Search Results (6,447)

The Sugars Will Eventually be Exported Transporters (SWEET) family plays a crucial role in the carbohydrate distribution, phloem loading, and stress response of plants, yet the evolutionary characteristics and functional diversification of SWEET genes in the endangered timber species Phoebe bournei (Hemsl.) Yen C. Yang remain largely unexplored. In this study, 21 PbSWEET genes were identified and classified into four subfamilies (A-D). Subfamily A exhibited a unique lineage expansion, mainly driven by tandem and segmental duplications. The nonsynonymous-to-synonymous substitution ratio (Ka/Ks) values of all duplicate gene pairs were all less than 1, indicating a strong selective suppression effect; consistent with this evolutionary constraint, the majority of PbSWEET proteins harbor the conserved Medicago truncatula Nodulin 3/saliva (MtN3_slv) domain, with only a few exceptions lacking a complete version. Promoter and hormone response analyses revealed that under abscisic acid (ABA) stress, PbSWEET4 exhibited an immediate burst, whereas PbSWEET10 showed a delayed burst. Physiological data indicated that soluble sugars may be more dominant osmolytes than proline (Pro), a pattern that points to a potential carbon-centric regulatory strategy. PbSWEET4 showed an early burst before sugar/oxidative peaks, suggesting a possible non-canonical signaling role, whereas PbSWEET10 exhibited a late increase coinciding with sugar/malondialdehyde (MDA) peaks, suggesting potential involvement in sugar redistribution. Under methyl jasmonate (MeJA) treatment, PbSWEET10 was rapidly induced, yet sugar accumulation occurred only at 24 h, a temporal decoupling that suggests a possible transcription–metabolism decoupling. Collectively, these correlative patterns point to a possible dual-wave transcriptional mechanism and nominate PbSWEET10 as a candidate for stress response, though these inferences require functional validation. Full article

Chilling injury is a major problem limiting the postharvest storage and marketability of mango fruit at low temperature. The present study investigated the individual and combined effects of sodium nitroprusside (SNP), L-arginine (Arg) and salicylic acid (SA) on chilling tolerance, regulation of oxidative stress and the postharvest quality of ‘Keitt’ mango fruit stored at 5 ± 1 °C for 28 days followed by 4 days of shelf life at 23 °C. Fruits were pre-treated with 1 mM SNP, 1 mM Arg, 2 mM SA or their binary combinations before storage. The chilling injury, membrane damage, lipid peroxidation, protein oxidation and fruit softening were greatly enhanced by cold storage in untreated fruits. In contrast, all the treatments significantly ameliorated these deteriorative changes, and the combined treatments were superiorly effective. Among these, SNP + Arg was the most effective treatment, which reduced the chilling injury index from 4.05 in control fruits to 1.00 after shelf life, completely inhibiting the incidence of decay and reducing electrolyte leakage and malondialdehyde accumulation by 47.4 and 48.2%, respectively. The same treatment also maintained higher firmness, titratable acidity, visual appearance and ascorbic acid content than untreated fruits. The enhanced chilling tolerance was accompanied by increased antioxidant defense, as SNP + Arg significantly stimulated the activities of superoxide dismutase, catalase and peroxidase, but suppressed the activity of pectin methylesterase. Multivariate analyses, such as PCA, clustered heatmap and integrated stress index, demonstrated a strong negative relationship between oxidative stress markers and antioxidant metabolism. The results showed that combined SNP and Arg treatments enhanced chilling tolerance through increasing antioxidant capacity, preserving membrane integrity, and retarding ripening-related metabolism, which provides an effective way to maintain the postharvest quality of cold-stored mango fruit. Full article

Background/Objectives: Tordylium trachycarpum Boiss. (Apiaceae) is traditionally used in Kurdish ethnomedicine for the management of gastrointestinal disorders; however, its pharmacological efficacy and safety profile remain insufficiently investigated. This study evaluated, for the first time, the gastroprotective activity and associated antioxidant, inflammatory, and apoptotic responses of the methanolic extract of T. trachycarpum using an ethanol-induced gastric ulcer model in Sprague–Dawley rats. Methods: Preliminary phytochemical screening revealed the presence of phenolics, flavonoids, terpenoids, tannins, coumarins, and glycosides. Acute oral toxicity testing demonstrated no signs of toxicity at doses up to 5 g/kg. Gastric ulceration was induced by absolute ethanol, and animals were pretreated with the extract (250 and 500 mg/kg) or omeprazole (20 mg/kg). Results: The extract significantly decreased the gastric lesion area from 258.50 ± 6.38 mm² in the ulcer control group to 143.70 ± 0.76 mm² and 115.50 ± 0.76 mm², corresponding to ulcer inhibition rates of 44.41% and 55.31%. Additionally, the extract increased mucus production, maintained mucosal structure, and raised stomach pH. Biochemical analysis showed a significant increase in antioxidant enzymes [superoxide dismutase (SOD) and catalase (CAT)] and a reduction in malondialdehyde (MDA) levels, indicating attenuation of oxidative stress. In addition, the extract modulated pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-10). Blood-based ELISA analysis demonstrated increased expression of heat shock protein 70 (HSP70) and reduced Bax levels, suggesting anti-apoptotic activity. Conclusions: These findings indicate that T. trachycarpum exerts significant gastroprotective activity through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms, supporting its traditional use and highlighting its potential as a natural therapeutic candidate for the management of gastric ulcers. Full article

Insulin (Ins) regulates multiple intracellular signalling pathways involved in cell survival, oxidative stress responses, and tau phosphorylation. Dysregulation of these pathways has been implicated in neurodegenerative disorders, including Alzheimer’s disease (AD). The present study evaluated the effects of insulin on protein kinase B/glycogen synthase kinase-3 beta (AKT/GSK-3β) signalling, tau phosphorylation, and oxidative stress-related markers in SH-SY5Y neuroblastoma cells. Cell metabolic activity was assessed using the (diphenyltetrazolium bromide) MTT assay, while cell number and viability were evaluated by Trypan Blue exclusion, necrosis by lactate dehydrogenase (LDH) release, and apoptosis by Caspase-3 activity. Western blot analysis was performed to evaluate the expression of phosphorylated AKT (p-AKT), phosphorylated GSK-3β (p-GSK-3β Ser9), phosphorylated TAU (pTAU), nuclear factor erythroid 2-related factor 2 (NRF2), manganese superoxide dismutase (Mn-SOD), and copper/zinc superoxide dismutase (Cu/Zn-SOD). Lipid peroxidation was determined by measuring malondialdehyde (MDA) levels using a colorimetric/fluorometric assay. Insulin treatment increased MTT reduction (31.25%) and cell metabolic activity (119.15%) while reducing LDH release (19.2%) and Caspase-3 activity (31.26%). In addition, insulin significantly increased p-AKT (34.2%) and p-GSK-3β (Ser9) (19.9%) levels. A reduction in pTAU levels (53.39%) was also observed following insulin treatment. Furthermore, insulin increased NRF2 expression (18.77%), Cu/Zn-SOD (37.29%), and Mn-SOD (50.16%) and reduced MDA levels (13.95%). These findings indicate that insulin modulates signalling pathways associated with tau phosphorylation and cellular redox regulation in SH-SY5Y cells. Insulin treatment was associated with increased AKT and GSK-3β phosphorylation, reduced tau phosphorylation, and changes in oxidative stress-related markers in SH-SY5Y neuroblastoma cells. These findings support a role for insulin in the modulation of molecular pathways implicated in cellular stress responses and tau regulation. Further studies using differentiated neuronal models and disease-relevant conditions are required to determine the relevance of these observations to neurodegenerative disorders. Full article

Identifying cold-resistance genes is essential for improving the ability of apples (Malus × domestica) to tolerate low temperatures, as cold stress significantly limits their growth and productivity. The MdWRKY31 gene was cloned from apple, and its sequence characteristics, expression pattern, and biological function were systematically investigated. Bioinformatic analysis indicated that MdWRKY31 belongs to the group II WRKY transcription factors and is localized in the nucleus. Expression analysis revealed that MdWRKY31 transcript levels were markedly upregulated under low-temperature stress. To further explore its function, MdWRKY31 was heterologously overexpressed in tomato (Solanum lycopersicum). Following low-temperature treatment, transgenic tomato plants exhibited significantly reduced accumulation of reactive oxygen species, markedly enhanced activities of antioxidant enzymes (SOD, POD, and CAT), increased contents of proline and soluble protein, and a notable decrease in malondialdehyde levels. Additionally, transcript levels of SlCBF1, SlCBF2, SlCBF3, SlICE1, along with the ABA signaling-related genes SlNCED1 and SlABI5, were markedly elevated. Further molecular docking showed that the MdWRKY31 protein has strong binding affinity to the W-box elements in the promoters of SlCBF1 suggesting that it may regulate the expression of these genes through direct protein–DNA interactions. These findings indicate that MdWRKY31 improves plant cold tolerance by CBF-dependent pathways to modulate antioxidant defenses and osmotic balance. These findings identify candidate genetic resources for breeding cold-resistant apple cultivation. Full article

This study evaluated the effects of adding zinc oxide nanoparticles (ZnNP), L-arginine (L-Arg), or a combination of both to the diets of growing rabbits to mitigate the physiological and productive consequences of heat stress. Two hundred and eighty 35-day-old New Zealand White rabbits were randomly assigned to four experimental treatments, with 70 rabbits per treatment and seven replicates (10 rabbits/replicate). The control group (Ctr) received the base diet without additives, while the diets of the other groups were fortified with arginine (L-Arg; 3 g/kg), zinc oxide nanoparticles (ZnNP; 40 mg/kg), or a combination of both (Arg-Zn). The results showed that the combined Arg-Zn significantly improved weight gain rate, feed conversion rate, carcass weight, and nutrient digestibility compared to the control group (p < 0.05). At the physiological level, we observed increased serum levels of total antioxidant capacity (T-AOC), glutathione peroxidase (GPx), superoxide dismutase (SOD), immunoglobulin G (IgG), immunoglobulin A (IgA), and triiodothyronine (T3), along with decreased levels of malondialdehyde (MDA), alanine aminotransferase (ALT), and aspartate aminotransferase (AST, p < 0.05) in Arg-Zn-fed rabbits. However, adding the Arg-Zn mixture contributed to a reduction in pathogenic bacteria counts and increased the volatile fatty acid (VFA) levels. At the molecular level, the gene expression of the inflammatory cytokines IL-6 and tumor necrosis factor alpha (TNF-α) decreased; however, the gene expression of claudins-1 (CLDN-1), cationic amino acid transporter-1 (CAT-1), mucin-2 (MUC-2), sodium-glucose co-transporter-1 (SGLT-1), and interferon gamma (IFNγ) increased (p < 0.05) in Arg-Zn-fed rabbits. These results suggest that dietary supplementation with ZnNP and L-Arg may serve as an effective nutritional strategy for improving growth performance, antioxidant status, immune function, and intestinal integrity in rabbits exposed to high ambient temperatures. Full article

Copper sulphate pentahydrate is widely used in agriculture to control bacterial and fungal diseases in various crops. Despite its extensive application, limited data exist regarding its potential toxic effects on juvenile rats following early-life exposure. In addition to oxidative stress and inflammation, copper overload may also trigger cuproptosis, a recently identified copper-dependent form of regulated cell death. This study aimed to investigate the histopathological, biochemical, and molecular effects of copper sulphate exposure on major organs in juvenile rats and to elucidate the associated inflammatory and oxidative stress-related mechanisms. Male and female Sprague–Dawley rats (30–40 days old, 50–70 g) were randomly assigned to control and experimental groups. Following copper sulphate exposure, histopathological examinations were performed on major organs, including the liver, kidney, heart, lung, and reproductive tissues (testis in males and ovary in females). Immunohistochemical analyses of tumor necrosis factor-alpha (TNF-α) and nuclear factor kappa B (NF-κB) were conducted. Oxidative stress parameters, including malondialdehyde (MDA), total antioxidant status (TAS), and total oxidant status (TOS), were measured using ELISA. Gene expression levels of TNF-α and NF-κB were evaluated by quantitative real-time PCR (qRT-PCR). Copper sulphate exposure induced significant histopathological alterations in all examined tissues of both male and female juvenile rats. Biochemical findings revealed increased oxidative stress, evidenced by elevated MDA and TOS levels along with altered TAS values. Furthermore, immunohistochemical and gene expression analyses demonstrated upregulation of TNF-α and NF-κB, indicating activation of inflammatory pathways. Copper sulphate exposure leads to widespread morphological changes in juvenile rats, potentially mediated by oxidative stress and inflammation. These findings provide insight into the biological impact of early-life pesticide exposure. Further studies are warranted to clarify the underlying molecular mechanisms and to develop effective preventive or therapeutic approaches. Full article

Background/Objectives: Obesity-related insulin resistance is accompanied by chronic low-grade inflammation, but the extent to which weight loss modifies circulating cytokines in a sex-specific manner remains insufficiently understood. The aim of this study was to assess sex-specific cytokine responses and metabolic adaptation in adults with obesity and insulin resistance following a six-month weight-reduction program (WRP). Methods: Thirty-six participants (24 women and 12 men) with a value of Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) ≥ 2 underwent an individualized low-calorie diet combined with moderate physical activity and health education. Anthropometric, body composition, biochemical, oxidative stress, and cytokine parameters were evaluated before and after the intervention. Results: Both women and men showed significant reductions in body mass, Body Mass Index (BMI), waist circumference, visceral fat area (VFA), body fat mass (BFM), fasting glucose, HOMA-IR, modified Atherogenic Index of Plasma (new-AIP), malondialdehyde (MDA), and Oxidative Stress Index (OSI). Women additionally showed significant decreases in fat-free mass (FFM), skeletal-muscle mass (SMM), total body water (TBW), glycated hemoglobin A_1c (HbA1c), and triacylglycerols, whereas cholesterol in high-density lipoproteins (HDL-C) increased significantly in men. Cytokine changes were selective rather than uniform. Interleukin-1 receptor antagonist (IL-1ra), Interleukin 6 (IL-6), and Tumor Necrosis Factor alpha (TNF-α) decreased in both women and men. In sex-stratified analyses, IL-1β decreased significantly only in women, whereas IL-7 decreased significantly only in men. ClinicalTrials.gov Registration: [NCT07645105] (retrospectively registered on [11 June 2026]). Conclusions: A 6-month lifestyle-based weight-reduction program in adults with overweight or obesity and insulin resistance was associated with metabolic improvement, reduced oxidative stress, and partial attenuation of obesity-related low-grade inflammation. The observed cytokine and metabolic changes suggest sex-related patterns of immunometabolic adaptation to weight reduction. However, these findings should be interpreted cautiously because of the relatively small sex-stratified subgroups and the number of cytokine endpoints analyzed, and they require confirmation in larger, sex-balanced studies. Full article

Heat stress severely constrains wheat productivity, yet the mechanisms underlying thermotolerance remain incompletely understood. This study integrated physiological, biochemical, molecular, and ultrastructural analyses to characterize heat-stress responses in four bread wheat (Triticum aestivum L.) genotypes contrasting in heat tolerance. Membrane injury was assessed by membrane damage rate, lipid peroxidation by malondialdehyde accumulation, antioxidant defense by SOD, CAT, GPX, and BPX activities, and stress-responsive regulation by qRT-PCR analysis of DREB, HSP16.9, and SOD isoforms. HSP16.9 protein accumulation was further evaluated by Western blotting. Heat stress increased membrane damage and MDA accumulation in all genotypes; however, tolerant Murov 2 and Zirva 85 showed lower oxidative membrane injury than sensitive Aran and Gyzyl bugda. Thermotolerance was associated with stronger antioxidant activation, enhanced DREB and HSP16.9 induction, and more coordinated FeSOD and MnSOD expression. The HSP16.9 protein accumulated after heat treatment, supporting its role as a stress-responsive molecular chaperone. Separate correlation analyses of tolerant and sensitive genotypes revealed stronger coordination among transcriptional, chaperone-related, and antioxidant markers in tolerant genotypes, whereas sensitive genotypes showed a more fragmented response. Microscopy further showed better preservation of chloroplast, mitochondrial, and mesophyll organization in the tolerant genotype relative to the sensitive counterpart, indicating integrated cellular protection. Together, these responses define a coordinated tolerance strategy that may guide the selection of heat-resilient wheat genotypes. Full article

This study used Poacynum hendersonii (Hook. f.) Woods. seedlings as experimental material. A soil drought group (gradual soil drying) and a PEG-simulated drought group (15% PEG-6000 treatment) were established. By combining physiological measurements, metabolomics, and transcriptomics, we investigated the physiological and molecular mechanisms of P. hendersonii in response to drought stress. The results showed that under drought stress, P. hendersonii alleviated oxidative damage by activating the antioxidant enzyme system (catalase, CAT; superoxide dismutase, SOD; peroxidase, POD), and enzyme activities recovered significantly after rehydration. In the osmotic stress group (PEG), hydrogen peroxide (H₂O₂) and malondialdehyde (MDA) contents increased significantly in the later stages, whereas membrane damage was milder in the soil drought group. Metabolomics analysis revealed significant enrichment of starch and sucrose metabolism pathways during early drought, shifting to unsaturated fatty acid biosynthesis and carbon metabolism in later stages. PEG-simulated drought specifically induced the accumulation of arachidonic acid, which may be associated with ferroptosis-like processes, although direct evidence is lacking. Transcriptomics analysis identified 23,623 differentially expressed genes (DEGs), with transcription factor families such as bHLH, MYB, and NAC playing key roles in drought response. Weighted Gene Co-expression Network Analysis (WGCNA) further revealed gene modules significantly correlated with physiological traits, indicating that enhanced respiratory metabolism (glycolysis, tricarboxylic acid (TCA) cycle) is an important strategy for P. hendersonii to adapt to drought. The study also found that while PEG-simulated drought could simulate the physiological effects of soil drought, significant differences existed in molecular pathways, particularly during later stress stages. This research provides a theoretical basis for elucidating the drought resistance mechanisms of P. hendersonii and offers potential targets for crop drought resistance breeding. Full article

Lupinus angustifolius is an important ornamental plant; however, its poor tolerance to alkaline soils limits its cultivation and production. Based on the alkaline-tolerance-related Gshdz4-GsNAC019-GsEXPA8 regulatory module previously screened and identified in soybean, we used Agrobacterium rhizogenes-mediated transformation to overexpress in lupine roots the combinations Gshdz4-GsNAC019-GsEXPA8 (HNE), Gshdz4-GsNAC019 (HN), and GsNAC019-GsEXPA8 (NE) to investigate their effects on root development and alkaline tolerance. RT-PCR confirmed the successful generation of all overexpression lines. Under 100 mM NaHCO₃ stress, all overexpression lines exhibited less wilting and longer survival than the wild type (WT), with the HNE line showing the best phenotype. Physiological measurements showed that the overexpression lines had significantly higher proline content, antioxidant enzyme (SOD, CAT, POD) activities, and root activity, as well as lower malondialdehyde content. DAB and NBT staining of leaves indicated reduced accumulation of O₂⁻ and H₂O₂, suggesting enhanced antioxidant capacity. Root architecture analysis revealed that root length, surface area, volume, tip number, and fork number were significantly increased in HNE, HN, and NE lines compared with WT, with the most pronounced effect observed in HNE. Bioinformatics analysis and qPCR confirmed that Gshdz4 binds to and activates the promoter of the endogenous LaNAC072 (the lupine homolog of GsNAC019), while GsNAC019 binds to and activates the promoter of the endogenous LaEXPA8 (the lupine homolog of GsEXPA8), thereby triggering the endogenous alkaline tolerance regulatory mechanism. Furthermore, the overexpression combinations significantly upregulated the expression of alkaline stress-responsive genes, including LaSOS1, LaNHX6, LaP5CS, LaMYB39, and LaDnaJ1. This study provides theoretical support for molecular breeding of alkaline-tolerant lupine. Full article

The physiological and metabolic responses of juvenile Chinese softshell turtles, Pelodiscus sinensis, exposed to single or double heatwaves (33 °C for 4 days) were investigated based on liver antioxidant assay and transcriptomic and metabolomic analyses. Heatwave exposure increased superoxide dismutase and catalase activities, but did not significantly alter malondialdehyde and reactive oxygen species levels, indicating enhanced antioxidant defense. Transcriptomic analysis revealed the differential expression of genes involved in carbohydrate metabolism, immune function, cardiovascular regulation, and signal transduction, with more pronounced alterations in single-heatwave-exposed turtles. Additionally, metabolic dysregulation in amino acids was revealed by significantly altered levels of some key amino acids and their derivatives. Compared with single-heatwave-exposed turtles, fewer differentially expressed genes and less metabolic disruptions in double-heatwave-exposed turtles probably indicated less physiological disorders under recurrent heat stress. Although P. sinensis can adopt physiological and metabolic adjustments to mitigate the adverse effects of short-term heatwaves, repeated heatwave exposure might still cause severe physiological consequences in aquatic turtles. These findings may have important implications for the conservation of freshwater turtle species under future climate change scenarios. Full article

Background/Objectives: Renal ischemia–reperfusion injury (IRI) is a major cause of acute kidney injury and delayed graft function after kidney transplantation. Oxidative stress, mitochondrial dysfunction, and tubular epithelial cell apoptosis are central events in renal IRI. Sophocarpine (SOP), a quinolizidine alkaloid derived from Sophora species, has reported antioxidant and anti-apoptotic activities, but its effects in renal IRI remain unclear. This study investigated the role and function of SOP in renal IRI. Methods: A bilateral renal IRI mouse model and a hypoxia/reoxygenation (H/R) model in HK-2 human proximal tubular epithelial cells were used. Renal function, histological injury, apoptosis, reactive oxygen species, malondialdehyde, superoxide dismutase activity, glutathione, mitochondrial morphology, mitochondrial membrane potential, and mitochondrial dynamics-related proteins were evaluated. SIRT1 dependency was examined using Sirt1 small interfering RNA in HK-2 cells and EX527-mediated SIRT1 inhibition in mice. Results: SOP pretreatment reduced serum creatinine and blood urea nitrogen levels, attenuated tubular injury and apoptosis, decreased oxidative stress, and preserved mitochondrial morphology and function after renal IRI. Similar protective effects were observed in HK-2 cells exposed to H/R. SOP increased SIRT1 and PGC-1α expression, whereas Sirt1 knockdown or pharmacological SIRT1 inhibition weakened the antioxidant and mitochondrial protective effects of SOP. Conclusions: SOP attenuates renal IRI-associated oxidative stress and mitochondrial dysfunction, at least in part through the SIRT1/PGC-1α axis. These findings support further investigation of SOP as a candidate renoprotective compound for ischemic kidney injury. Full article

This study systematically compared the effects of dietary supplementation with glutamine (Gln) and its precursors, including glutamic acid (GA) and α-ketoglutarate (AKG), on growth performance, serum antioxidant and immune parameters, and multi-region gastrointestinal microbiota in suckling lambs. Forty healthy suckling Hu lambs with similar body weight (7.37 ± 1.18 kg) and age (7 ± 0.8 d) were selected and randomly allocated into four groups (n = 10 per group): a control group (CON, without additive), and three treatment groups (GA, AKG, and Gln), each receiving 2 g per animal per day of the corresponding additive. The experimental period lasted for 42 d. All three additives showed a tendency to increase the final body weight (p = 0.056) and significantly increased the average daily gain (ADG) of lambs (p < 0.05). GA supplementation increased the dry matter intake throughout the entire trial (p < 0.05), whereas the addition of AKG and Gln increased the dry matter intake only during the later period (d 21–42) (p < 0.05). The feed-to-gain ratios did not differ among all groups (p > 0.05). Compared with the CON group, all three treatment groups showed elevated serum activities of catalase, glutathione peroxidase, and total antioxidant capacity, as well as increased IgA and IgG contents (p < 0.05). In addition, malondialdehyde concentration was decreased in all three treatment groups (p < 0.05). Moreover, GA supplementation reduced the ruminal alpha diversity while increasing the abundance of butyrate-producing bacteria (Ruminococcaceae UCG-014) (p < 0.05). All three interventions consistently decreased the abundance of the intestinal pathogen Escherichia-Shigella in the ileum (p < 0.05). Correlation analyses showed that ruminal Treponema 2 abundance was negatively correlated with ADG, whereas jejunal Methylobacterium and ileal [Eubacterium] coprostanoligenes group were positively correlated with final body weight or ADG. In conclusion, glutamine and its precursors play an important role in modulating gastrointestinal bacterial diversity and composition, enhancing antioxidant and immune functions, and improving the growth performance of suckling lambs. Full article

Oxidative stress biomarkers are elevated in liver cirrhosis, but their clinical utility for severity staging and complication prediction remains uncertain. This retrospective single-centre study enrolled 90 patients with decompensated cirrhosis (Child–Pugh classes B and C) to evaluate serum malondialdehyde (MDA) and 8-isoprostane (8-isoPGF2α) as predictors of Child–Pugh severity, severe ascites, and severe hepatic encephalopathy, and to quantify their incremental value within supervised machine learning models. Four algorithms—logistic regression, Random Forest, Gradient Boosting, and Support Vector Machine—were evaluated using stratified 10-fold cross-validation; logistic regression models with and without oxidative stress biomarkers were compared for the prediction of ascites and encephalopathy. Routine biochemical parameters effectively discriminated Child–Pugh class B from C, with machine learning models achieving AUC-ROC values of 0.921–0.972. Neither MDA nor 8-isoPGF2α differed between Child–Pugh classes or across ascites categories, and both failed to improve ascites prediction (ΔAUC = −0.015). For severe hepatic encephalopathy, the extended model showed modest but consistent improvements in accuracy (+3.4 percentage points), sensitivity (+6.4%), and model fit, suggesting an outcome-specific complementary role consistent with the established involvement of lipid peroxidation in ammonia neurotoxicity. These findings support the use of machine learning for automated cirrhosis severity classification and indicate that oxidative stress biomarkers hold selective relevance for hepatic encephalopathy rather than global disease staging. Full article