Search Results (10,286)

Identifying physiological changes during the transition period is essential for improving the health and productivity of dairy goats. This study evaluated hematological, biochemical, hormonal, oxidative stress, and molecular alterations in Shami goats during the pre-pregnancy, late pregnancy, and early lactation periods. Eighty clinically healthy goats were examined, and blood samples were analyzed for hematological indices, metabolic and hormonal profiles, oxidative stress biomarkers, and relative expression of genes associated with energy metabolism, antioxidant defense, inflammation, and autophagy. Late pregnancy was characterized by significant (p < 0.05) increases in red blood cell count (RBCs), hemoglobin concentration (Hb), neutrophils, albumin, globulin, urea, insulin-like growth factor-1 (IGF-I), and malondialdehyde (MDA), accompanied by decreased glucose, cholesterol, total protein (TP), antioxidant markers, total leukocyte count, packed cell volume, and monocytes. Early lactation was associated with higher non-esterified fatty acid, triiodothyronine (T3), and thyroxine (T4) levels. Genes involved in lipid mobilization and oxidation, ketogenesis, inflammation, cellular stress, and autophagy; sirtuin 1 (SIRT1), peroxisome proliferator-activated receptor alpha (PPARA), carnitine palmitoyltransferase 1a (CPT1A), 3-hydroxy-3-methylglutaryl-coenzyme a synthase 2 (HMGCS2), cluster of differentiation 36 (CD36), lipase E (LIPE), protein kinase amp-activated catalytic subunit alpha 1 (PRKAA1), solute carrier family 2 member 1 (SLC2A1), haptoglobin (HP), interleukin 6 (IL6), heat shock protein 70 (HSP70), heme oxygenase 1 (HMOX1), beclin 1 (BECN1), and autophagy-related protein 5 (ATG5) were significantly upregulated, whereas antioxidant- and glucose transport-related genes nuclear factor erythroid 2-related factor 2 (Nrf2), glutathione peroxidase 1 (GPX1), catalase (CAT), thioredoxin (TXN), and solute carrier family 2 member 4 (SLC2A4) were downregulated during the transition period. The results indicate well-orchestrated metabolic and molecular adaptations that can be employed as biological indicators to track the physiological status of Shami goats. These findings fulfilled the study objective and identified potential biomarkers of the transition period in Shami goats. Full article

Background/Objectives: Primary open-angle glaucoma (POAG) is a complex multifactorial optic neuropathy involving genetic, vascular, oxidative, inflammatory, and neurodegenerative mechanisms. Despite advances in genome-wide studies, the contribution of genetic variants remains incompletely characterized in underrepresented Latin American populations. This study aimed to characterize the genetic landscape of POAG in a Colombian cohort by identifying previously reported glaucoma-associated variants, rare candidate variants, and pharmacogenomic markers and integrating these findings into biologically relevant pathways. Methods: An exploratory descriptive study was conducted in 21 Colombian patients with confirmed POAG. Whole-exome sequencing (WES) was performed at an average sequencing depth of approximately 100×. Variants were quality-filtered, functionally annotated, and prioritized within 446 POAG-associated genes retrieved from DisGeNET. Previously reported glaucoma-associated variants and rare candidate variants were identified, while pharmacogenomic variants related to latanoprost and timolol response were evaluated using ClinPGx/PharmGKB. Identified genes were classified according to major biological pathways relevant to glaucoma pathophysiology. Results: Of the 446 POAG-associated genes, 381 were detected in the patients’ exomes. A total of 10,220 molecular variants were identified, of which 1,187 synonymous variants were excluded, leaving 9,033 variants for downstream analysis. Among these, 955 were non-synonymous SNVs, including 26 variants previously reported in association with glaucoma and 929 potentially novel coding variants. Previously reported variants included loci in SIX6, LOXL1, CYP1B1, NOS3, and SOD2. Two rare candidate variants (minor allele frequency <1%) were identified in FMNL2 and C3. Pharmacogenomic variants in PTGS1, ADRB1, and ABCC4 with potential implications for response to latanoprost or timolol were also detected. Functional integration highlighted pathways involving oxidative stress, extracellular matrix remodeling, vascular regulation, neurodegeneration, and inflammation. Conclusions: This exploratory analysis identifies known glaucoma-associated variants, rare candidate variants, and pharmacogenomic markers in Colombian patients with POAG. The findings support a multifactorial biological framework involving interconnected oxidative, structural, vascular, neurodegenerative, and inflammatory pathways. The FMNL2 and C3 variants represent candidates for further investigation, while the identified pharmacogenomic variants highlight the potential relevance of genomic profiling for personalized glaucoma management. Larger ancestry-informed case–control studies are required to validate these observations and determine their clinical significance. Full article

Background: Conventional tyrosinase (TYR) inhibitors irritate skin and trigger rebound pigmentation, necessitating safer and more effective depigmenting agents. Methods: Biocompatibility was assessed by cell viability. Melanin content and TYR activity were measured spectrophotometrically. Reactive oxygen species (ROS), adenosine triphosphate (ATP), and inflammatory cytokines were detected by fluorescence, luminescence, and ELISA. Western blot and RT-qPCR assessed oxidative stress, inflammatory, and melanogenic targets. Molecular docking simulated Ganoderic Acid A (GAA) interactions with key proteins. Results: GAA exhibits good biocompatibility, inhibits melanin synthesis and TYR activity in B16-F10 cells, and reverses ultraviolet B-induced pigmentation. Mechanistically, GAA restores mitochondrial homeostasis by scavenging ROS, replenishing ATP, activating the nuclear factor erythroid 2-related factor 2 (Nrf2) axis, and inhibiting nuclear factor kappa-B (NF-κB) and cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) to regulate the inflammatory microenvironment. This synergistic regulation inhibits the mitogen-activated protein kinase (MAPK) signaling pathway and down-regulates the microphthalmia-associated transcription factor (MITF) transcriptional network and the expression of TYR, tyrosinase-related protein 1 (TRP-1), and tyrosinase-related protein 2 (TRP-2). Conclusion: GAA eliminates ultraviolet B-induced hyperpigmentation through a multi-target mechanism of mitochondrial repair, inflammation inhibition, and direct binding to tyrosinase, and is a potential natural candidate drug for the treatment of skin diseases. Full article

Background/Objectives: Recovery nutrition must restore near-term readiness without indiscriminately suppressing biological signals that contribute to repair and training adaptation. This review evaluates recovery–adaptation coupling (RAC) as a research framework and clarifies its contribution relative to established recovery, nutrient-periodization, and athlete-monitoring models. Methods: Targeted narrative searches of PubMed/MEDLINE, Scopus, and Web of Science were supplemented by Google Scholar citation tracking and backward and forward screening. Peer-reviewed English-language literature available through 31 May 2026 was considered. Human athlete studies, randomized trials, systematic reviews, meta-analyses, consensus statements, and position stands were prioritized; mechanistic evidence was used to explain pathways rather than to support stand-alone performance recommendations. The final cited corpus comprised 130 records. No formal risk-of-bias tool, certainty grading, PRISMA denominator, or quantitative pooling was used. Claims were instead identified as established practice (EP), context-dependent evidence (CDE), mechanistic rationale (MR), or RAC hypothesis (RH). Results: The most consistent applied support concerns adequate energy availability, distributed high-quality protein, carbohydrate restoration when recovery windows are short, and individualized fluid and sodium replacement. Evidence for polyphenol-rich products, curcumin, omega-3 fatty acids, and creatine is context- and product-dependent. Collagen or gelatin evidence is mainly mechanistic or pilot-level, while RAC recovery-pattern categories and multimodal monitoring rules remain unvalidated hypotheses. RAC differs from existing frameworks by jointly specifying the next athletic demand, dominant recovery bottleneck, possible adaptive cost of intervention, and response-verification plan. Conclusions: RAC should presently be interpreted as an evidence-organization and hypothesis-generation architecture, not as a validated predictive, diagnostic, or treatment algorithm. Prospective comparative studies are required before RAC-specific decision rules can guide individualized practice. Full article

Aging is accompanied by a progressive decline in mitochondrial quality, bioenergetic flexibility, and stress resilience. Aging mitochondria are increasingly recognized as active inflammatory signaling platforms rather than passive targets of cellular damage. Excess mtROS, leaked mtDNA, defective mitophagy, altered NAD⁺ metabolism, and impaired pyruvate oxidation together create a cellular environment that favors persistent inflammatory activation. These signals engage NF-κB, NLRP3 inflammasome, cGAS–STING, and SASP pathways, allowing mitochondrial stress to spread from organelle dysfunction to tissue-level inflammation. Within this framework, pyruvate dehydrogenase kinase 4 (PDK4) is of particular interest because it directly controls mitochondrial pyruvate entry through inhibition of the pyruvate dehydrogenase complex. By phosphorylating and inhibiting the pyruvate dehydrogenase complex, PDK4 limits mitochondrial pyruvate oxidation and favors lactate accumulation, fatty acid utilization, and redox-inflammatory signaling. Recent work in senescent cells links PDK4-dependent lactate accumulation to NOX1-derived ROS and SASP activity, suggesting a direct route by which altered fuel handling may reinforce inflammation. Here, we review mitochondrial dysfunction as the organizing principle of age-associated meta-inflammation, discuss PDK4 as a central metabolic checkpoint, examine tissue-specific consequences in muscle, adipose tissue, brain, and kidney, and evaluate therapeutic strategies aimed at restoring mitochondrial function to suppress chronic inflammation and preserve healthspan. Full article

Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive immunometabolic liver disorder involving lipid dysregulation, inflammation, fibrosis, and extrahepatic immune–neural responses, yet therapies capable of modulating these interconnected processes remain limited. Berberine (BBR), an isoquinoline alkaloid derived from traditional medicinal plants including Coptis chinensis Franch. (Coptidis Rhizoma), has shown metabolic and anti-inflammatory activities; however, its effects on hepatic inflammation and the liver–brain inflammatory axis in MASH remain unclear. Here, network pharmacology and molecular docking were used to predict BBR targets and pathways, followed by in vivo validation in a methionine- and choline-deficient diet-induced mouse model. Liver injury and metabolic alterations were assessed using serum biochemistry and lipid profiles, histological changes by hematoxylin and eosin and Sirius Red staining, and hepatic and hypothalamic inflammation by qRT-PCR, flow cytometry, and Iba-1/GFAP immunostaining. SREBF1, AKT1, and TGFB1 were identified as core BBR targets, with pathways linked to lipid metabolism, oxidative stress, inflammation, and fibrogenesis. BBR attenuated liver injury, steatosis, steatohepatitis, and fibrosis, suppressed SREBF1-associated lipogenic signaling and fibrogenic gene expression, remodeled circulating monocyte subsets, reduced Kupffer cell accumulation, and inhibited hypothalamic microglial activation. These findings suggest that BBR alleviates MCD-induced steatohepatitis through multi-target regulation of hepatic metabolic dysfunction, immune remodeling, and hypothalamic neuroinflammation. Full article

Hydrogen sulfide (H₂S) is an important endogenous gaseous signaling molecule that regulates diverse physiological and pathological processes through protein persulfidation. As a central regulator of inflammation and immune responses, NF-κB signaling is precisely controlled by post-translational modifications, and its dysregulation contributes to various inflammatory diseases. Recent studies reveal that H₂S-mediated persulfidation is a key mechanism for fine-tuning NF-κB activity by targeting critical components, including p65, IKKβ, IκBα, and upstream regulators. Through site-specific S-sulfhydration, H₂S modulates IKK activation, IκBα degradation, and p65 nuclear translocation, thereby limiting excessive NF-κB activation and inflammatory cytokine production. This review provides an integrated view of how endogenous H₂S production and persulfidation-dependent signaling regulate inflammatory responses. Rather than simply summarizing individual pathways, we focus on the molecular mechanisms underlying H₂S-mediated regulation of NF-κB-associated networks, including TLR4/NF-κB, PI3K/Akt/NF-κB, and MAPK/NF-κB pathways, and highlight its roles in oxidative stress, apoptosis, pyroptosis, and tissue repair. We further discuss current challenges in identifying persulfidation sites, understanding endogenous H₂S regulation, and improving detection technologies. By proposing H₂S as a precision modulator of inflammatory signaling, this review provides new insights into H₂S biology and highlights future opportunities for developing targeted H₂S-based therapeutic strategies. Full article

Diabetes mellitus (DM) induces significant endocrine disruption and oxidative stress (OS) within the testes, resulting in impaired spermatogenesis, increased sperm abnormalities, and compromised reproductive function. This study aimed to evaluate the combined protective effects of Semaglutide (SEM) combined with Carica papaya (papaya) juice against type 2 diabetes-induced testicular damage in rats. Forty adult male albino rats were divided into four experimental groups: a control group, a Streptozotocin (STZ)-induced diabetic group, a diabetic group treated with SEM (0.3 mg/kg), and a diabetic group treated with SEM (0.3 mg/kg) in combination with 10% papaya juice, administered for eight weeks. Statistically significant superiority over SEM alone was observed for selected endpoints; the findings primarily support the potential of papaya as a dose-sparing adjunct rather than demonstrating uniformly enhanced efficacy. They significantly improved systemic metabolic parameters, as evidenced by reduced fasting blood glucose (FBG) and glycated hemoglobin (HbA_1c) levels and restoration of the lipid profile. Importantly, it also attenuated diabetes-induced testicular injury, as demonstrated by improved reproductive hormone levels, enhanced sperm parameters, restoration of antioxidant defenses, modulation of inflammatory and apoptotic signaling, and marked histopathological recovery of seminiferous tubular architecture. Antioxidant markers revealed a notable reduction in malondialdehyde (MDA) and cytochrome P450 2E1 (CYP2E1), along with significant increases in reduced glutathione, catalase (CAT), and superoxide dismutase (SOD). Furthermore, a marked modulation of key pro-inflammatory and pro-apoptotic mediators was observed, including forkhead box protein O1 (FOXO1), microRNA-155 (miR-155), tumor necrosis factor-alpha (TNF-α), nuclear factor kappa B cell subunit 1 (NF-κB1), interleukin-6 (IL-6), caspase-3 (CASP3), and BCL2-Associated X Apoptosis Regulator (Bax), while a significant upregulation of sirtuin-1 (SIRT1), microRNA-34c (miR-34c), and B-cell lymphoma-2 (Bcl-2) was also detected. Histopathological assessments confirmed the restoration of normal testicular architecture in the treated groups. These findings indicate that the combination strategy may have the potential to achieve dose savings while maintaining efficacy comparable to the standard-dose SEM, through the enhancement of the antioxidant defenses, modulation of inflammation, and apoptosis, specifically via the modulation of the miR-34c/miR-155 and SIRT1/FOXO1 signaling. Full article

Myocardial infarction with non-obstructive coronary arteries (MINOCA) is a clinically important but heterogeneous syndrome associated with substantial long-term morbidity and adverse cardiovascular outcomes. Pharmacologic management remains largely extrapolated from obstructive coronary artery disease, creating a persistent mismatch between treatment strategies and the diversity of underlying mechanisms. Accurate diagnostic adjudication using cardiac magnetic resonance imaging, intracoronary imaging, coronary functional testing, and mechanistic biomarkers is therefore central to a phenotype-guided therapeutic approach. Inflammation, endothelial dysfunction, oxidative stress, autonomic dysregulation, coronary microvascular dysfunction, plaque-related injury, and adverse ventricular remodeling represent potentially targetable biological domains across selected MINOCA phenotypes. Empagliflozin and colchicine exert overlapping but distinct effects on several of these pathways and have demonstrated cardiovascular benefits in related clinical settings; however, direct evidence in MINOCA remains limited and predominantly observational. This article integrates the available mechanistic and clinical evidence into a comparative, phenotype-linked therapeutic framework and proposes a pragmatic trial strategy incorporating diagnostic adjudication, phenotype enrichment, biomarker-guided stratification, and adaptive or factorial designs. The proposed framework is hypothesis-generating and is intended to inform prospective investigation rather than support off-label prescribing or changes to current clinical practice. Full article

Alkaptonuria (AKU) is a rare metabolic disorder caused by homogentisic acid accumulation and characterised by ochronosis, oxidative stress, chronic inflammation, and progressive connective tissue damage. This study aimed to define the circulating proteomic alterations associated with AKU and assess their relationship with nitisinone treatment. Plasma samples from 11 patients with AKU and 6 age- and sex-matched healthy controls were analysed by liquid chromatography coupled to tandem mass spectrometry using label-free quantification. Differentially abundant proteins were identified using thresholds of |log₂FC| ≥ 1 and Benjamini–Hochberg false discovery rate ≤ 0.01, followed by functional enrichment and treatment-stratified analyses. Twenty-two proteins were differentially abundant between AKU patients and controls. Complement components (C1R, C1S, C9, C4BPA, CPN2), fibronectin, clusterin, PGLYRP2, and haemoglobin subunits showed increased abundance, whereas most immunoglobulin chains, kallikrein, apolipoprotein A2, and alpha-1-antitrypsin showed decreased abundance. Functional enrichment highlighted complement activation, B-cell-mediated and humoral immune responses, immunoglobulin-related functions, platelet activation, and erythrocyte gas-exchange pathways. Correlation analysis linked several proteins, particularly CPN2, APOA2, C1R and C1S, to core biochemical parameters of disease activity. Treatment-stratified analysis identified fourteen proteins that remained significantly altered in both treated and untreated patients, forming a treatment-resistant core of the signature, while several complement-, coagulation-, and lipid-related proteins were significant only in one treatment subgroup. These findings define an AKU plasma proteomic signature dominated by complement activation and humoral immune alterations, together with extracellular matrix, erythrocyte-, and coagulation-associated changes. The persistence of most alterations across treatment groups suggests that residual systemic proteomic dysregulation remains despite nitisinone treatment. Full article

Oxidative stress and inflammation are the causes of many colonic diseases. Therefore, the aim of this study was to maximize the biological activity of hawthorn seed preparations aimed at modulating oxidative stress and the inflammatory response in the colon through selective fractionation and enrichment in compounds with antioxidant, anti-inflammatory, and cytotoxic potential. Fractionation of hawthorn seed extract (CE) was performed using C18 resin, and detailed phytochemical analysis was performed using ultra-performance liquid chromatography (UPLC-MS/MS). This work resulted in four fractions (F1-F4), with differential distribution of 28 identified polyphenolic compounds. Phenolic acids dominated in F1, flavan-3-ols in F2, and flavonols in F3 and F4. In terms of quantitative composition, the obtained fractions can be ranked in the order F1 > F2 > F3 > F4. In biological activity studies, the highest antioxidant activity in a chemical model was demonstrated for F2, which was also confirmed in a cellular model–colonocyte cells (CCD841CoN line) stimulated with H₂O₂. F2 also demonstrated the highest inhibition of ROS production by colonocytes and NO production by macrophages. High F2 activity was also demonstrated in studies of the proliferation, migration, and invasion of colon cancer cells. These findings underscore the validity of fractionation of hawthorn seed extract and its potential use in the prevention and treatment of colon diseases. Future studies should include in vivo models and estimation of the activity of the fraction truly bioavailable after digestion. Full article

Potassium is the predominant intracellular cation and plays a fundamental role in maintaining membrane potential, cellular metabolism, enzyme activity, protein synthesis, acid–base homeostasis, and mitochondrial bioenergetics. Although hypokalemia is readily identified by decreased serum potassium concentration, serum potassium represents only a small fraction of total-body potassium stores and therefore may not accurately reflect intracellular potassium status. Consequently, chronic total-body potassium depletion and intracellular potassium deficiency may remain clinically unrecognized despite serum potassium concentrations within the reference range. Growing experimental and clinical evidence suggests that disturbances of potassium homeostasis are associated with multiple metabolic abnormalities involving the cardiovascular, neuromuscular, endocrine, renal, and gastrointestinal systems. Intracellular potassium depletion has been associated with mitochondrial dysfunction, oxidative stress, impaired insulin secretion and insulin sensitivity, metabolic alkalosis, chronic low-grade inflammation, and anabolic resistance. However, these relationships are complex and frequently bidirectional, indicating that potassium deficiency should be regarded as one component of an integrated metabolic network rather than an isolated pathogenic mechanism. This narrative review critically summarizes current evidence regarding the physiological regulation of potassium homeostasis, distinguishes hypokalemia from total-body potassium depletion and intracellular potassium deficiency, and discusses the mechanisms through which potassium depletion may contribute to systemic metabolic dysfunction. Particular attention is given to the clinical manifestations, diagnostic evaluation, and current therapeutic approaches to disorders of potassium homeostasis. Finally, important knowledge gaps are highlighted, including the need for reliable biomarkers of intracellular potassium deficiency and prospective studies evaluating whether correction of chronic potassium depletion improves long-term metabolic and clinical outcomes beyond normalization of serum potassium concentration. Full article

Background: Diclofenac is a widely consumed non-steroidal anti-inflammatory drug, yet its clinical utility is limited by severe hepatotoxicity, acute kidney injury, and gastric ulceration. While the RhoA/ROCK pathway is implicated in inflammation, its potential as a therapeutic target for multi-organ NSAID toxicity remains unexplored. Methods: This study evaluated the dose-dependent protective effects of the ROCK inhibitor, fasudil, against diclofenac-induced damage and investigated the underlying ROCK2/TLR4/SIRT1 axis. Five separate cohorts were established using thirty male Sprague-Dawley rats. Alongside a normal control and fasudil control group, one experimental group was treated with 100 mg/kg diclofenac. Furthermore, two distinct groups were pretreated with fasudil for seven days before induction, receiving either a 10 mg/kg or a 30 mg/kg dose prior to diclofenac administration. Results: Diclofenac provoked severe hepatic, renal, and gastric injury accompanied by marked oxidative stress. Pretreatment with fasudil markedly reversed these effects and improved hepatic and renal function biomarkers. Mechanistically, fasudil reduced renal and hepatic ROCK2 and TLR4 expression, which consequently suppressed downstream systemic inflammatory markers, including NF-κB and TNF-α. Furthermore, fasudil halted apoptosis by restoring SIRT1 expression and reducing cleaved caspase-3, alongside preserving gastric barrier integrity. Conclusions: Fasudil dose-dependently ameliorates diclofenac-induced hepatic, renal, and gastric injury by silencing the ROCK2/TLR4 inflammatory axis, restoring SIRT1 survival networks, and protecting epithelial tight junctions. Full article

Background/Objectives: Endometriosis is a chronic estrogen-dependent disease with a complex and incompletely understood etiology. Environmental exposure to toxic elements, including cadmium, lead, mercury, and arsenic, may contribute to its development and progression. Proposed mechanisms include endocrine disruption, oxidative stress, chronic inflammation, and epigenetic alterations. Methods: This narrative review was based on a structured literature search of the PubMed, Scopus, and Web of Science databases for studies published up to 15 June 2026. The search included the following keywords: endometriosis, cadmium, lead, mercury, arsenic, toxic elements, heavy metals, environmental exposure, diet, nutrition, and biomonitoring. Results: This review summarizes current evidence on the relationship between toxic element exposure and endometriosis, including sources of exposure, biomonitoring findings, proposed biological mechanisms, and human studies. The influence of nutritional status on metal bioavailability is also considered. Among the toxic elements reviewed, cadmium has been studied most extensively and shows the most consistent association with endometriosis. Evidence for lead is less consistent, whereas data on mercury and arsenic remain limited. Although the available epidemiological evidence does not establish a causal relationship, biomonitoring and experimental studies support a possible role of toxic elements in the development and progression of endometriosis. Conclusions: Current evidence supports a possible role of toxic elements in endometriosis, although a causal relationship has not been established. Cadmium has been investigated most extensively, while evidence for other toxic elements remains limited. Nutritional status should be considered when evaluating biomonitoring findings, particularly in relation to cadmium exposure. Full article

Excessive cyanobacterial proliferation and toxin production increasingly threaten freshwater ecosystems, drinking water systems, and public health. Among cyanotoxins, microcystin-LR (MC-LR) is one of the most prevalent variants and is recognized for its hepatotoxicity, with evidence showing it can also alter gut microbiota composition. Previous studies, including our own, demonstrate that MC exposure can induce inflammation, oxidative stress, and changes in gene expression associated with immune responses, even at concentrations below guideline limits. This study investigated the protective effect of an MC-degrading bacterium, Sphingopyxis sp. IM1 (IM1) with a known enzymatic MC degradation pathway, against MC-LR-induced hepatotoxicity under in vitro conditions. Human Hep3B hepatocytes were pretreated with varying ratios of IM1 bacteria and subsequently exposed to 9.95 ppm of MC-LR for 24 h. RT-qPCR analysis demonstrated that MC-LR exposure strongly increased the expression of the inflammatory markers TNFα and TGF-β1, whereas pretreatment with IM1 significantly attenuated these responses. Mass spectrometric analysis of cell pellets and spent culture media demonstrated reduced concentrations of intact MC-LR in IM1-pretreated samples compared to MC-LR-only controls, accompanied by increased detection of tetrapeptide degradation products generated during mlr-mediated MC degradation. These results demonstrate that IM1-mediated degradation of MC-LR attenuates toxin-induced hepatotoxic and inflammatory responses, highlighting the potential of a novel microbial-based therapeutic approach to mitigate MC-induced toxicity. Full article