Search Results (40,171)

Spirulina-derived protein hydrolysates (SPPHs) have attracted considerable attention as bioactive agents due to their potential metabolic and physiological benefits. This study evaluated the therapeutic efficacy of different enzyme-specific SPPHs—Pepsin (SPPH-P), Trypsin (SPPH-T), Chymotrypsin (SPPH-C), and a combined hydrolysate (SPPH-PTC)—in high-fat diet (HFD)-induced male Wister rats, compared with Spirulina platensis protein extract (SPPE, formulated using freeze–thaw cycles and ultrasonication followed by centrifugation) and atorvastatin as a Positive Control. The animals were randomly allocated into seven groups (n = 6 per group) and received their respective treatments orally for 4 weeks. Across treatment groups, significant improvements in obesity-related anthropometric indices were observed, including reductions in BMI, Lee Index, and abdominal circumference to thoracic circumference ratio (AC:TC), with the strongest effects noted in the atorvastatin and SPPH-PTC groups. Protein metabolism markers showed enhanced hepatic and serum protein status, reflected by increased albumin and total protein concentrations. Lipid profile analysis revealed marked decreases in total cholesterol, triglycerides, and LDL in both serum and liver homogenates, while HDL exhibited non-significant but favorable elevations. Liver function markers (bilirubin, ALT, AST) and renal parameters (uric acid, BUN) demonstrated notable improvements, particularly in enzyme-derived hydrolysate groups and Positive Control. Antioxidant assessments indicated substantial reductions in MDA levels and significant increases in SOD, CAT, and GSH activities in serum and liver tissues, confirming enhanced oxidative stress resistance. Among all treatments, SPPH-PTC consistently produced the most robust therapeutic outcomes. Overall, Spirulina protein hydrolysates, especially the combined PTC formulation, exert comprehensive beneficial effects on metabolic regulation, hepatic and renal function, and oxidative balance. These findings support their potential application as functional bioactive agents for managing obesity-associated metabolic disturbances. Full article

White-nose syndrome (WNS), caused by the psychrophilic fungus Pseudogymnoascus destructans, poses a severe threat to wild bat populations. Caves serve as unique microecosystems. Exploring antagonistic microorganisms and their volatile antifungal compounds within these native environments has emerged as a promising ecological control strategy. In this study, we isolated four antagonistic bacterial strains from bat cave soil that completely inhibit P. destructans. Additionally, we identified benzaldehyde (BzH) and 2,5-dimethylpyrazine (2,5-DMP) as their primary antifungal volatile organic compounds (VOCs). Combined physiological, biochemical, and multi-omics analyses revealed that these two VOCs disrupt the structural integrity of the fungal cell wall and membrane. This disruption triggers abnormal energy metabolism and compensatory ATP accumulation, leading to a significant intracellular burst of reactive oxygen species and the impairment of primary antioxidant defenses. This sustained oxidative stress causes irreversible DNA damage, endoplasmic reticulum stress, and basal metabolic dysfunction. Consequently, this cascade induces apoptosis and significantly downregulates the expression of essential virulence genes. In conclusion, this study systematically elucidates the molecular network through which VOCs released by cave soil microorganisms antagonize P. destructans. These findings provide a theoretical foundation and candidate intervention molecules for the contactless biocontrol of WNS. Full article

Mandibular condylar cartilage (MCC) exhibits greater susceptibility to mechanical stress-induced degeneration than tibial articular cartilage (TAC). This study investigated whether differential epigenetic regulation of nuclear factor erythroid 2-related factor 2 (Nrf2), a master regulator of antioxidant responses, is associated with distinct antioxidant capacities between these cartilage types. Cartilage tissues from 5-week-old male ICR mice (n = 16 for gene analyses, n = 8 for protein analyses) were obtained using laser microdissection. Gene and protein expression was analyzed by microarray, real-time RT-PCR, and immunohistochemistry. DNA methylation of the Nrf2 promoter was evaluated using pyrosequencing and high-resolution melting analysis. Nrf2 expression in MCC was approximately 1/10 that in TAC at mRNA level and only 5% at protein level. Downstream antioxidant enzymes (NQO1, G6PD, HO-1) showed significantly reduced expression in MCC. Oxidative DNA damage marker 8-OHdG was significantly elevated in MCC compared to TAC (20.0% vs. 10.7%, p < 0.05). The Nrf2 promoter region showed higher DNA methylation levels in MCC, confirmed by high-resolution melting analysis. Higher Nrf2 promoter methylation in MCC is associated with reduced antioxidant capacity and elevated oxidative damage. This epigenetic–antioxidant relationship may contribute to MCC’s vulnerability to mechanical stress-induced degeneration and represents a potential therapeutic target for temporomandibular joint disorders. Full article

Background/Objectives: Endocrine-disrupting chemicals (EDCs) interfere with hormonal homeostasis and have been implicated in gynecological malignancy pathogenesis. This narrative review synthesizes current evidence regarding EDC exposure and breast, endometrial, ovarian, and cervical cancers, examining molecular mechanisms, epidemiology, and diagnostic and clinical implications. Methods: We conducted a literature review using PubMed/MEDLINE, Embase, Scopus, and Cochrane databases through April 2026, including systematic reviews, meta-analyses, prospective cohorts, case-control studies, and mechanistic investigations examining EDC-cancer associations. Methodological quality was appraised using the Newcastle-Ottawa Scale and AMSTAR-2, with overall certainty of evidence rated using the GRADE framework. Results: Major EDC classes—bisphenol compounds, phthalates, polychlorinated biphenyls, organochlorine pesticides, and per- and polyfluoroalkyl substances—demonstrate carcinogenic potential through estrogen receptor modulation, epigenetic alterations, oxidative stress, and oncogenic signaling disruption. Breast cancer shows the strongest evidence, with prenatal and early-life DDT/DDE exposure associated with up to a 3.7-fold increased risk. Endometrial cancer demonstrates associations with xenoestrogen mixtures exhibiting non-monotonic dose-responses, whereas ovarian and cervical cancers show emerging but limited associations. Common mechanisms include receptor crosstalk, epigenetic dysregulation with transgenerational effects, oxidative genomic instability, metabolic reprogramming, and cancer stem cell enrichment. Conclusions: Evidence supports EDC contributions to gynecological malignancy through convergent pathways, though causal inference remains constrained by observational epidemiology, long latency periods, and challenges in characterizing real-world mixture exposures. Diagnostic and prevention strategies should integrate EDC exposure into risk-prediction models, leverage multi-omics biomarkers for early detection, and emphasize exposure reduction during critical developmental windows alongside regulatory reform. Full article

Strenuous exercise is a well-established physiological stimulus that enhances muscular strength and hypertrophy but can also increase reactive oxygen species production, leading to oxidative stress (OS). Numerous studies have investigated whether dietary supplements can attenuate exercise-induced OS, yet findings remain inconsistent, and methodological quality varies. This systematic review aimed to synthesize current clinical evidence on dietary supplementation for OS management in young adults undergoing intensive exercise and to evaluate study methodology critically. The review was conducted in accordance with PRISMA 2021 guidelines and the Cochrane Risk of Bias (RoB 2.0) framework and was prospectively registered in PROSPERO. A comprehensive search of MEDLINE (PubMed), Scopus, Cochrane Central, ClinicalTrials.gov, OpenGrey, and ISRCTN identified interventional and observational human studies assessing supplementation and OS biomarkers. Forty-six studies met the inclusion criteria. The analysis revealed substantial heterogeneity in study design and reporting quality. Frequent methodological limitations included incomplete reporting of allocation concealment, participant and investigator blinding, examiner involvement, and deviations from intended interventions. Despite these limitations, several studies reported favorable effects of specific supplements on OS modulation and post-exercise recovery. Overall, the findings highlight widespread methodological shortcomings and emphasize the need for standardized trial designs, consistent biomarker selection, and transparent reporting. Well-designed, long-term randomized controlled trials are required to establish robust, evidence-based guidelines for dietary supplement use in managing exercise-induced OS in young adults. Full article

Magnesium (Mg) deficiency is common in acidic orchard soils and can limit fruit crop growth and quality. This study evaluated whether foliar-applied magnesium oxide nanoparticles (MgO NPs) could improve Mg nutrition and fruit quality in ‘Ninghaibai’ loquat grown under Mg-deficient acidic soil conditions. Pot and field experiments were conducted using water as the control and MgSO₄-50eq as an equimolar Mg comparator. MgO NPs showed a concentration-dependent effect, and 200 mg/L produced the best overall performance among the tested concentrations. At this concentration, total biomass increased by 47.27%, compared with CK, accompanied by enhanced chlorophyll accumulation, antioxidant enzyme activities, and Mg uptake. In fruit, 200 mg/L MgO NPs increased soluble solids content by 45.67% and reduced titratable acidity by 53.26%, while also improving fruit size and sugar–acid balance. Leaf transcriptome analysis suggested that MgO NPs altered the expression of genes involved in metabolism, stress response, and secondary metabolite biosynthesis. At the 50 mg/L level, MgO NPs produced stronger responses than the equimolar MgSO₄ treatment in Mg uptake, nutrient acquisition, and several fruit-quality traits. However, excessive application at 500 mg/L weakened growth and quality improvement. Overall, foliar application of 200 mg/L MgO NPs may represent a promising strategy for improving loquat growth and fruit quality under the tested Mg-deficient conditions. Full article

Per- and polyfluoroalkyl substances (PFAS) are persistent environmental contaminants increasingly associated with cardiovascular disease. Identifying early manifestations of vascular aging before the onset of overt disease is essential for improving cardiovascular risk stratification and prevention. Emerging evidence suggests that PFAS exposure contributes to early vascular and atherosclerotic alterations detectable by imaging techniques, including increased carotid intima–media thickness (CIMT), arterial stiffness, and endothelial dysfunction. In contrast, evidence for associations with coronary artery calcium progression and coronary stenosis remains scarce. Mechanistically, PFAS exposure promotes endothelial dysfunction, oxidative stress, chronic inflammation, lipid dysregulation, and genetic and epigenetic modifications, all of which contribute to premature vascular aging and metabolic disturbances. The integration of imaging and molecular biomarkers may provide complementary insights into the structural, functional, and biological processes underlying PFAS-related vascular damage; however, to date, this field remains largely unexplored. This narrative review summarizes current evidence on imaging and molecular biomarkers of PFAS-induced vascular aging and discusses their potential role in cardiovascular risk assessment. It also highlights key knowledge gaps and the need for robust epidemiological and multi-omics studies to validate these biomarkers, clarify causal mechanisms, and support their application in cardiovascular and environmental health surveillance. Full article

Lipopolysaccharide (LPS) impairs the function of ovine follicular granulosa cells (GCs), representing a primary cause of follicular atresia. Selenium (Se), an essential trace element, possesses anti-inflammatory and cytoprotective properties; however, its effects on GC ultrastructure remain largely unknown. In this study, primary ovine GCs were exposed to LPS (10 µg/mL) and treated with sodium selenite (25 nM). Transmission electron microscopy (TEM), JC-1 staining, enzyme-linked immunosorbent assay (ELISA), reactive oxygen species (ROS) detection, flow cytometry, and quantitative real-time PCR (qRT-PCR) were employed to evaluate cellular ultrastructure, mitochondrial membrane potential (ΔΨm), and downstream physiological processes. LPS induced severe mitochondrial pyknosis, cristae loss, and reduced ΔΨm, accompanied by inflammation, oxidative stress, apoptosis, and impaired steroidogenesis. Se intervention markedly ameliorated these ultrastructural injuries, preserving mitochondrial morphology and ΔΨm. Functionally, Se suppressed the release of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β); enhanced the activities of antioxidant enzymes including superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) while attenuating ROS accumulation; inhibited apoptosis by upregulating BCL-2 and downregulating BAX and CASPASE-3; and restored E₂ and P₄ secretion via upregulation of STAR and NR5A1. This study provides direct morphological evidence that Se protects ovine GCs from LPS-induced damage by repairing mitochondrial ultrastructure. This structural restoration is central to its integrated anti-inflammatory, antioxidant, anti-apoptotic, and steroidogenic effects. These in vitro findings suggest that Se may serve as a promising nutritional strategy for mitigating inflammation-driven follicular atresia, pending further in vivo validation. Full article

Aging of Styrene–butadiene–styrene (SBS)-modified asphalt accelerates the degradation of both the SBS polymer network and asphalt components, resulting in deterioration of the durability of asphalt concrete. This study investigates the use of zinc diethyldithiocarbamate (ZDC), a multifunctional antioxidant, in SBS-modified asphalt to improve its aging resistance. Physical property tests, dynamic rheological analysis, multiple stress creep recovery (MSCR) and Fourier transform infrared spectroscopy (FTIR) assays were conducted to evaluate the rheological and chemical properties of asphalt binders before and after thermo-oxidative and UV aging. The results indicate that the incorporation of ZDC improved the deformation resistance and elastic recovery of SBS-modified asphalt. After aging, the ZDC/SBS composite-modified asphalt exhibited lower performance change rate than conventional SBS-modified asphalt, indicating enhanced resistance to permanent deformation and aging-induced damage. FTIR analysis demonstrated that ZDC effectively inhibited the formation of oxygen-containing functional groups during aging, suggesting suppressed oxidative reactions within the asphalt binder. The 5% ZDC dosage reduces the carbonyl index of SBS-modified asphalt by 36.48% after thermo-oxidative aging, and by 21.89% after UV aging, showing a stronger chemical inhibition effect on thermo-oxidative reactions. From the perspective of rheological performance stability, ZDC lowers the variation amplitude of non-recoverable creep compliance by 35.32% before and after thermo-oxidative aging and 41.46% before and after UV aging, and delivers a more prominent mitigating effect on property fluctuations triggered by UV aging. This indicates that ZDC exerts differentiated anti-aging mechanisms on thermo-oxidative and UV aging, with considerable potential to improve the comprehensive aging resistance of polymer-modified asphalt binders. Full article

Tuberculosis (TB) remains a leading cause of death from a single infectious agent, and its outcome is shaped not only by Mycobacterium tuberculosis (Mtb) itself, but also by the host’s metabolic state. This review synthesises current understanding of how Mtb reprograms macrophage immunometabolism and how this reprogramming propagates to a systemic level, culminating in skeletal muscle dysregulation and TB-associated cachexia. We describe the molecular mechanisms by which Mtb subverts phagosomal maturation, the glycolytic (Warburg-like) switch governed by HIF-1α and accumulation of immunomodulatory tricarboxylic acid cycle intermediates, and the M1/M2 polarisation balance that dictates bacterial containment versus persistence. We then trace the cytokine- and metabolite-mediated circuits (TNF-α, IL-6, IL-1β, lactate, ketone bodies, free fatty acids) that link infected macrophages to ubiquitin–proteasome and autophagy–lysosome-driven muscle proteolysis, mitochondrial dysfunction and oxidative stress. Building on these mechanisms, we propose an immunometabolic and muscle-derived biomarker framework that, although still requiring clinical validation, may offer value for diagnosis, host-response stratification and treatment monitoring, and we discuss host-directed therapeutic strategies that target macrophage metabolism and muscle preservation. By integrating immunity, metabolism and systemic pathology at the molecular level, this work highlights translational opportunities relevant to the host immunity, diagnosis and treatment of tuberculosis. Full article

Neuropathic pain (NP) arises from diverse conditions, including peripheral nerve injury, spinal cord injury (SCI), and painful diabetic neuropathy, yet these disorders share oxidative stress, mitochondrial dysfunction, lipid dysregulation, and altered neuronal excitability. We investigated whether dietary omega-3 polyunsaturated fatty acids modulate ferroptotic stress-associated pathways, defined as lipid peroxidation susceptibility and impaired antioxidant defense rather than overt ferroptotic cell death. Female Sprague–Dawley rats received either a soy oil control diet (SOD) or fish oil omega-3-enriched diet (FOD) before chronic constriction injury (CCI). Behavioral outcomes were assessed using Hargreaves and CatWalk testing, followed by dorsal root ganglion (DRG) RNA sequencing, RT-PCR, and GPX4 ELISA. Previously generated SCI metabolomics and human diabetic serum metabolomic/lipidomic datasets were re-analyzed for shared pathways. FOD attenuated CCI-induced thermal hypersensitivity and improved gait parameters. DRG transcriptomics showed reduced injury-associated transcriptional disruption, enrichment of selenoamino acid metabolism, nonsense-mediated decay, and ribosomal quality-control pathways, and reduced mitochondrial dysfunction pathway activity. Omega-3 increased Gpx1/Gpx4 expression and GPX4 protein, reduced pain-associated genes including Scn10a, Piezo2, Trpa1, and Oprm1, and aligned with selenoamino acid enrichment in SCI and human datasets. Human lipidomics showed MG/DG/PC/PE pathway remodeling. These findings support ferroptotic stress as a plausible shared downstream mechanism modulated by omega-3 supplementation across NP models. Full article

Congenital toxoplasmosis, caused by the obligatory intracellular apicomplexan protozoan Toxoplasma gondii, can lead to severe complications during pregnancy, including fetal malformations and spontaneous abortion. In the present study, the anti-T. gondii effects of the natural flavonoid quercetin were evaluated using in vitro, ex vivo, and in silico models. Cell viability and intracellular proliferation of the parasite were determined via colorimetric assays. The lipid droplet assay was analyzed using Nile Red staining, the antioxidant and oxidative stress parameters were determined by biochemical assays, and the cytokine levels were quantified by immunoassays. Our results demonstrated that non-cytotoxic concentrations of quercetin (CC₅₀ > 100 μM) significantly inhibited parasite proliferation (IC₅₀ = 14.10 ± 2.83 μM; SI > 7.09) in an irreversible manner. Quercetin impairs parasite adhesion, invasion, and reinfection capacity. In parallel, quercetin reduced lipid droplet accumulation, restored antioxidant balance by modulating redox biomarkers, and regulated cytokine production, notably increasing IL-4, IL-6, and IL-8 levels. Corroborating the in vitro findings, quercetin significantly reduced T. gondii proliferation in human placental villous explants while preserving tissue architecture and viability. In silico analyses revealed that quercetin binds to the active site of T. gondii hypoxanthine-guanine phosphoribosyltransferase (TgHGPRT) and exhibits favorable pharmacokinetic and drug-likeness properties. Full article

Transcranial magnetic stimulation (TMS) is a non-invasive brain stimulation method with neuromodulatory capacity in neurodegenerative diseases such as multiple sclerosis (MS). Its therapeutic value is linked to its activity against oxidative stress by activation of antioxidant defenses. The sex hormones, estrogens (E), progesterone (P) and testosterone (T), have demonstrated their power as adjuvants to TMS, improving cortical excitability. The aim of this study was to evaluate the effect of these hormones as adjuvants to extremely low-frequency electromagnetic fields (ELFEFs) in the treatment of experimental autoimmune encephalomyelitis (EAE), the experimental model of MS. The effect of these hormones as replacement therapy was also evaluated in ovariectomized rats treated with ELFEFs. Sixty-five female Dark Agouti rats were divided into 13 groups (5 rats/group), in which biomarkers of oxidative stress and the glutathione redox cycle in non-nervous organs (kidney, liver, heart, intestines and blood) were analyzed. The results show that ELFEFs alone are more effective against oxidative stress. However, P and E were more effective than ELFEFs, both as adjuvants and in hormone replacement therapy, in activating the glutathione system. Therefore, it could be concluded that sex hormones play an important role against MS, enhancing the antioxidant effect of ELFEFs. Full article

The toxicity of oxybenzone (benzophenone-3; BP-3), a UV filter present in coral reef waters at toxic concentrations, has been incompletely characterized for oxidative stress responses in adult cnidarians. In order to examine this, Aiptasia pallida (an anemone commonly used as a coral research model) was exposed to oxybenzone at concentrations of 0.02, 0.2, 2.0, and 3.0 mg/L for 5, 10, and 30 days (n = 4 tanks per treatment). Catalase (CAT) and superoxide dismutase (SOD) activity, glutathione levels, and the alkaline comet assay (% DNA in tail) were analyzed. CAT increased significantly at all concentrations and timepoints, with 80.6% maximum induction at 2.0 mg/L on Day 30 and a LOEC of 0.02 mg/L. SOD showed no significant response at any timepoint. The levels of glutathione increased at Day 5 for the two highest concentrations, but decreased at Day 10 for 3.0 mg/L. Genotoxic effects were significant at Days 5 and 10, with a threshold between 0.02 and 2.0 mg/L. A significant positive correlation between group mean CAT activity and % DNA in the tail contrasted with a null SOD–DNA association, identifying hydrogen peroxide, not superoxide, as the proximate genotoxic driver in adult cnidarian tissue. These results indicate that oxybenzone induces oxidative stress responses in A. pallida. Full article

Psychological stress can affect female reproductive function through behavioral, endocrine, ovarian, and oxidative mechanisms. Antioxidant supplements have therefore attracted attention for their potential to mitigate stress-related reproductive alterations. Coenzyme Q10 (CoQ10) is a lipid-soluble quinone involved in mitochondrial energy metabolism and is widely used as a dietary supplement. However, whether CoQ10 modulates female reproductive responses to repeated psychological stress remains unclear. Although water avoidance stress (WAS) is a well-established psychogenic stress model, its effects on female reproductive outcomes are still not fully defined. In this study, we examined how repeated WAS affects female reproductive outcomes and whether CoQ10 modifies these effects. Twenty-eight regularly cycling female rats were assigned to sham control, WAS, CoQ10, or WAS + CoQ10 groups. WAS was applied for 1 h/day for 10 days, and CoQ10 was administered orally at 100 mg/kg/day. Repeated WAS did not significantly alter sexual incentive motivation parameters, reproductive hormones, corticosterone, total antioxidant capacity (T-AOC), 8-hydroxy-deoxyguanosine (8-OHdG), or mast cell count under the present experimental conditions (all p > 0.05). However, WAS reduced male-directed active investigation time (p = 0.008) and male investigation preference ratio (p = 0.024), increased absolute ovarian and adrenal gland weights (p = 0.035 and p = 0.016, respectively), reduced primordial follicle number (p = 0.030), decreased germinative epithelium thickness (p = 0.017), lowered VEGF histoscore (p = 0.033) regardless of CoQ10 treatment, and reduced corpus luteum angiogenesis in animals not receiving CoQ10 (p = 0.030). CoQ10 reduced total investigation time toward the male (p = 0.032), male investigation preference ratio (p = 0.037), 17-β estradiol (E2) (p = 0.003), testosterone (p = 0.021), and germinative epithelium thickness (p < 0.001) regardless of WAS exposure. CoQ10 also decreased kisspeptin-1 levels under non-stressed conditions (p = 0.010), while increasing corpus luteum angiogenesis under stress conditions (p = 0.003). Overall, repeated WAS produced selective behavioral and ovarian alterations rather than broad reproductive dysfunction. CoQ10 was not associated with a broadly protective or uniformly beneficial profile in this model, and its endocrine, behavioral, and ovarian effects should be interpreted with caution. Full article