Search Results (5,710)

Metabolic and cardiometabolic diseases are closely associated with mitochondrial dysfunction and redox imbalance. Ubiquinol–cytochrome c reductase core protein 2 (UQCRC2), a non-catalytic structural core subunit of mitochondrial respiratory chain Complex III, is increasingly recognized as a regulator of Complex III integrity, electron transfer, oxidative phosphorylation, and mitochondrial redox homeostasis. Under metabolic stress, reduced expression or functional impairment of UQCRC2 may promote electron leakage, mitochondrial reactive oxygen species (mtROS) generation, lipid peroxidation, impaired antioxidant defense, and disrupted glucose–lipid metabolism. These alterations may contribute to insulin resistance (IR), metabolic dysfunction-associated steatotic liver disease (MASLD), obesity, and cardiovascular disease (CVD). This review summarizes current evidence linking UQCRC2 dysfunction to mitochondrial bioenergetic failure, oxidative stress, inflammatory signaling, and cardiometabolic injury. We further discuss redox-regulatory pathways, including Nrf2, AMPK–SIRT1–PGC-1α, glutathione metabolism, and mitophagy, as well as pharmacological agents and natural compounds that may modulate UQCRC2-related mitochondrial responses. Collectively, these findings highlight UQCRC2 as a redox-sensitive mitochondrial node linking Complex III dysfunction to cardiometabolic injury and targeted redox-based interventions. Full article

Oxidative stress is a primary driver of sperm deterioration during chilled storage of poultry semen, and identifying effective natural antioxidant supplements for semen extenders is an important practical goal for poultry reproductive management. This study evaluated the protective effects of ginseng extract (Panax ginseng) supplementation on sperm viability, motility, oxidative stress biomarkers, antioxidant defense, and fertility in chilled Leung Hang Kao rooster semen. Pooled semen was diluted in IGGKPh extender supplemented with ginseng extract at 0, 1, 2, 3, or 4 mg/mL and stored at 5 °C for 0, 24, and 48 h. Sperm viability, total motility, progressive motility, malondialdehyde (MDA) concentration, total antioxidant capacity (T-AOC), glutathione peroxidase (GPx) activity, catalase (CAT) activity, and fertility following artificial insemination were evaluated at each time point. All ginseng-supplemented groups showed significantly lower MDA concentrations and higher GPx activity than the unsupplemented control throughout storage. At 48 h, total motility and progressive motility were highest in the 2 and 3 mg/mL groups, while T-AOC was best maintained in the 1 and 2 mg/mL groups. CAT activity did not differ significantly among groups at 48 h (p = 0.2498). Fertility was significantly higher in the 1 and 2 mg/mL groups than in the control after 24 and 48 h of storage, and the alignment between T-AOC and fertility across storage time points indicated that overall antioxidant buffering capacity was a stronger determinant of fertilizing competence than individual enzyme activities or MDA concentration alone. Concentrations of 3–4 mg/mL, despite producing lower MDA at 48 h, did not confer superior fertility outcomes, suggesting a hormetic dose–response relationship. Based on integrated evidence from sperm quality, antioxidant status, and in vivo fertility, ginseng extract supplementation at 1–2 mg/mL is recommended as the most suitable range for preserving chilled Leung Hang Kao rooster semen and may represent a practical natural antioxidant strategy for Thai native poultry breeding programs. Full article

Silage maize (Zea mays L.) serves as a key source of high-quality roughage for ruminants, yet its production and the development of the silage maize industry in Xinjiang are severely constrained by saline–alkali stress. In this study, root growth phenotypes, root energy metabolism, cell membrane stability, osmotic regulatory substances, and reactive oxygen species (ROS) metabolism were examined to elucidate the mechanisms by which iron chlorin e6 (ICe6) enhances saline–alkali tolerance in maize roots. The results showed that saline–alkali stress significantly suppressed root growth in maize seedlings, leading to increased malondialdehyde (MDA) content and relative conductivity. This suggests that membrane lipid peroxidation has intensified, resulting in increased cell membrane permeability. Meanwhile, ICe6 enhanced antioxidant enzyme (SOD, POD, CAT, and APX) activities, scavenged H₂O₂ accumulation, reduced MDA content, and stabilized cell membrane integrity, as indicated by reduced ion leakage. Moreover, ICe6 optimized root respiratory pathways, improved root vigor, and ATP synthesis to provide adequate energy for growth, while decreasing free proline accumulation to maintain cellular osmotic balance. These findings demonstrate that ICe6 mitigates saline–alkali stress in silage maize roots through coordinated regulation of energy metabolism, antioxidant defense, and osmotic adjustment. Full article

The safety profile for bio-derived phenols post-oxidation and their related antioxidant/redox potential remain largely under-explored. Oxidation by fungi, in terms of environmental impacts via fungal oxidation by enzymes, remains an attractive strategy under milder conditions, since it is one route by which many naturally occurring lignocellulosic phenols are modified; thus, an immediate need still exists for characterizing the effects that these modified phenolic compounds may have. Methodology: We examined four different biomass-derived phenolics—vanillin, ferulic acid, syringaldehyde and guaiacol—that were oxidized with fungal laccase and characterized their effects on normal human lung fibroblasts and levels of cellular oxidative stress. Laccase activity was evaluated via the ABTS method and through simple observation and UV-Vis spectroscopic scanning of the phenolics in question, and compared with the untreated version of each phenolic. In addition to assessing the cytotoxic effect and oxidative stress generated by the phenols alone, an ELISA-based measurement assay was used to investigate the relative abundance of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and reduced glutathione (GSH) in the human normal lung fibroblast cell line under varying treatment regimes, complemented by phase-contrast microscopy. Scores integrating the biomarkers were analyzed via clustering, PCA, radar and Pearson correlation analyses, to discern distinct trends in antioxidant potential after laccase conversion. Observations: Each of the four tested phenolics demonstrated the presence of laccase activity, leading to substantial differences in visible appearance compared with the control and characteristic absorbance shifts at differing wavelengths from the original molecule. Cell viability dropped dramatically as phenol concentration was increased and the untreated phenolics resulted in diminished confluence and induced greater levels of oxidative damage, from guaiacol and syringaldehyde. Laccase treatment resulted in higher MTT reduction activity and improved cellular morphology compared with the corresponding untreated phenolic compounds. Untreated phenols induced the highest levels of MDA, while decreasing SOD, CAT, GPx and GSH levels. Post-oxidation with laccase, there were lower amounts of lipid peroxidation, along with improved levels of antioxidant activity compared with the control phenol. Multi-technique analyses show clear distinctness between the untreated and laccase-converted phenolic groups. Clustering with multivariate techniques separated all cell groups in line with control samples, grouping the laccase-converted treatments towards the middle and displaying an inverse relationship between MDA and the antioxidant markers. Conclusions: Laccase conversion markedly decreases the adverse effects that bio-derived phenols have on normal cell viability and induces fewer detrimental effects on the cellular redox balance. This is a critical discovery in terms of finding greener methods by which to upgrade bio-derived substances as we research these lignocellulosic phenols. By employing ELISA-based measurements along with multiple analysis techniques, we present a suitable paradigm for studying biological effects in all bio-based goods intended for pharmaceuticals, packaging materials, nutraceuticals or a host of different applications. Full article

This research paper focused on the synthesis of 1-[2-hydroxy-3-(phenylcarbamoyloxy)propyl]-4-(R¹, R²-substituted phenyl)piperazin-1-ium chlorides (I)–(III), containing R¹, R² = H, Cl and/or OCH₃, and the evaluation of some of their physicochemical parameters. The in vitro biological investigation of these N-arylpiperazine (NAP) derivatives consisted in assessing their impact on purinergic P2X7-associated signaling, that is, the evaluation of antioxidant, anti-inflammatory and immunomodulatory characteristics. The ultraviolet type C (UVC) irradiation (λ = 254 nm, 0.954 kJ/m²) induced a pronounced stress response in human leukocytes without marked cytotoxicity while maintaining high cell viability (≥90%), as evidenced by increased interleukin (IL)-1β production (94%), elevated IL-1β mRNA expression, enhanced lipid peroxidation (66%), and increased intracellular adenosine 5′-triphosphate (ATP; 97%), respectively. Under basal conditions, these lipophilic NAPs, defined with logarithmic values of retention (capacity) factors corresponding to 100% water in isocratic elution RP-HPLC, i.e., k_w descriptors (varying from 2.3829 to 4.3689), and isocratic chromatographic hydrophobicity index (φ₀) parameters (ranging from 0.7578 to 0.8842), reduced IL-1β production (by 26–63%) and enhanced superoxide dismutase (SOD) activity (up to 64%) without inducing oxidative damage. Under UVC-induced stress, all evaluated compounds decreased lipid peroxidation (up to 45%) and significantly increased antioxidant enzyme activities, including SOD (up to 223%) as well as catalase (up to 145%). The observed effects were associated with changes in intracellular ATP levels and redox-related parameters. In the experiments described in this paper, intracellular ATP was measured so that no direct conclusions could be drawn regarding the extracellular ATP-dependent activation of purinergic receptors, including P2X7. Overall, the results demonstrated that variations within the structure of these NAPs significantly affected compounds’ biological activity, highlighting their potential for further optimization as cytoprotective and anti-inflammatory agents. Full article

Background/Objectives: Melatonin is a multifunctional indoleamine with recognized antitumor activity; however, its subtype-specific effects in breast cancer remain incompletely understood. This study aimed to investigate the impact of melatonin on cellular and metabolic processes associated with tumor progression in two human breast cancer cell lines representing distinct molecular subtypes: MCF-7 (luminal A) and MDA-MB-468 (triple-negative). Methods: Breast cancer cells were treated with micromolar concentrations of melatonin, and assays were performed to evaluate cell viability, migration, invasion, mitochondrial status, redox balance, protein expression, and biogenic amine profiles. Results: Melatonin significantly reduced cell viability, migration, and invasion in both cell lines, with more pronounced effects in MCF-7 cells. At the molecular level, melatonin downregulated key metabolic and hypoxia-related proteins, including GAPDH and HIF-1α, while citrate synthase was selectively reduced in MCF-7 cells, indicating suppression of mitochondrial metabolic capacity. This was accompanied by a reduction in mitochondrial status, reflected by decreased MitoGreen staining. Melatonin also induced redox imbalance, as evidenced by increased lipid peroxidation and protein carbonylation, along with subtype-dependent modulation of antioxidant enzymes. In addition, alterations in biogenic amine profiles were observed, suggesting broader metabolic remodeling. Conclusions: Collectively, these findings demonstrate that melatonin exerts subtype-dependent antitumor effects by targeting metabolic, mitochondrial, and redox pathways, supporting further investigation of melatonin as a potential therapeutic adjuvant in breast cancer, while recognizing that the concentrations used in this study exceed physiological circulating levels. 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

Fatty acid-binding protein 7 (FABP7) is a multifunctional lipid chaperone that is enriched in radial glia and astrocytes within the central nervous system (CNS) and is frequently upregulated in glioma. Beyond its established roles in glial development, lipid homeostasis, and circadian regulation, growing evidence positions FABP7 at the intersection of tumor metabolism, neuronal activity, and immune modulation in the brain. In this review, we integrate the physiological functions of FABP7 in glial cells with its tumor-intrinsic and microenvironmental roles in glioma. We summarize how gliomas co-opt FABP7-dependent metabolic, transcriptional, and post-transcriptional programs to promote stemness, lipid remodeling (e.g., altered fatty acid composition, lipid droplet formation, and lipid peroxidation resistance), inflammatory signaling, and invasive growth, including nuclear FABP7-mediated transcriptional activation linked to oncogene status. Furthermore, we discuss the role of FABP7 in shaping the tumor–neuro–immune interface, including regulating immunosuppressive gene networks, pro-tumoral macrophage polarization, resistance to T-cell-induced ferroptosis and immunotherapy, and tumor microtube-mediated integration into neuronal circuits to support glioma progression. Finally, we highlight therapeutic opportunities and challenges, including small-molecule FABP7 inhibitors, brain-directed delivery strategies, chronotherapeutic considerations, and combination approaches with immunotherapy. Collectively, this work positions FABP7-centered metabolic, circadian, and neuro-immune networks as potential vulnerabilities in glioma, linking fundamental glial biology to glioma therapeutics. Full article

Chronic coronary syndromes (CCSs) are increasingly recognized as complex immunometabolic vascular disorders in which coronary microvascular dysfunction (CMD), persistent low-grade inflammation, oxidative stress, and maladaptive cellular remodeling contribute to ischemic symptoms and adverse outcomes beyond epicardial stenosis. CMD represents a heterogeneous condition comprising both functional and structural endotypes and constitutes a major determinant of myocardial ischemia, heart failure progression, and adverse cardiovascular outcomes, even in the absence of obstructive coronary artery disease. Emerging evidence indicates that immunometabolic reprogramming of endothelial cells, vascular smooth muscle cells, and immune cells sustains microvascular dysfunction in CCSs. Metabolic shifts toward glycolysis, mitochondrial dysfunction, redox imbalance, and dysregulated lipid metabolism promote chronic inflammatory activation within the coronary microenvironment. Convergent mitochondrial stress (including NAD⁺ decline) and redox injury promote endothelial senescence and increase susceptibility to regulated cell death, progressively limiting vasodilatory reserve and predisposing to microvascular rarefaction. Pyroptosis and ferroptosis-like lipid peroxidation further exacerbate endothelial barrier disruption and inflammatory amplification. In parallel, inflammasome activation, iron-dependent lipid peroxidation, impaired autophagy, and endoplasmic reticulum stress form interconnected molecular networks that amplify vascular injury through self-reinforcing mechanisms. This narrative review integrates mechanistic and translational evidence linking immunometabolic dysregulation, mitochondrial stress, thromboinflammatory signaling, endothelial senescence, and regulated cell death to distinct CMD endotypes. We propose a systems-level framework in which coronary microvascular dysfunction is conceptualized as an immunometabolic vascular network disorder, with reduced coronary flow reserve (CFR)—often termed myocardial flow reserve (MFR) in PET studies—emerging as the integrative functional endpoint of these interacting molecular perturbations and a robust predictor of major cardiovascular events. Full article

Background: Glioblastoma (GBM) is the most aggressive primary brain tumor in adults and remains associated with poor prognosis despite multimodal treatment. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation and redox imbalance, has recently emerged as a potential therapeutic vulnerability in glioma. This review summarizes current knowledge on the molecular regulation of ferroptosis in glioma and discusses its implications for tumor progression, therapeutic resistance, and translational targeting. Methods: A structured narrative review of the literature was conducted using PubMed/MEDLINE, Scopus, and Web of Science databases. Experimental, translational, and clinically relevant studies investigating ferroptosis-related mechanisms and therapeutic strategies in glioma and GBM were qualitatively analyzed. Results: Ferroptosis in glioma is regulated by interconnected pathways involving iron metabolism, phospholipid remodeling, oxidative stress, and antioxidant defense systems, particularly the SLC7A11–glutathione–GPX4 axis. Additional protective mechanisms mediated by FSP1 and DHODH, together with regulatory networks involving NRF2, ATF4, p53, and hypoxia-related signaling, contribute to adaptive resistance to ferroptosis. Increasing evidence indicates that ferroptosis interacts bidirectionally with the glioma tumor microenvironment and may exert both antitumor and immunosuppressive effects. Preclinical studies further suggest that ferroptosis induction may enhance the efficacy of temozolomide, radiotherapy, and immunotherapy, although clinical translation remains limited by tumor heterogeneity, blood–brain barrier penetration, and resistance mechanisms. Conclusions: Ferroptosis represents a biologically plausible and therapeutically promising target in glioma. Improved understanding of ferroptosis regulation, tumor microenvironment interactions, and biomarker-guided therapeutic strategies may support the future development of more effective treatments for GBM. Full article

Iron overload disrupts cellular homeostasis and drives ferroptosis through dysregulated iron metabolism. Non-coding RNAs (ncRNAs) are considered as key regulators of various biological functions and targets for a new generation of RNA therapeutics and biomarkers. However, few studies have investigated the regulatory roles of ncRNAs, particularly competitive endogenous RNAs (ceRNAs) in iron overload. This study performed whole-transcriptome sequencing to characterize the ceRNA network in ferric ammonium citrate (FAC)-induced iron-overloaded HT-1080 fibrosarcoma cells. A total of 208 differentially expressed mRNAs, 83 lncRNAs, and 170 circRNAs (q < 0.05) were identified, with hierarchical clustering revealing distinct expression patterns between control and iron-treated groups. KEGG enrichment implicated vitamin B6 metabolism (q < 0.001) and lysine degradation (q < 0.001) as key disrupted pathways. ceRNA network was conducted and further demonstrated lncRNA/circRNA-mediated regulation of ferroptosis genes via shared miRNA response elements. Notably, LINC-PINT-232 was implicated in the regulation of both ferritin heavy chain (FTH) and sequestosome 1 (SQSTM1), two ferroptosis-associated mRNAs. FTH upregulation mitigates iron toxicity through ferroxidase activity, while SQSTM1 modulates lipid peroxidation in ferroptosis. These findings provide a preliminary transcriptomic landscape for hypothesis generation regarding ncRNA-mediated regulatory mechanisms in iron overload-induced ferroptosis and offer a computational foundation for future functional and therapeutic investigations. Full article

Cytokinins are key regulators of plant root development, but their dose-dependent effects on rice seedling roots and their physiological association with ethylene-related responses remain incompletely understood. In this study, rice seedlings were exposed to two exogenous cytokinins, 6-benzyladenine (6-BA) and kinetin (KT), at different concentrations for 3 and 6 d, and Ag⁺ was used as an inhibitor of ethylene action to evaluate its alleviating effect. Both 6-BA and KT significantly inhibited primary root elongation in a concentration- and time-dependent manner. At high cytokinin concentrations, primary root length was reduced by more than 60% relative to the control, accompanied by reductions in total root length, lateral root number, absorptive area, and root vigor, as well as increased MDA and ethylene levels. Ag⁺ partially alleviated cytokinin-induced primary root inhibition, with the strongest rescue effect observed near 0.08 μM. The recovery effect was particularly evident under moderate and high cytokinin concentrations. Correlation and principal component analyses further indicated that root morphological traits were negatively associated with MDA and ethylene but positively associated with root vigor. These results suggest that exogenous cytokinins restrict rice seedling root growth through a coordinated physiological response associated with ethylene accumulation and increased membrane lipid peroxidation, while Ag⁺ partially relieves this inhibition in association with mitigation of ethylene-related restriction. Because the study was based on short-term exogenous treatments and pharmacological inhibition, the findings should be interpreted as physiological evidence for ethylene-related involvement rather than direct proof of a complete signaling mechanism. Full article

Background/Objectives: Anemia and iron dysregulation are common in chronic heart failure (CHF), but additional metabolic mechanisms may contribute to these alterations. This study aimed to evaluate purine metabolism and oxidative stress markers in patients with CHF and to explore their potential relationship with anemia. Methods: In this cross-sectional study, 176 patients with CHF and 29 control individuals were included. CHF phenotypes were classified according to left ventricular ejection fraction (HFpEF, HFmrEF, HFrEF). Purine metabolites (guanine, hypoxanthine, adenine, xanthine, and uric acid) were measured using high-performance liquid chromatography, while lipid peroxidation (LPO) and advanced oxidation protein products (AOPPs) were assessed spectrophotometrically. Non-parametric statistical tests with correction for multiple comparisons were applied. Results: Anemia was present in 40.3% of patients with CHF. Serum iron and platelet counts were significantly lower in CHF compared with controls (p = 0.001). Among purine metabolites, adenine levels were higher in CHF (nominal p = 0.009), whereas other metabolites did not differ significantly between groups. LPO levels were lower and AOPP levels were higher in CHF (p = 0.021 and p = 0.008, respectively). No statistically significant associations were observed between hemoglobin levels and purine metabolites. Conclusions: CHF is associated with alterations in iron status and oxidative stress markers, as well as changes in purine metabolism. However, no significant associations between purine metabolites and anemia were identified in this cohort, and these findings should be interpreted cautiously given the exploratory design and sample size limitations. Full article

Prostate cancer remains a major therapeutic challenge, particularly after progression to castration-resistant disease, where persistent androgen receptor signaling, metabolic adaptation, immune escape, and treatment resistance jointly limit clinical benefit. Regulated cell death (RCD) is increasingly recognized not only as an endpoint of tumor cell elimination but also as a dynamic regulator of prostate cancer progression, therapeutic vulnerability, and tumor–immune interactions. In this review, we propose an immunometabolic framework in which androgen receptor signaling, lipid and redox metabolic reprogramming, oxidative stress, and therapeutic pressure converge to shape the susceptibility of prostate cancer cells to distinct RCD modalities. We focus on autophagy and ferroptosis as two extensively studied and translationally relevant pathways, while also discussing emerging roles of necroptosis, pyroptosis, and cuproptosis. Particular attention is given to how RCD-associated signals, including damage-associated molecular patterns, inflammatory mediators, and lipid peroxidation products, may remodel the tumor immune microenvironment and influence the transition between immune-cold and immune-inflamed phenotypes. We further summarize RCD-targeted therapeutic strategies, including ferroptosis induction, autophagy inhibition, nanodrug delivery systems, rational combination therapy, and biomarker-guided patient stratification. Finally, we discuss key translational barriers, including context-dependent biological effects, limited clinical validation, tumor heterogeneity, adaptive resistance, and insufficient predictive biomarkers. By integrating cell death biology with metabolic reprogramming, immune remodeling, and therapeutic resistance, this review highlights RCD as a promising but context-dependent therapeutic vulnerability in advanced prostate cancer. Full article

This study evaluated the effects of monolaurin intake per finishing feedlot cattle on growth performance, metabolic status, ruminal environment, and meat fatty acid profile. Twenty-four castrated Holstein males (379 ± 8.5 kg; 12 months old) were randomly assigned to two treatments: basal diet (control) or basal diet with α-monolaurin (treated: 0.762 g/kg dry matter intake; ≈6.63 g/animal/day) for 79 days. Feed intake, body weight, and feed efficiency were recorded, and blood and ruminal samples were collected during the trial. Ruminal fermentation parameters, protozoa counts, hematological and biochemical variables, oxidative status biomarkers, ruminal microbiota composition (16S rRNA sequencing), and Longissimus dorsi fatty acid profile were analyzed. Monolaurin feed did not affect dry matter intake or final body weight, but increased total weight gain, average daily gain, and feed efficiency (p ≤ 0.05), indicating improved nutrient utilization. Hematological and serum biochemical variables were largely unchanged, although total leukocyte counts were lower in treated cattle. Animals receiving monolaurin showed reduced reactive oxygen species and lower superoxide dismutase activity, suggesting improved oxidative balance without changes in lipid peroxidation. During the adaptation phase (day 14), treated cattle exhibited lower acetate, propionate, valerate, and total volatile fatty acid concentrations and higher protozoa counts, but these differences disappeared by day 79, indicating ruminal adaptation. Microbiota diversity was not altered overall, although specific genera differed in relative abundance between treatments. In meat, monolaurin increased lauric, linoleic, and arachidonic acids, reduced palmitic and heptadecanoic acids, decreased total saturated fatty acids, and increased polyunsaturated fatty acids (p ≤ 0.05). Overall, dietary monolaurin improved feed efficiency, modulated oxidative status, induced transient ruminal microbial adjustments, and enhanced the nutritional quality of beef lipids without compromising metabolic health. Full article