markedly lowered elevated serum ALT and AST levels. The extract also significantly mitigated t-BHP-induced increases in serum Cr and UA. However, no significant increase in the levels of the antioxidant enzymes SOD and CAT or in GSH was observed at all tested doses. Malondialdehyde and 8-OHdG levels increased markedly following t-BHP exposure, whereas pretreatment with M. frivaldszkyana at all tested doses significantly ameliorated these oxidative alterations. These findings suggest that the methanolic extract of M. frivaldszkyana confers protective effects against t-BHP-induced toxicity, potentially through stabilisation of cell membranes, inhibition of lipid peroxidation, and reduction in DNA damage. The extract may therefore serve as a potential natural therapeutic agent against injuries caused by oxidative stress. Full article

Ionizing radiation induces reactive oxygen species (ROS) and inflammatory signaling that contribute to both therapeutic efficacy and normal tissue toxicity. While the effects of high-dose radiation are well characterized, responses to low-dose-rate radiation (LDRR) remain inconsistent and are not adequately explained by conventional linear dose–response models. To address this gap, we conducted a narrative review of recent experimental studies across multiple biological systems, including body fluids, joint microenvironments, and reproductive tissues, focusing on redox and immune-related responses under LDRR conditions (dose rates: 0.39–3.49 mGy/h). Literature was identified through PubMed/MEDLINE, Web of Science, and Google Scholar, with emphasis on studies published between 2015 and 2026. These studies demonstrate that LDRR elicits nonlinear, dose-dependent effects that vary across biological compartments and involve coordinated changes in oxidative stress, immune signaling, and metabolic regulation. Based on this synthesis, we propose a unifying framework of nonlinear redox–immune coupling, in which oxidative stress functions as a threshold-dependent regulator and immune responses follow a biphasic trajectory characterized by activation at lower dose rates and attenuation or adaptation at higher levels. These responses are strongly influenced by the local microenvironment, resulting in compartment-specific variability. This integrated perspective supports a shift from dose-centric to systems-level interpretations of radiation biology and provides a basis for improving biomarker development, risk assessment, and therapeutic strategies in chronic low-dose radiation exposure settings. Future research priorities include time-resolved mechanistic studies to define compartment-specific redox thresholds, validation of candidate biomarkers under identical multi-compartment experimental conditions (e.g., GSH/GSSG ratio, 8-OHdG, circulating cytokine panels including IL-10/TNF-α ratio), and integration of subject-specific biological variables (e.g., age, sex, and baseline redox capacity) into predictive models of LDRR response. Full article

This study evaluated the effects of dietary supplementation with 25-hydroxyvitamin D₃ (25-OH-D3), canthaxanthin (Cx), copper (Cu), and gluco-oligosaccharides (GO) on performance, egg quality, fertility, and hatchability of broiler breeder hens during early production (30 to 41 weeks of age). A total of 210 breeder hens and 21 males were allocated to three dietary treatments. Birds were fed a standard broiler breeder diet (control) or the same diet in which 0.5 kg/MT of an additive premix replaced sand. This premix supplied 16.6–17.7 mg/kg canthaxanthin (Cx) and 3700–4700 IU/kg 25-OH-D3 in Treatment 1, and 9.2–11.1 mg/kg Cx and 4100–4700 IU/kg 25-OH-D3 in Treatment 2. Treatment 2 also included Cu and GO (≥44 mg/g within the additive), with Cu provided at industry-standard levels. Each treatment consisted of seven replicates, with birds housed in floor pens containing 10 females and 1 male per replicate. Hen performance was recorded weekly, while egg quality was assessed at 30, 35, and 41 weeks. Fertility and hatchability were evaluated at 30 and 41 weeks. Treatment 2 improved lay rate, albumen height, Haugh unit, and feed conversion ratio (FCR) at selected time points. Both supplemented diets consistently produced darker yolk color compared with the control. Supplementation consistently enhanced yolk color, whereas effects on albumen height, Haugh unit, shell thickness, and FCR were observed only at specific ages or weeks. Lay rate differed among treatments only at week 40, with a trend observed at week 41. Fertility and hatchability were not significantly affected by dietary treatment. Full article

Street-food grilling is a common occupation in Asia, yet the occupational health risks associated with cooking-generated polycyclic aromatic hydrocarbons (PAHs) exposure, occurring alongside plausible unmeasured co-exposures such as ambient heat and physical workload, remain under-researched. This study investigated the internal dose of PAH exposure and its association with early biological effects and physiological strain among grill restaurant workers. A cross-sectional study was conducted involving grill workers and 20 age/BMI-matched controls. Urinary 1-hydroxypyrene (1-OHP) was utilized as the primary exposure biomarker. The study assessed early biological effects such as oxidative stress (8-OHdG, F₂-isoprostanes), lung epithelial integrity (CC16), and genotoxicity (BPDE-DNA adducts) via ELISA. Physiological parameters, including blood pressure and heart rate, were recorded to evaluate acute cardiovascular strain. Workers had significantly elevated urinary 1-OHP levels compared to controls (Hodges–Lehmann ratio = 3.66, 95% CI: 1.68–7.12, representing a 3.7-fold median increase), with exposure levels increasing proportionally to smoke proximity. Notably, workers demonstrated a significantly higher median resting heart rate (HL ratio = 1.13, 95% CI: 1.05–1.23; +12.9%) and systolic blood pressure (HL ratio = 1.09, 95% CI: 1.00–1.18; +8.9%) compared to their office-based peers. Although strong correlations were observed among biological effect biomarkers (r_s = 0.42–0.63), there were no significant differences between groups for 8-OHdG, CC16, or BPDE-DNA adducts, suggesting that cardiovascular parameters reflect acute short-term responses, while genomic damage markers may require higher cumulative exposure thresholds to become detectable. The study revealed that grill restaurant workers face substantial internal PAH exposure and significant cardiovascular strain, occurring alongside plausible unmeasured co-exposures including ambient heat and physical workload. The prevalence of chronic cough and elevated heart rate is a critical early warning sign for occupational health. Our findings indicate that current general ventilation is inadequate, highlighting an urgent need for localized engineering controls and comprehensive health surveillance, including cardiovascular monitoring in the service sector. Full article

Allergic diseases are complex conditions in which oxidative stress contributes to pathogenesis, yet the metabolic mechanisms linking oxidative stress to immunoglobulin E (IgE)-mediated responses remain unclear. This study analyzed 124 children at an 8-year follow-up, identifying those with eczema, rhinitis, and asthma. Oxidative stress markers and ¹H-nuclear magnetic resonance (NMR) blood metabolomic profiles were assessed to determine associations between metabolic pathways and atopic indices. Results showed that glutathione peroxidase (GPx) activity was significantly lower in seafood-sensitized children, while FeNO and mite-specific IgE were elevated in children with rhinitis (p < 0.01). Fractional exhaled nitric oxide (FeNO) correlated positively with allergen-specific IgE and negatively with 8-hydroxy-2′-deoxyguanosine (8-OHdG) (p < 0.01) and rhinitis-related methionine. Furthermore, seafood-specific IgE showed negative correlations with glucose and threonine (p < 0.01). Among 22 metabolites linked to atopy, threonine correlated positively with GPx (p < 0.01), while serine and mannose were associated with total antioxidant capacity (TAC). Pathway analysis revealed that branched-chain amino acid (BCAA) and glycine-serine-threonine metabolism intersected significantly with oxidative stress and atopic indices. In conclusion, a metabolomics-based approach highlights that oxidative stress-related BCAA and threonine pathways are central to the metabolic signature of childhood allergies, providing potential targets for future therapeutic interventions. Full article

Background and Objectives: Migraine is a chronic, throbbing type of headache that affects large populations worldwide. This condition is associated with neuroinflammation. Materials and Methods: In this study, polymorphism analyses were performed by KASP PCR. Serum interleukin-6 (IL-6) and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels were measured using kits based on the enzyme-linked immunosorbent assay (ELISA) principle. Results: In the APE1 Asp148Glu (rs1130409) gene polymorphism analysis, the frequency of the mutant G (Glu) allele was 93.1% and 48.0% in the control and migraine populations, respectively, while the frequency of the wild-type T (Asp) allele was 6.9% and 52.0% (p < 0.001). The frequency of the T/T (Asp/Asp) genotype was high in the migraine group (p < 0.001), while the frequency of the G/G (Glu/Glu) genotype was higher in the control group at 86.2%, compared to the migraine group (p < 0.001). The total frequency of the T/G+ G/G (Asp/Glu+Glu/Glu) composite genotype was determined to be 65.9% in the control group and 34.1% in the migraine group (p < 0.001). There was no statistical difference in allele and genotype frequency between the control and migraine groups for the XRCC1 Arg399Gln (rs25487) gene polymorphism. Serum 8-OHdG and IL-6 levels were comparable between the groups, with no statistically significant differences observed. Conclusions: Future studies with larger and more homogeneous populations are needed to further elucidate the potential interactions between inflammatory processes and DNA damage in migraine. Consideration of attack duration and environmental exposures may improve interpretation of biomarker variability. Expanding the analysis to additional DNA repair gene polymorphisms may also contribute to a better understanding of the molecular background of migraine and the evaluation of potential biomarkers. Full article

Background/Objectives: We aimed to evaluate the efficacy and safety of a short-term dietary intervention using trigonelline-rich Sakurajima radish on vascular endothelial function in patients with metabolic syndrome (MetS). Methods: In this multicenter, open-label, randomized, three-period crossover phase IIb trial, 21 patients with MetS were assigned to three 14-day sequences (Sakurajima radish powder, Aokubi radish powder, and a usual diet), separated by 14-day washouts. The primary outcome was flow-mediated dilation (FMD). Key Secondary outcomes included blood pressure (BP), urinary nitric oxide metabolites (NOx), and the oxidative stress marker 8-hydroxy-2′-deoxyguanosine (8-OHdG). Results: Sakurajima radish did not improve FMD versus the usual diet (p = 0.58) or Aokubi radish (p = 0.59), although a significant negative carryover effect following the Aokubi period likely confounded this estimation. Despite successfully stimulating NO production (elevated urinary NOx, p = 0.03), the intervention paradoxically increased oxidative stress (elevated 8-OHdG/creatinine, p = 0.02) and significantly elevated systolic BP compared with the usual diet (+9.67 mmHg, p = 0.03) and Aokubi radish (+8.86 mmHg, p = 0.04). Conclusions: Sakurajima radish does not appear to improve endothelial function in patients with MetS within the constraints of this short-term crossover design. Importantly, the unexpected negative carryover effect inherently limits the interpretability of this primary FMD outcome, as it may have masked potential physiological benefits. Despite boosting NO production, the intervention paradoxically exacerbated systemic oxidative stress and elevated systolic BP. These findings suggest that in the pro-oxidant environment of MetS, NO-boosting functional foods may induce unintended adverse hemodynamic responses, underscoring the need for careful risk–benefit evaluation and parallel-group trial designs in this specific population. Full article

Background/Objectives: Cigarette smoking is a major risk factor for periodontitis, but the salivary host-response profile associated with smoking-related periodontal inflammation remains incompletely characterized. This study compared salivary NETosis-related and oxidative-inflammatory biomarkers among current smokers, former smokers, and never-smokers with periodontitis. Methods: This cross-sectional study included 159 systemically healthy adults with periodontitis (53 per group: current smokers, former smokers, never-smokers). Individuals with systemic diseases or concomitant medications that could interfere were excluded. Unstimulated whole saliva was analyzed for NETosis-related biomarkers (MPO-DNA complexes, citrullinated histone H3, neutrophil elastase, cell-free DNA) and oxidative-inflammatory markers (MMP-8, IL-1β, IL-6, TNF-α, 8-OHdG, total antioxidant capacity). Results: Salivary MPO-DNA complexes differed significantly among groups (current smokers 33.52 ± 9.96, former smokers 26.90 ± 8.38, never-smokers 19.20 ± 7.50 ng/mL; p < 0.001, η² = 0.317). The composite NETosis score (η² = 0.702) and oxidative-inflammatory score (η² = 0.718) showed the same graded pattern. Biochemical verification confirmed clear group separation (salivary cotinine: current smokers 312.3 ± 77.0, former smokers 9.7 ± 5.1, never-smokers 3.2 ± 1.4 ng/mL). Smoking exposure was positively correlated with biomarker levels and the severity of periodontal disease. Smoking status remained independently associated with MPO-DNA complexes and the NETosis score after covariate adjustment. Conclusions: Current smoking was associated with an enhanced salivary NETosis-related and oxidative-inflammatory phenotype. Former smokers displayed an intermediate profile. Salivary MPO-DNA complexes and composite biomarker scores warrant further investigation as candidate non-invasive indicators of smoking-associated periodontal inflammatory burden, pending diagnostic performance analyses and prospective validation. Full article

Doxorubicin (Dox) is a cornerstone in the treatment of pediatric acute lymphoblastic leukemia (ALL), but its use is limited by dose-dependent cardiotoxicity. Oxidative stress, arising from mitochondrial dysfunction, enzymatic generation of reactive oxygen species, and cardiotoxic metabolites, has been implicated as a central mechanism, with interindividual variability partly influenced by genetic factors. This study evaluated oxidative DNA damage 8-hydroxy-2′-deoxyguanosine (8-OHdG) as an integrative marker of redox-related pathways in Dox-induced cardiotoxicity. In a prospective case–control study, 93 pediatric patients with ALL treated with Dox and 63 controls were included. Cardiotoxicity was assessed by serial echocardiography, and 8-OHdG levels were measured by ELISA. Genotyping of ABCC1 rs3743527, NCF4 rs1883112, and CBR3 rs1056892 was performed, and multivariable analyses were conducted. Dox-treated patients showed higher 8-OHdG levels than controls, and patients with cardiotoxicity (n = 11) had higher levels than those without. A higher frequency and severity of cardiotoxicity was observed in female patients, although this finding should be interpreted cautiously. Although allele frequencies did not reach statistical significance, distinct distribution patterns were observed between groups. These findings suggest that 8-OHdG may function as an integrative marker of redox dysfunction associated with Dox-induced cardiotoxicity. Full article

Hypoxia-induced radioresistance remains a major obstacle in non-small cell lung cancer (NSCLC) radiotherapy. This study investigates whether artificially activating mitochondrial reverse electron transfer (RET) can enhance radiosensitivity in NSCLC by triggering oxidative stress. An in vitro hypoxia/reoxygenation (H/R) model was established in A549 cells to assess reactive oxygen species (ROS) levels, mitochondrial function, and metabolic alterations using fluorescence probes, flow cytometry, confocal microscopy, and targeted metabolomics. Mitochondrial complex inhibitors and dimethyl succinate (DM-S) were employed to validate the RET mechanism, and radiosensitivity was evaluated through clonogenic survival, apoptosis assays, and γ-H2AX staining. In vivo, A549 tumor-bearing mice received high oxygen (95% O₂) combined with DM-S and localized irradiation (4 Gy); tumor growth, histopathology, and immunohistochemistry were examined. H/R triggered substantial mitochondrial ROS production via complex I-mediated RET, dependent on a high mitochondrial membrane potential and electron transport chain imbalance, with succinate accumulation serving as a key metabolic switch. Exogenous DM-S exacerbated H/R-induced oxidative damage, DNA fragmentation (8-OHdG elevation, mtDNA integrity loss), and mitochondrial network disruption. H/R combined with DM-S significantly enhanced in vitro radiosensitivity, reducing clonogenic survival and increasing apoptosis to 53.4% ± 1.9% versus 10.3% ± 1.2% with irradiation alone. In vivo, the combination therapy markedly suppressed tumor growth, induced apoptosis and oxidative lipid damage (4-HNE), alleviated hypoxia (reduced HIF-1α), and showed no overt toxicity. These findings demonstrate that activating mitochondrial RET effectively enhances radiosensitivity in NSCLC. Succinate metabolism is a critical therapeutic target, and combining high oxygen with a succinate analog represents a promising radiosensitization strategy for hypoxic tumors. Full article

Background/Objectives: Idiopathic granulomatous mastitis (IGM) is a rare, benign, chronic inflammatory disease of the breast that may present with recurrent and treatment-resistant courses and can clinically and radiologically mimic breast cancer. Despite its benign nature, IGM may significantly impair quality of life, and its underlying pathophysiology remains unclear. This study aimed to evaluate oxidative stress and DNA damage in patients with IGM. Methods: In this prospective case–control study, 28 patients with clinically and histopathologically confirmed idiopathic granulomatous mastitis who had not received corticosteroid or immunosuppressive therapy within the previous six months were enrolled. An age-matched control group of 27 healthy women was included. Venous blood and urine samples were collected for the assessment of total oxidant status (TOS), total antioxidant status (TAS), and calculation of the oxidative stress index (OSI). Mononuclear leukocyte DNA damage was evaluated using the alkaline Comet assay, and urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels were measured by ELISA. Sociodemographic data, laboratory and imaging results of the patients were also evaluated. Results: The mean ages of the patient and control groups were 37.3 ± 5.3 and 35.4 ± 8.6 years, respectively, with no significant difference (p = 0.081). Patients exhibited significantly higher inflammatory markers and oxidative stress parameters, including TOS, OSI, and urinary 8-OHdG (p < 0.05), whereas TAS did not differ between groups (p = 0.534). Comet assay analysis demonstrated significantly increased tail intensity (%) and tail moment in the patient group (p = 0.029 and p = 0.016). Conclusions: IGM is associated with increased oxidative stress and mononuclear leukocyte DNA damage. These findings suggest that oxidative stress-induced DNA damage may play a role in the pathophysiology of IGM and highlight the potential value of antioxidant-based therapeutic strategies as adjunctive treatment options. Full article

Background/Objectives: Sepsis is a life-threatening syndrome arising from a dysregulated host response to infection, frequently leading to multiple organ dysfunction, with the lungs being among the most severely affected organs. Oxidative stress, inflammation, apoptosis, and DNA damage play key roles in the pathogenesis of sepsis-induced acute lung injury (ALI). Beyond its lipid-lowering effects, rosuvastatin possesses anti-inflammatory and antioxidant properties that may confer protective effects in sepsis. This study was designed to investigate the dose-dependent prophylactic efficacy of rosuvastatin in mitigating pulmonary damage in rats with cecal ligation and puncture (CLP)-induced sepsis. Methods: Sprague–Dawley rats were randomly divided into six groups: Sham, Sham + rosuvastatin (10 mg/kg), Sham + rosuvastatin (20 mg/kg), CLP, CLP + rosuvastatin (10 mg/kg), and CLP + rosuvastatin (20 mg/kg). Rosuvastatin was administered via oral gavage 4 h before the surgical procedures in the experimental groups. All animals were sacrificed 16 h following surgical procedures. Lung tissues were analyzed for biochemical markers, including malondialdehyde (MDA) and reduced glutathione (GSH), as well as histopathological changes and immunohistochemical expression of NF-κB/p65, caspase-3, and 8-OHdG. Results: CLP-induced sepsis significantly increased MDA levels while decreasing GSH levels, indicating enhanced oxidative stress. Rosuvastatin treatment significantly reversed these changes. Histopathological analysis revealed marked lung injury in the CLP group, including alveolar inflammation, interstitial inflammation, vascular congestion, and increased alveolar septal thickness, all of which were significantly reduced following rosuvastatin administration. Immunohistochemical findings demonstrated increased expression of NF-κB/p65, caspase-3, and 8-OHdG in the CLP group, whereas rosuvastatin significantly attenuated these expressions. No significant difference in prophylactic efficacy was observed between the 10 mg/kg and 20 mg/kg doses of rosuvastatin. Conclusions: Rosuvastatin demonstrated a protective effect against sepsis-induced pulmonary damage by reducing oxidative stress, inflammation, apoptosis, and DNA damage. These findings suggest that rosuvastatin may have prophylactic potential in sepsis; however, further support is needed from investigations of cellular pathways in different mechanistic directions. Full article

Background: Late-onset neonatal sepsis (LONS) remains a major cause of morbidity in preterm neonates admitted to the neonatal intensive care unit (NICU), yet the contribution of vitamin D status to neonatal infectious susceptibility remains uncertain. Objective: To evaluate clinical and demographic variables and serum vitamin D levels assessed at birth in preterm neonates with and without LONS. Methods: A retrospective observational cohort study was conducted in a tertiary NICU in northeastern Mexico between May 2023 and October 2024. Preterm neonates (<37 weeks of gestation) with serum 25(OH)D measured within the first hour of life were included. Vitamin D status was classified as sufficient (≥30 ng/mL), insufficient (20–29 ng/mL), or deficient (<20 ng/mL). LONS was defined as sepsis occurring after 72 h of life. Comparisons between neonates with and without LONS were performed using Fisher’s exact test for categorical variables and Student’s t-test or Mann–Whitney U test for continuous variables, as appropriate. Results: Twenty-nine preterm neonates were included (mean gestational age: 32.0 ± 2.6 weeks; mean birth weight: 1748 ± 545 g). The mean serum 25(OH)D level at birth was 35.5 ± 13.0 ng/mL. LONS occurred in 31% (9/29) of neonates, of which 55% were microbiologically confirmed. No significant differences were observed in vitamin D levels between neonates with and without LONS (35.0 ± 12.0 vs. 35.7 ± 13.7 ng/mL; p = 0.899). Vitamin D deficiency was not associated with LONS (OR 1.13, 95% CI 0.09–14.28). The prevalence of vitamin D deficiency was low (10%) in this cohort. Conclusions: A clear association between serum 25(OH)D levels at birth and the development of LONS could not be demonstrated in this small exploratory cohort. Given the limited sample size and low prevalence of vitamin D deficiency, further multicenter prospective studies are required to better understand the potential relationship between vitamin D status and neonatal infectious outcomes. Full article