Search Results (1,242)

Oxidative stress significantly contributes to the exacerbation of brain damage during cerebral ischemia-reperfusion injury (CIR/I). In our previous study, purified cornel iridoid glycoside (PCIG), consisting of morroniside (MOR) and loganin (LOG), showed neuroprotective effects against CIR/I. To further explore the antioxidative effects and underlying molecular mechanisms, we applied PCIG, MOR, and LOG to rats injured by middle cerebral artery occlusion/reperfusion (MCAO/R) as well as H₂O₂-stimulated PC12 cells. Additionally, the molecular docking analysis was performed to assess the interaction between the PCIG constituents and Kelch-like ECH-associated protein 1 (Keap1). The results showed that the treated rats experienced fewer neurological deficits, reduced lesion volumes, and lower cell death accompanied by decreased levels of malondialdehyde (MDA) and protein carbonyl, as well as increased activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). In H₂O₂-stimulated PC12 cells, the treatments decreased reactive oxygen species (ROS) production, mitigated mitochondrial dysfunction, and inhibited mitochondrial-dependent apoptosis. Moreover, the treatments facilitated Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) translocation into the nucleus and selectively increased the expression of NAD(P)H quinone oxidoreductase 1 (NQO-1) and heme oxygenase 1 (HO-1) through MOR and LOG, respectively. Both MOR and LOG demonstrated strong binding affinity to Keap1. These findings suggested that PCIG, rather than any individual components, might serve as a valuable treatment for ischemic stroke by activating the Nrf2/NQO-1 and Nrf2/HO-1 signaling pathway. Full article

Background/Objectives: Metabolic syndrome (MetS) is a multifactorial condition characterized by abdominal obesity, dyslipidemia, insulin resistance, hypertension, and chronic inflammation. As its global prevalence rises, there is increasing interest in natural, multi-targeted approaches to manage MetS. Curcuma longa Linn. (turmeric), especially its active compound curcumin, has shown therapeutic promise in preclinical studies. This systematic review and meta-analysis evaluated the effects of Curcuma longa and its derivatives on MetS-related outcomes in rodent models. Methods: A comprehensive search was conducted across six databases (PubMed, Scopus, AMED, LILACS, MDPI, and Google Scholar), yielding 47 eligible in vivo studies. Data were extracted on key metabolic, inflammatory, and oxidative stress markers and analyzed using random-effects models. Results were presented as mean differences (MD) with 95% confidence intervals (CI). Results: Meta-analysis showed that curcumin significantly reduced body weight (rats: MD = −42.10; mice: MD = −2.91), blood glucose (rats: MD = −55.59; mice: MD = −28.69), triglycerides (rats: MD = −70.17; mice: MD = −24.57), total cholesterol (rats: MD = −35.77; mice: MD = −52.61), and LDL cholesterol (rats: MD = −69.34; mice: MD = −42.93). HDL cholesterol increased significantly in rats but not in mice. Inflammatory cytokines were markedly reduced, while oxidative stress improved via decreased malondialdehyde (MDA) and elevated superoxide dismutase (SOD) and catalase (CAT) levels. Heterogeneity was moderate to high, primarily due to variations in curcumin dosage (ranging from 10 to 500 mg/kg) and treatment duration (2 to 16 weeks) across studies. Conclusions: This preclinical evidence supports Curcuma longa as a promising functional food component for preventing and managing MetS. Its multi-faceted effects warrant further clinical studies to validate its translational potential. Full article

This study investigated the effects of reducing organic trace minerals below commercial inclusion levels and compared them with both low-dose and commercial levels of inorganic trace minerals, focusing on growth performance, carcass traits, tibia characteristics, oxidative stress (superoxide dismutase [SOD] and malondialdehyde [MDA]), and immune response (serum IgG) in broilers. A total of 384 one-day-old Ross 308 chicks were randomly assigned to three dietary treatments: (1) commercial-level inorganic trace minerals (ILI; Zn 100 ppm; Cu 15 ppm; Fe 100 ppm; Mn 80 ppm; Se 0.2 ppm; I 3 ppm); (2) low-level organic trace minerals (LLO; Zn 30 ppm; Cu 4 ppm; Fe 11 ppm; Mn 30 ppm; Se 0.225 ppm; I 3 ppm), and (3) low-level inorganic trace minerals (LLI; Zn 30 ppm; Cu 4 ppm; Fe 11 ppm; Mn 30 ppm; Se 0.2 ppm; I 3 ppm). Each treatment consisted of eight replicates with 16 birds per replicate, and diets were provided in two phases: starter (days 1–21) and grower (days 22–35). The results showed that the LLO group demonstrated a significantly improved feed conversion ratio (FCR) during the starter phase, 2.4% better than that of the ILI and LLI groups (p = 0.02). Additionally, filet and thigh muscle yields in the LLO group were higher by 11.9% (p = 0.03) and 13.9% (p = 0.02), respectively, compared to the ILI group. Other carcass traits, as well as pH and drip loss, were not significantly affected. However, tibia breaking strength at day 35 was 15.1% lower in the LLO group compared to the ILI group (p = 0.02). No significant differences were observed in oxidative stress markers or IgG levels among groups. This study demonstrated that reducing the inclusion level of inorganic trace minerals did not negatively affect broiler growth performance, whereas supplementation with low levels of organic trace minerals improved both growth performance and carcass quality. Full article

Browning significantly impacts the commercial value of luffa (luffa cylindrica) and is primarily driven by the metabolic processes of phenolic acids. Investigating changes in phenolic acids during browning aids in understanding the physiological mechanisms underlying this process and provides a basis for improving storage, processing, variety breeding, and utilization of germplasm resources. This study compared browning-resistant (‘30’) and browning-sensitive (‘256’) luffa varieties using high-throughput sequencing and metabolomics techniques. The results revealed 55 genes involved in the phenylpropanoid biosynthesis pathway, including 8 phenylalanine ammonia-lyase (PAL) genes, 20 peroxidase (POD) genes, 2 polyphenol oxidase (PPO) genes associated with tyrosine metabolism, and 37 peroxisome-related genes. Real-time quantitative (qPCR) was employed to validate 15 browning-related genes, revealing that the expression levels of LcPOD21 and LcPOD6 were 12.5-fold and 25-fold higher in ‘30’ compared to ‘256’, while LcPAL5 and LcPAL4 were upregulated in ‘30’. Enzyme analysis showed that catalase (CAT) and phenylalanine ammonia-lyase (PAL) activities were higher in ‘30’ than in ‘256’. Conversely, superoxide dismutase (SOD) and polyphenol oxidase (PPO) activities were reduced in ‘30’, whereas CAT activity was upregulated. The concentrations of cinnamic acid, p-coumaric acid, trans-5-O-(4-coumaroyl)mangiferic acid, and caffealdehyde were lower in browning-resistant luffa ‘30’ than in browning-sensitive luffa ‘256’, suggesting that their levels influence browning in luffa. These findings elucidate the mechanisms underlying browning and inform strategies for the storage, processing, and genetic improvement of luffa. Full article

Temperature fluctuations caused by climate change and global warming pose a threat to fish. The burbot (lota lota) population is particularly sensitive to increased water temperature, but the systematic impacts of high-temperature exposure on their liver and intestinal health remain unclear. In January of 2025, we collected wild adult burbot individuals from the Ussuri River (water temperature: about 2 °C), China. The burbot were exposed to 2 °C, 7 °C, 12 °C, 17 °C, and 22 °C environments for 96 h; then, the liver and intestinal contents were subsequently collected for histopathology observation, immunohistochemistry, biochemical index assessment, and transcriptome/16S rDNA sequencing analysis. There was obvious liver damage including hepatocyte necrosis, fat vacuoles, and cellular peripheral nuclei. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were elevated and subsequently decreased. Additionally, the malondialdehyde (MDA) level significantly increased with increasing temperature. These results indicate that 7 °C (heat stress temperature), 12 °C (tipping point for normal physiological metabolism status), 17 °C (tipping point for individual deaths), and 22 °C (thermal limit) are critical temperatures in terms of the physiological response of burbot during their breeding period. In the hepatic transcriptome profiling, 6538 differentially expressed genes (DEGs) were identified, while KEGG enrichment analysis showed that high-temperature stress could affect normal liver function by regulating energy metabolism, immune, and apoptosis-related pathways. Microbiomics also revealed that acute heat stress could change the intestinal microbe community structure. Additionally, correlation analysis suggested potential regulatory relationships between intestinal microbe taxa and immune/apoptosis-related DEGs in the liver. This study revealed the potential impact of environmental water temperature changes in cold habitats in winter on the physiological adaptability of burbot during the breeding period and provides new insights for the ecological protection of burbot in the context of global climate change and habitat warming. Full article

Quercetin is a biologically active flavonoid compound that exerts numerous beneficial effects in humans and animals, including anti-diabetic activity. Its action has been explored in rodent models of type 1 and type 2 diabetes. It was revealed that quercetin mitigated diabetes-related hormonal and metabolic disorders and reduced oxidative and inflammatory stress. Its anti-diabetic effects were associated with advantageous changes in the relevant enzymes and signaling molecules. Quercetin positively affected, among others, superoxide dismutase, catalase, glutathione peroxidase, glucose transporter-2, glucokinase, glucose-6-phosphatase, glycogen phosphorylase, glycogen synthase, glycogen synthase kinase-3β, phosphoenolpyruvate carboxykinase, silent information regulator-1, sterol regulatory element-binding protein-1, insulin receptor substrate 1, phosphoinositide 3-kinase, and protein kinase B. The available data support the conclusion that the action of quercetin was pleiotropic since it alleviates a wide range of diabetes-related disorders. Moreover, no side effects were observed during treatment with quercetin in rodents. Given that human diabetes affects a large part of the population worldwide, the results of animal studies encourage clinical trials to evaluate the potential of quercetin as an adjunct to pharmacological therapies. Full article

Background: Aicardi-Goutières Syndrome (AGS) is a rare neuroinflammatory condition characterized by early-onset symptoms that extend outside the nervous system. Due to the rarity of the disease, the pathogenesis is not well understood, and its diagnosis and treatment remain elusive. We recently demonstrated mitochondrial abnormalities and increased reactive oxygen species (ROS) levels in lymphoblastoid cell lines (LCLs) derived from RNASEH2B- and RNASEH2A-mutated AGS patients. On this background, we turned our attention to metformin, the first-choice drug for type 2 diabetes, as a possible treatment acting on oxidative stress in RNASEH2-mutant AGS cells. Methods and Results: By means of flow cytometry, we found that metformin treatment significantly decreases ROS production in RNASEH2B- and RNASEH2A-mutated AGS LCLs. Of note, metformin treatment reduces the green JC-1 monomeric signal and, concurrently, increases the red JC-1 signal in both mutated LCLs, accounting for restoration of the mitochondrial membrane potential. Immunofluorescence staining shows a decrease in 8-oxoG levels only in RNASEH2B- mutated AGS LCLs. Finally, the significant upregulation of Forkhead Box O3 (FOXO3), cytochrome C somatic (CYCS), and superoxide dismutase 2 (SOD2) mRNA levels in RNASEH2B-mutated AGS LCLs after metformin treatment points to FOXO3 signaling as a possible mechanism to reduce oxidative stress. Conclusions: In conclusion, even if these pilot results need to be confirmed on a larger cohort, we shed light on metformin treatment as a valid approach to ameliorate oxidative stress-related inflammation in AGS patients. Full article

Acute hepatopancreatic necrosis disease (AHPND), caused by the bacterium Vibrio parahaemolyticus, is a major threat to global shrimp aquaculture. In this study, we evaluated the therapeutic effects of phage therapy in Litopenaeus vannamei challenged with AHPND-causing Vibrio parahaemolyticus. Phage application at various concentrations significantly improved shrimp survival, with the 1 ppm group demonstrating the highest survival rate. Enzymatic assays revealed that phage-treated shrimp exhibited enhanced immune enzyme activities, including acid phosphatase (ACP), alkaline phosphatase (AKP), and lysozyme (LZM). In addition, antioxidant defenses such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX), and total antioxidant capacity (T-AOC) significantly improved, accompanied by reduced malondialdehyde (MDA) levels. Serum biochemical analyses demonstrated marked improvements in lipid metabolism, particularly reductions in triglyceride (TG), total cholesterol (TC), and low-density lipoprotein (LDL), alongside higher levels of beneficial high-density lipoprotein (HDL). Transcriptomic analysis identified 2274 differentially expressed genes (DEGs), notably enriched in pathways involving fatty acid metabolism, peroxisome functions, lysosomes, and Toll-like receptor (TLR) signaling. Specifically, phage treatment upregulated immune and metabolic regulatory genes, including Toll-like receptor 4 (TLR4), myeloid differentiation primary response protein 88 (MYD88), interleukin-1β (IL-1β), nuclear factor erythroid 2-related factor 2 (Nrf2), and peroxisome proliferator-activated receptor (PPAR), indicating activation of innate immunity and antioxidant defense pathways. These findings suggest that phage therapy induces protective immunometabolic adaptations beyond its direct antibacterial effects, thereby providing an ecologically sustainable alternative to antibiotics for managing bacterial diseases in shrimp aquaculture. Full article

Origanum majorana L. (O. majorana) (Lamiaceae) is an aromatic Mediterranean plant widely used in food, cosmetics, and traditional medicine due to its aroma and rich content of bioactive compounds. While its leaves and flowers are commonly utilized, lignified stems are often discarded. This study compared hydroalcoholic extracts from the leaves and flowers (valuable fraction, VF) and stems (by-product, BP). Phytochemical analysis revealed qualitatively similar profiles, identifying 20 phenolic compounds, with Rosmarinic acid and Salvianolic acid B as the most and second most abundant, respectively. Antioxidant activity was evaluated in vitro using DPPH (IC₅₀ [µg/mL]: VF 30.11 ± 3.46; BP 31.72 ± 1.46), H₂O₂ (IC₅₀ [µg/mL]: VF 103.09 ± 4.97; BP 119.55 ± 10.58), and O₂^•− (IC₅₀ [µg/mL]: VF 0.71 ± 0.062; BP 0.79 ± 0.070). Both extracts (20 µg/mL) fully restored oxidative balance in hemin-stressed AC16 cardiomyocytes, without altering the expression of catalase, heme-oxygenase 1, superoxide dismutase 2, or ferritin. Anti-inflammatory activity in LPS-stimulated RAW 264.7 macrophages showed that VF (IC₅₀ 400 µg/mL) reduced ^•NO release to control levels, while BP achieved a ~60% reduction. Cytotoxicity was assessed on cancer cell lines: CaCo-2 (IC₅₀ [µg/mL]: VF 154.1 ± 6.22; BP 305.2 ± 15.94), MCF-7 (IC₅₀ [µg/mL]: VF 624.6 ± 10.27; BP 917.9 ± 9.87), and A549 (IC₅₀ [µg/mL]: VF 720.8 ± 13.66; BP 920.2 ± 16.79), with no cytotoxicity on normal fibroblasts HFF-1 (IC₅₀ > 1000 µg/mL for both extracts). Finally, both extracts slightly inhibited only CYP1A2 (IC₅₀ [µg/mL]: VF 497.45 ± 9.64; BP 719.72 ± 11.37) and CYP2D6 (IC₅₀ [µg/mL]: VF 637.15 ± 14.78, BP 588.70 ± 11.01). These results support the potential reuse of O. majorana stems as a sustainable source of bioactive compounds for nutraceutical and health-related applications. Full article

Oxidative stress is a key mediator of physiological dysfunction in aquatic organisms under environmental challenges, yet its comprehensive impacts on gill physiology require further clarification. This study investigated the molecular and cellular responses of Eriocheir sinensis gills to hydrogen peroxide (H₂O₂)-induced oxidative stress, integrating antioxidant defense, ion transport regulation, and stress-induced cell apoptosis and autophagy. Morphological alterations in the gill filaments were observed, characterized by septum degeneration, accumulation of haemolymph cells, and pronounced swelling. For antioxidant enzymes like catalase (CAT) and glutathione peroxidase (GPx), activities were enhanced, while superoxide dismutase (SOD) activity was reduced following 48 h of exposure. Overall, the total antioxidant capacity (T-AOC) showed a significant increase. The elevated concentrations of malondialdehyde (MDA) and H₂O₂ indicated oxidative stress. Ion transport genes displayed distinct transcription patterns: Na⁺-K⁺-2Cl⁻ co-transporter-1 (NKCC1), Na⁺/H⁺ exchanger 3 (NHE3), aquaporin 7 (AQP7), and chloride channel protein 2 (CLC2) were significantly upregulated; the α-subunit of Na⁺/K⁺-ATPase (NKAα) and carbonic anhydrase (CA) displayed an initial increase followed by decline; whereas vacuolar-type ATPase (VATP) consistently decreased, suggesting compensatory mechanisms to maintain osmotic balance. Concurrently, H₂O₂ triggered apoptosis (Bcl2, Caspase-3/8) and autophagy (beclin-1, ATG7), likely mediated by MAPK and AMPK signaling pathways. These findings reveal a coordinated yet adaptive response of crab gills to oxidative stress, providing new insights into the mechanistic basis of environmental stress tolerance in crustaceans. Full article

This study aimed to investigate the effects of dietary supplementation with different levels of ursolic acid (UA) on the growth performance, immune function, intestinal antioxidant capacity, and anti-inflammatory responses of weaned rabbits. A total of 160 Hyla meat rabbits aged 35 days were randomly assigned to four groups. Each treatment group consisted of 8 replicates, with 5 rabbits per replicate. The rabbits were fed a basal diet (control group, CON) or experimental diets supplemented with 50, 100, or 200 mg/kg UA for 28 days. Dietary supplementation with 50 mg/kg UA significantly increased (p < 0.05) the average daily gain and average daily feed intake. The villus height, crypt depth, and villus height to crypt depth ratio exhibited quadratic responses (p < 0.05) to increasing dietary UA levels, with rabbits fed 50 mg/kg UA showing optimal ileal morphology. Compared with the CON group, dietary supplementation with 50 mg/kg UA significantly enhanced (p < 0.05) cecal catalase activity, secretory immunoglobulin A, and interleukin-10 (IL-10) levels, while the addition of 200 mg/kg UA increased (p < 0.05) serum catalase activity. The concentrations of serum tumor necrosis factor-α (TNF-α) and cecal IL-10 responded quadratically (p < 0.01 and p = 0.01, respectively) as the dietary UA level increased. With increasing UA supplementation, cecal Kelch-like ECH-associated protein 1 and IL-10 mRNA expression showed linear upregulation (p < 0.05), whereas nuclear factor erythroid 2-related factor 2 (Nrf2), superoxide dismutase 1 (SOD1), quinone oxidoreductase 1 (NQO1), TNF-α, interleukin-6, and interleukin-8 displayed quadratic responses (p < 0.05). Dietary UA at 50 mg/kg significantly downregulated cecal TNF-α and interleukin-1β mRNA expression while upregulating Nrf2, NQO1, and SOD1 mRNA levels (p < 0.05). In conclusion, dietary supplementation with 50 mg/kg UA significantly improved the growth performance of weaned rabbits by improving intestinal morphology, immune function, and antioxidant and anti-inflammatory capacities, demonstrating its efficacy as a natural phytogenic feed additive. Full article

This study was conducted through in vivo and in vitro experiments and aimed to reveal the regulatory effect of water extract of Artemisia annua L. (WEAA) on the antioxidant function of mutton sheep and the underlying mechanism. In the in vivo experiment, 32 Dorper × Han female sheep (3 months old; avg. body weight: 24 ± 0.09 kg) were allocated to four groups (eight lambs/group) and fed a diet containing 0, 500, 1000, and 1500 mg/kg WEAA, respectively. In the in vitro experiments, peripheral blood lymphocytes (PBLs) were cultured with different doses of WEAA (0, 25, 50, 100, 200, 400 µg/mL) to determine the optimal concentration, followed by a 2 × 2 factorial experiment with four treatment groups (six replicates per treatment group): the ML385(−)/WEAA(−) group, the ML385(−)/WEAA(+) group, the ML385(+)/WEAA(−) group, and the ML385(+)/WEAA(+) group. The results showed that WEAA supplementation dose-dependently increased serum, liver and spleen tissue total antioxidant capacity, glutathione peroxidase (GSH-Px), and catalase (CAT) activity while reducing malondialdehyde level (p < 0.05). Moreover, WEAA supplementation significantly upregulated the liver and spleen expression of nuclear factor erythroid 2-related factor 2, superoxide dismutase 2, GSH-Px, CAT and NAD(P)H quinone dehydrogenase 1 (p < 0.05) while significantly downregulating the kelch-like ECH associated protein 1 expression in a dose-dependent manner (p < 0.05), thereby activating the Keap1/Nrf2 pathway with the peak effect observed in the 1000 mg/kg WEAA group. Additionally, supplementation with 100 µg/mL of WEAA had significant antioxidation activity in the culture medium of PBLs. Its action mechanism involved the Keap1/Nrf2 pathway; specifically, WEAA exerted its antioxidant effect by upregulating the gene expression related to the Keap1/Nrf2 pathway. In conclusion, WEAA enhances sheep’s antioxidant capacity by up-regulating Keap1/Nrf2 pathway genes and boosting antioxidant enzyme activity. The results provided experimental support for the potential application of WEAA in intensive mutton sheep farming. Full article

In this study, we identify cortical molecular biomarkers potentially associated with learning in mice using artificial intelligence (AI), inclusive of established and novel feature selection combined with supervised learning technologies. We applied multiple machine learning (ML) algorithms, using public domain ML software, to a public domain dataset, in order to support reproducible findings. We developed technologies tasked with predicting whether a given mouse was shocked to learn, based on protein expression levels extracted from their cortices. Results indicate that it is possible to predict whether a mouse has been shocked to learn or not based only on the following cortical molecular biomarkers: brain-derived neurotrophic factor (BDNF), NR2A subunit of N-methyl-D-aspartate receptor, B-cell lymphoma 2 (BCL2), histone H3 acetylation at lysine 18 (H3AcK18), protein kinase R-like endoplasmic reticulum kinase (pERK), and superoxide dismutase 1 (SOD1). These results were obtained with a novel redundancy-aware feature selection method. Five out of six protein expression biomarkers (BDNF, NR2A, H3AcK18, pERK, SOD1) identified have previously been associated with aspects of learning in the literature. Three of the proteins (BDNF, NR2A, and BCL2) have previously been associated with pruning, and one has previously been associated with apoptosis (BCL2), implying a potential connection between learning and both cortical pruning and apoptosis. The results imply that these six protein expression profiles (BDNF, NR2A, BCL2, H3AcK18, pERK, SOD1) are highly predictive of whether or not a mouse has been shocked to learn. Full article

A high-fat diet (HFD) has significant effects on health, leading to cardiovascular, metabolic, neurodegenerative, and psychiatric conditions and contributing to obesity and type 2 diabetes. Mitochondria, essential for energy production and oxidative metabolism, are adversely affected by a HFD, causing oxidative stress and impaired cellular function. Mutations in the OPA1 (OPtic Atrophy 1) gene, crucial for mitochondrial dynamics and functions, are responsible for dominant optic atrophy (DOA), a mitochondrial neurodegenerative disease associated with increased reactive oxygen species (ROS). The expressivity of DOA is highly variable, even within the same family. This suggests that both modifying genetics and environmental factors could influence the penetrance of the disease. We previously demonstrated that genetic background modulates DOA expressivity and now ask if this is also the case for external cues. We thus explore how OPA1 deficiency interacts with HFD-induced metabolic disturbances, hypothesizing that long-term HFD consumption impairs brain mitochondrial function and disrupts oxidative metabolism. OPA1^+/− mice were thus subjected to a HFD for a period of 12 weeks, and ROS levels and the expression of antioxidant genes were evaluated by Western blot and spectrophotometry. Cortices from high-fat diet-fed OPA1^+/− mice showed lower aconitase activity than those of their wild-type (WT) litter mates, indicative of an unbalanced increase in mitochondrial ROS. Accordingly, OPA1^+/− mice present lower levels of the antioxidant enzyme superoxide dismutase 2 compared to WT mice. Therefore, this study (i) reveals the onset of oxidative stress in brain cortices from OPA1^+/− mice challenged with a HFD, (ii) shows that diet is a modifying factor for DOA, and (iii) suggests that food control could be used to moderate the severity of the disease. Full article

Background/Objectives: Epicardial adipose tissue (EAT) is metabolically active and is in dynamic crosstalk with the surrounding cardiomyocytes, modulating their function and metabolism. Oxidative stress is a key contributor to cell death and cardiac remodeling, is a hallmark of diabetes (DM) and cardiovascular disease, such as coronary artery disease (CAD). However, little is known about these processes in EAT from patients undergoing cardiac surgery. This study investigates changes in mitochondrial dynamics, reactive oxygen species (ROS) production, and antioxidant defense levels in EAT compared to subcutaneous adipose tissue (SAT) in patients undergoing cardiac surgery, with a focus on the impact of DM and CAD. Methods: Adipose tissue biopsies were collected from 128 patients undergoing surgical cardiac intervention. Mitochondrial dynamics and oxidative stress markers were analyzed. Results: EAT exhibited increased expression of mitochondrial fusion markers [mitofusin 1 (p ≤ 0.001), mitofusin 2 (p = 0.038), and optic atrophy 1 (p ≤ 0.001)], as well as fission markers [fission 1 (p ≤ 0.001) and dynamin-related protein 1 (p ≤ 0.001)] relative to SAT. Additionally, ROS levels (dihydroethidium, p = 0.004) were elevated, while lipid peroxidation (malondialdehyde, p ≤ 0.001) was reduced in EAT compared to SAT. Reduced glutathione (GSH) levels (p ≤ 0.001) and the redox buffer ratio between reduced and oxidized glutathione (GSH/GSSG, p ≤ 0.001) were significantly increased in EAT. Interestingly, glutathione peroxidase activity (p ≤ 0.001) and the antioxidant defense markers catalase (p ≤ 0.001) and superoxide dismutase 2 (p = 0.001) were significantly reduced in EAT compared to SAT. Conclusions: The findings provide a unique molecular insight into the mitochondrial dynamics and oxidative stress profiles of EAT, highlighting potential avenues for a novel diagnostic method and therapeutic strategies for cardiac disease. Full article