Search Results (9,378)

The increasing contamination of agricultural soils with microplastics (MPs) represents an emerging environmental challenge. While conventional plastics such as low-density polyethylene (LDPE) persist for decades, biodegradable alternatives like polybutylene adipate terephthalate (PBAT) are promoted as eco-friendly solutions. However, their environmental safety for crop plants and soil microbiota remains poorly understood. In this study, we evaluated the effects of LDPE and PBAT microplastics (1% w/w) on the growth and physiological state of winter wheat (Triticum aestivum L.) cultivated in soil, either alone or in combination with the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) and the plant-beneficial fungus Trichoderma citrinoviride. Growth parameters (root and shoot length and mass), germination index, chlorophyll content, antioxidant enzyme activity, and lipidomic profiles of wheat were assessed. PBAT stimulated biomass accumulation but simultaneously triggered oxidative stress and remodeled membrane phospholipids, indicating physiological disturbance. T. citrinoviride enhanced wheat growth and mitigated oxidative stress under non-contaminated conditions; however, its beneficial effect was generally suppressed in the presence of PBAT and/or 2,4-D. The results suggest that, despite its biodegradability, PBAT may pose a higher phytotoxic potential than conventional LDPE, particularly by altering oxidative balance and membrane lipid composition in wheat. Full article

Bovine milk is a complex biological fluid whose lipid fraction plays essential roles in nutrition, processing, and product quality. While conventional analyses have traditionally focused on total fat content and fatty acid composition, recent advances in liquid chromatography–mass spectrometry (LC–MS) have unveiled the molecular diversity of polar lipids, particularly phospholipids and sphingolipids. These compounds, largely associated with the milk fat globule membrane (MFGM), include key molecular species such as phosphatidylcholine (PC), phosphatidylethanolamine (PE), sphingomyelin (SM), ceramides (Cer), and lysophospholipids, which collectively contribute to emulsion stability, flavor development, and bioactive functionality. This review summarizes current progress in the determination of sphingolipids and phospholipids in bovine milk, with a specific focus on analytical strategies enabling their accurate detection, identification, and quantification. We discuss how advanced LC–MS platforms have been applied to investigate factors shaping the milk polar lipidome, including lactation stage, animal diet, metabolic and inflammatory stress, and technological processing. Accumulating evidence indicates that specific lipid species and ratios, such as PC/PE balance, SM and ceramide profiles, and Lyso-PC enrichment, act as sensitive molecular indicators of membrane integrity, oxidative status, heat stress, and processing history. From an applied perspective, these lipidomic markers hold strong potential for dairy quality control, shelf-life assessment, and authenticity verification. Overall, advanced lipidomics provides a robust analytical framework to translate molecular-level lipid signatures into actionable tools for monitoring cow health, technological performance, and the nutritional valorization of bovine milk. Full article

Quercetin (Q), a bioactive flavonoid, exerts potent antioxidant and redox-modulating effects by activating the nuclear factor erythroid 2-related factor 2/antioxidant response Element (Nrf2/ARE) pathway and upregulating endogenous antioxidant defenses, including enzymatic antioxidants such as superoxide dismutase (SOD) and catalase (CAT), as well as non-enzymatic glutathione (GSH) and lipid peroxidation (MDA). Gemcitabine (Gem), a widely used antimetabolite chemotherapeutic, often shows limited efficacy under hypoxic and oxidative stress conditions driven by hypoxia-inducible factor 1-alpha (HIF-1α) and vascular endothelial growth factor (VEGF)-mediated angiogenesis. This study investigated the redox-mediated synergistic effects of Q and Gem in MDA-MB-231 human breast cancer cells. Combination treatment significantly reduced cell viability beyond the expected Bliss value, indicating a synergistic interaction and enhanced apoptosis compared with single-agent treatments. Increased reactive oxygen species (ROS) production was accompanied by depletion of GSH and accumulation of MDA, establishing a pro-apoptotic oxidative stress environment. Q alone enhanced SOD and CAT activities, whereas the combination induced exhaustion of antioxidant defenses under oxidative load, reflecting a redox-adaptive response. Molecular analyses revealed downregulation of HIF-1α and VEGF, alongside upregulation of Bax and Caspase-3, confirming suppression of hypoxia-driven survival and activation of the intrinsic apoptotic pathway. Transcriptomic and enrichment analyses further identified modulation of oxidative stress- and apoptosis-related pathways, including phosphoinositide-3-kinase–protein kinase B/Akt (PI3K/Akt), HIF-1 and VEGF signaling. Collectively, these results indicate that Q potentiates Gem cytotoxicity via redox modulation, promoting controlled ROS elevation and apoptosis while suppressing hypoxia-induced survival mechanisms, highlighting the therapeutic potential of redox-based combination strategies against chemoresistant breast cancer. Full article

Fruit shrubs’ lignocellulosic biomass remaining as waste after harvesting and/or after pruning is an underutilized, little-explored bioresource. Sea buckthorn (Hippophae rhamnoides L.), aronia (Aronia melanocarpa) and blackcurrant (Ribes nigrum) berries are rich in biologically active compounds, so these shrubs’ woody biomass derivatives are prospective investigation objects. The influence of pre-treated biomass, extracts, and purified proanthocyanidins on the oxidative stability of lipid-based systems was studied by accelerated oxidation method. Emulsion stability, antimicrobial activity against bacteria that causes acne—Cutibacterium acnes; contaminating wounds; skin care products—Streptococcus pyogenes, Pseudomonas aeruginosa, Staphylococcus aureus, and Bacillus cereus; cytotoxicity and phototoxicity of extracts and proanthocyanidins on HaCaT human keratinocytes were tested. The study established that biomass, lipophilic extracts obtained using liquefied hydrofluorocarbon, and hydrophilic extracts obtained by aqueous ethanol increased oxidative stability of lipid-based formulations. Compounds with skin-protecting properties were detected. Sea buckthorn and aronia hydrophilic extracts and proanthocyanidins had the highest antimicrobial activity. Low phototoxicity was revealed, emphasizing safety and applicability in topical formulations; human HaCaT keratinocyte viability was the best with aronia extracts, but none of the other samples decreased cell viability by more than 50%. It was proven that agro-waste biomass is a prospective source of multifunctional ingredients for cosmetic and pharmaceutical topical formulations. Full article

The objective of this study was to evaluate the protective effect of curcumin (Cur) on reproductive toxicity induced by fumonisin B₁ (FB₁) in laying ducks during the peak egg-laying period. A total of seventy-two 50-week-old Cherry Valley ducks were randomly assigned to four groups: control, FB₁ (30 mg/kg), Cur (200 mg/kg), and Cur + FB₁ (200 mg/kg + 30 mg/kg). The experiment lasted for 35 days. Our results showed that cur supplementation effectively restored the reductions in final body weight (p = 0.005) and oviduct length (p = 0.020) induced by FB₁ exposure. Residual FB₁ concentrations in serum, liver, and ovaries were markedly increased in the FB₁-treated group, while Cur significantly decreased the FB₁ residual in duck liver (p < 0.05). Meanwhile, Cur supplementation markedly counteracted the FB₁-induced reductions in serum total protein, albumin, triglycerides, and high-density lipoprotein induced by FB₁ exposure. Cur supplementation effectively regulated FB₁-induced oxidative stress, inflammation, and endocrine disruption. Specifically, Cur lowered FB₁-induced malondialdehyde levels (p < 0.010), attenuated interleukin-1β increase (p = 0.083), and reversed the reduction in immunoglobulin G levels. FB increased the levels of hormones associated with duck reproduction, including estradiol, follicle-stimulating hormone, and luteinizing hormone; in contrast, curcumin supplementation decreased the levels of these hormones (p < 0.010). Histopathological analysis revealed that Cur significantly alleviated the inflammation and necrosis in the liver, kidneys, ovaries, and oviducts induced by FB₁. In conclusion, dietary Cur supplementation effectively alleviated FB₁-induced reproductive toxicity in laying ducks by enhancing antioxidant capacity, improving lipid metabolism, and restoring hormonal homeostasis. Full article

This systematic review aimed to summarize the effects of astaxanthin (ASX) supplementation on oxidative stress, inflammation, and metabolic regulation in human studies. A systematic search was conducted in Scopus, Web of Science (WOS), and PubMed for articles published between 2020 and 2025. Fifteen studies involving human participants were included, while in vitro and animal studies were excluded. ASX consistently reduced pro-inflammatory cytokines (IL-6, TNF-α, TGF-β1) and oxidative stress indices while increasing antioxidant capacity (SOD, TAC). Combined ASX and exercise interventions improved body composition, lipid profiles, insulin sensitivity, and immune recovery. In women with Polycystic Ovary Syndrome (PCOS) or endometriosis, ASX downregulated endoplasmic reticulum stress–related apoptotic pathways and improved oocyte and embryo quality. Cardiometabolic and respiratory outcomes showed improved endothelial function and reduced disease severity. Astaxanthin demonstrates broad antioxidant and anti-inflammatory properties, supporting its role as a promising adjunctive therapy for metabolic, reproductive, and cardiovascular health. Further well-designed clinical trials are needed to confirm optimal dosing and mechanisms of action. Full article

Phosphatidylserine (PS) externalization is a conserved membrane stress signal that becomes chronically dysregulated in cancer cells and tumor-associated endothelium. In vivo, PS does not exist as a free lipid signal but is presented in specific membrane-associated forms, including apoptotic or stressed cell surfaces, PS-rich extracellular vesicles, and circulating lipid particles. Unlike apoptosis-associated transient PS exposure, malignant PS externalization arises from metabolic rewiring, oxidative stress, epigenetic silencing of flippases, and microenvironmental cues, creating an immunosuppressive interface across the tumor–host boundary. This review synthesizes mechanistic, immunological, and clinical evidence on PS biology, including its roles in tumor immune evasion, extracellular vesicle-mediated systemic suppression, and vascular remodeling. We further summarize the development and evaluation of PS-targeted therapeutic platforms—such as bavituximab, SapC-DOPS/BXQ-350, and PS-directed imaging agents—and highlight their translational potential in combination with radiotherapy, chemotherapy, and checkpoint inhibitors. Chronic PS externalization, as manifested through distinct cellular and vesicular carriers, represents a unifying biomarker of tumor stress, immune suppression, and therapeutic vulnerability, offering a next-generation axis for theragnostic cancer management. Full article

Membrane rupture, induced by lipid peroxidation, is a severe threat to osmotic balance, as membrane pores contribute to ferroptosis, an iron-dependent cell death. To alleviate osmotic stress, membrane constituents dynamically reconstruct the membrane and interact with intracellular molecules. Tumor-derived acidosis shift glycolysis-dependent metabolism toward lipid metabolism, increasing polyunsaturated fatty acids (PUFAs). PUFAs enhance membrane fluidity but make cancer susceptible to lipid peroxidation. Also, the ionization of phospholipids under low pH can accelerate membrane rupture. This stress can be mitigated by the redistribution of cholesterol, which maintains tension–compression balance and acts as antioxidants. When excessive reactive aldehydes—byproducts of lipid peroxidation—overwhelm cholesterol’s protective role, lipid peroxides promote membrane cracks. Moreover, a deficiency in glutathione can alter cholesterol’s function, turning it into a pro-oxidant. In contrast, ceramide, derived from membrane lipids, indirectly prevents ferroptosis by facilitating cytochrome c release. This review integrates recent findings on how membrane components and environmental stressors influence ferroptosis. It also suggests potential therapeutic strategies. This could advance our understanding of ferroptosis in cancer. Full article

Structural and physicochemical deterioration in frozen foods is largely driven by ice crystal formation and growth during storage. Although biofoams offer sustainable alternatives to plastic packaging, bio-based systems designed to mitigate ice crystal-induced quality loss remain limited. In this study, a sodium alginate-based biofoam was synthesized via a facile one-pot method and evaluated for frozen fried chicken packaging. Its moisture, mechanical, and optical properties were compared with those of conventional plastic and paper packaging. The quality of frozen fried chicken was assessed in terms of moisture absorption, color, texture, pH, lipid oxidation (TBARs), and the overall appearance under different freezing conditions. The alginate biofoam exhibited exceptionally high moisture absorption (>2400%) due to its porous and hydrophilic structure, enabling effective moisture management during frozen storage. Samples packaged with the biofoam showed reduced moisture loss, lower lipid oxidation, and improved color and surface texture stability compared with conventional packaging, particularly under freeze–thaw conditions. These findings demonstrate that sodium alginate-based biofoam is a promising eco-friendly packaging material for maintaining the physicochemical quality of frozen ready-to-eat foods. Full article

Metabolic syndrome (MetS) is a multifactorial disorder characterized by central obesity, insulin resistance, dyslipidemia, and hypertension, all of which increase the risk of type 2 diabetes and cardiovascular diseases. This study investigates the potential complementary effects of the standardized green and black ADM ComplexTea Extract (CTE) and the heat-treated postbiotic (BPL1^® HT) on the cardiometabolic alterations associated with MetS in a murine model. C57BL/6J mice were fed a high-fat/high-sucrose (HFHS) diet and treated with CTE, BPL1^® HT, or their combination for 20 weeks. Metabolic, inflammatory, oxidative, vascular parameters, and fecal microbiota composition were assessed. Both CTE and BPL1^® HT individually attenuated weight gain, organ hypertrophy, insulin resistance, and inflammation. However, their combined administration exerted synergistic effects, fully normalizing body weight, adipocyte size, lipid profiles, HOMA-IR index, and insulin sensitivity to levels comparable to lean controls. Co-treatment also restored PI3K/Akt signaling in liver and muscle, reduced hepatic steatosis, and normalized the expression of inflammatory and oxidative stress markers across multiple tissues. Furthermore, vascular function was significantly improved, with enhanced endothelium-dependent relaxation and reduced vasoconstrictor responses, particularly to angiotensin II. CTE, BPL1^®HT, and the blend prevented bacterial richness reduction caused by HFHS; the blend achieved higher bacterial richness than mice in Chow diet. Additionally, the blend prevented the increase in Flintibacter butyricus, which is associated with MetS clinical parameters, and showed a tendency to increase the abundance of Bifidobacterium. These findings suggest that the combination of CTE and BPL1^® HT offers a potential nutritional strategy to counteract the metabolic and cardiovascular complications of MetS through complementary mechanisms involving improved insulin signaling, reduced inflammation and oxidative stress, enhanced vascular function, and modulation of gut microbiota. Full article

Background: Intestinal failure-associated liver disease (IFALD) is a serious complication in patients receiving parenteral nutrition, often exacerbated by inflammation, lipid overload, and oxidative stress. Nobiletin (NOB), a polymethoxylated flavone, is known for its anti-inflammatory and lipid-regulating properties. Methods: We employed an in vitro model using THLE-2 human hepatocytes and primary human cholangiocytes exposed to Intralipid (INT) and lipopolysaccharide (LPS) to simulate IFALD conditions. NOB was tested at non-toxic concentrations (10 and 25 µM) to assess its protective effects. MTT viability assays, multiplex bead-based immunoassays (MAGPIX), RT-qPCR, and Western blotting were used to evaluate changes in inflammation markers, gene expression, and protein signaling. Moreover, ALT and AST activities were used to assess hepatocellular injury. Results: NOB maintained high cell viability in THLE-2 hepatocytes and cholangiocytes, confirming its low cytotoxicity. NOB normalized ALT and AST activities in both tested cell lines, but the effect reached statistical significance only for ALT in cholangiocytes. Under IFALD-like conditions (LPS+INT), NOB significantly preserved metabolic activity in both cell types. In THLE-2 and cholangiocytes, NOB markedly reduced the phosphorylation of pro-inflammatory proteins JNK, NF-κB, and STAT3, indicating a broad inhibition of inflammatory signaling. Moreover, in THLE-2 cells, NOB upregulated lipid metabolism-related genes (PRKAA2, CYP7A1, and ABCA1) and decreased oxidative stress, thereby enhancing the nuclear translocation of Nrf2 and increasing SOD1 level, which supports the activation of antioxidant defenses. Conclusions: NOB exhibits hepatoprotective properties under IFALD-like conditions in vitro, likely through modulation of inflammation-related signaling and lipid metabolism pathways. Full article

Heme released during blood digestion represents a major oxidative challenge for hematophagous insects, promoting the generation of reactive oxygen species (ROS) and redox imbalance. Although Aedes aegypti has evolved specialized mechanisms to mitigate heme toxicity, how these responses vary across developmental stages remains poorly understood. Here, we applied quantitative proteomics to compare the effects of heme exposure in larvae and adult females. In larvae, heme treatment predominantly led to downregulation of metabolic and antioxidant proteins, consistent with a shift toward energy conservation and growth regulation. Nonetheless, selective upregulation of proteins associated with mitochondrial MnSOD activity, lipid remodeling, and cytoskeletal organization indicates the engagement of complementary protective mechanisms. In contrast, adults exhibited a coordinated bioenergetic response, characterized by enrichment of mitochondrial pathways, redox-related proteins, and molecular chaperones, reflecting enhanced resilience to oxidative stress. Enrichment of cuticle-associated proteins in both stages further suggests heme-induced structural remodeling. Together, these findings demonstrate that A. aegypti employs divergent, stage-specific proteomic strategies to cope with heme toxicity: larvae suppress metabolic activity while maintaining structural and redox homeostasis, whereas adults reinforce mitochondrial function and proteostatic defenses. These insights advance our understanding of mosquito redox biology and highlight stage-specific vulnerabilities that may be exploited for innovative vector control strategies. Full article

Understanding the molecular basis of heat tolerance in microalgae is crucial for developing resilient strains for industrial biotechnology. This study identified two desert Chlorella strains, XDA024 (thermotolerant) and XDA121 (heat-sensitive), through short-term thermal screening. The thermotolerant strain XDA024 survived exposure to 50 °C for 3 h, whereas XDA121 succumbed within 1 h at 40 °C. Physiological analyses revealed that the superior heat resistance of XDA024 was associated with enhanced activities of key antioxidant enzymes, including superoxide dismutase, catalase, and peroxidase, which effectively mitigated oxidative damage, alongside an elevated proline content contributing to osmoregulation. Transcriptomic profiling under acute heat stress (45 °C, 3 h) revealed that the unique thermotolerance of XDA024 was underpinned by the upregulation of genes related to photosystem stability and lipid synthesis, processes supported by activated calcium signaling and antioxidant pathways. In contrast, XDA121 exhibited significant downregulation of photosynthesis-related genes and promoted lipid degradation, resulting in membrane instability. Exogenous application of phosphatidylethanolamine (PE) and monoethanolamine (MEA) markedly increased the survival rate of XDA121 by more than threefold, primarily by alleviating membrane damage through enhanced membrane integrity and modulated antioxidant enzyme activities. These findings indicate that thermotolerance in desert Chlorella (Chlorophyta) is governed by the integrated coordination of antioxidant defense mechanisms, lipid metabolism, and photosystem protection. This research provides crucial insights and practical strategies for engineering heat-resistant microalgal strains for sustainable biofuel and bioproduct production. Full article

Atherosclerosis is a chronic, multifactorial vascular disease and the leading global cause of cardiovascular morbidity. Its development reflects interconnected disturbances in lipid metabolism, endothelial function, inflammation, smooth muscle cell (SMC) phenotypic switching, and extracellular matrix remodeling. Genetic predisposition, including monogenic disorders such as familial hypercholesterolemia and polygenic risk variants, modulates disease susceptibility by altering lipid homeostasis as well as inflammatory and thrombotic pathways. Epigenetic regulators and noncoding RNAs, such as histone modifications, microRNAs, and long noncoding RNAs, further shape gene expression and link environmental cues to vascular pathology. Endothelial injury promotes lipoprotein retention and oxidation, triggering monocyte recruitment and macrophage-driven foam cell formation, cytokine secretion, and necrotic core development. Persistent inflammation, macrophage heterogeneity, and SMC plasticity collectively drive plaque growth and destabilization. Emerging insights into immune cell metabolism, intracellular signaling networks, and novel regulatory RNAs are expanding therapeutic possibilities beyond lipid-lowering. Current and evolving treatments include statins, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, anti-inflammatory agents targeting interleukin-1 beta (IL-1β) or NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3), and advanced approaches such as gene editing, siRNA, and nanoparticle-based delivery. Integrating multi-omics, biomarker-guided therapy, and precision medicine promises improved risk stratification and next-generation targeted interventions. This review summarizes recent molecular advances and highlights translational opportunities for enhancing atherosclerosis prevention and treatment. Full article

Background: Metabolic-dysfunction-associated steatotic liver disease (MASLD) is a multifactorial liver disease in which mitochondrial dysfunction, oxidative stress, and inflammation play key roles in driving the progression toward metabolic dysfunction-associated steatohepatitis (MASH) and hepatocellular carcinoma (HCC). Dysfunctional mitochondria generate excess reactive oxygen species (ROS), impair antioxidant defenses, activate pro-inflammatory pathways and hepatic stellate cells, and perpetuate liver injury. Mitochondrial Complex I is a major ROS source, particularly under conditions of dysregulated energy metabolism. Since Complex I inhibition by metformin was shown to reduce ROS and activate the adenosine monophosphate-activated protein kinase (AMPK), this study aimed to evaluate whether a novel Complex I Modulator (CIM, BI4500) could attenuate oxidative stress, inflammation, and consequently reduce lipid accumulation and fibrosis in a methionine- and choline-deficient diet (MCD)-fed rat model of MASH. Methods: Rats were fed an MCD or an isocaloric control diet for six weeks. From week four, animals received daily oral treatment with CIM (10 mg/kg) or vehicle (Natrosol). At the endpoint, liver tissue was collected for histological, biochemical, and molecular analyses. Lipid droplet area, inflammatory infiltration, and collagen deposition were evaluated on tissue sections; total lipid content and oxidative stress markers were assessed in homogenates and isolated mitochondria. Molecular pathways related to oxidative stress, lipid metabolism, and fibrosis were assessed at protein and mRNA levels. Results: CIM treatment significantly reduced oxidative stress (ROS, lipid peroxidation, nitrogen species), promoting AMPK activation and metabolic reprogramming. This included increased expression of peroxisome proliferator-activated receptor alpha (PPAR-α) and its target genes, and decreased sterol regulatory element binding protein-1c (SREBP-1c)-driven lipogenesis. These changes halted fibrosis progression, as confirmed by Picro-Sirius Red staining and fibrosis markers. Conclusions: these findings indicate that Complex I modulation may represent a promising strategy to counteract MASLD progression toward MASH. Full article