Targeting GPX4 in neurodegenerative disorder: Unlocking ferroptosis as a therapeutic frontier.

Integrated transcriptomic and metabolomic analysis of intestinal responses of Litopenaeus vannamei under acute freshwater stress.

Refrigerated braised beef: Impacts of different preservation strategies on dominant spoilage microbiota dynamics, flavor profiles, and metabolism.

Astragalin alleviates ulcerative colitis via FPR1 inhibition and restores Microbiota-Metabolite Homeostasis: A mechanism revealed by deep learning.

Radiotherapy represents a cornerstone treatment modality in oncology and primarily mediates tumor cell death through the generation of reactive oxygen species (ROS). Nevertheless, elevated glutathione (GSH) levels within tumor cells can scavenge these ROS, thereby compromising the efficacy of radiotherapy and promoting the emergence of radioresistance. The contemporary understanding of redox regulation in cancer underscores the strategic relevance of targeting GSH metabolism in the context of radiotherapy. This review comprehensively describes the mechanisms through which GSH metabolism contributes to radioresistance and surveys novel therapeutic approaches aimed at inhibiting GSH synthesis or promoting its depletion to achieve radiosensitization. Both pharmacological compounds and nanotechnology‑enabled delivery systems have been investigated, with an emphasis on their ability to intensify oxidative stress in tumors characterized by high GSHcontent, thus potentially improving radiotherapeutic outcomes.

Omics insights into the mechanisms of flavor changes in Eriocheir sinensis under different restraint methods during live transportation.

Interaction of nanoplastics and atrazine in a hydroponic system: Antagonistic phytotoxicity mediated by plant-microbe crosstalk and root endophytic bacteria restructuring.

Glutathione decline coordinates mitochondria to license histone acetylation and zygotic genome activation.

Propyl gallate mitigates diabetic liver injury via suppressing SLC7A11/GPX4-mediated hepatic ferroptosis and modulating gut-liver axis.

Phthalate esters (PAEs) are emerging atmospheric contaminants in facility agriculture, yet their foliar transformations and phytotoxic mechanisms remain unclear. We compared the uptake, translocation, metabolism, and physiological effects of dibutyl phthalate (DBP) and di(2-ethylhexyl) phthalate (DEHP) in lettuce after foliar exposure. The more hydrophobic DEHP accumulated in cuticular wax and leaves and caused oxidative lipid damage, whereas DBP was weakly retained in wax, translocated more readily to roots, and elicited stronger antioxidant responses. Both compounds were converted to monoesters, which accumulated at higher concentrations than their parent PAEs. Metabolomics revealed that DBP specifically upregulated arginine metabolism, suggesting an enhanced defense, whereas DEHP was associated with glutathione metabolism and ABC transporter pathways, consistent with responses to membrane peroxidation. These findings show that PAE physicochemical properties govern their fate in plants and drive compound-specific metabolic disturbances with important implications for crop safety under atmospheric PAE pollution.

Volatile organic compounds from the salt-tolerant Glutamicibacter halophytocola KLBMP 5180 enhance salt stress tolerance in tomato seedlings by regulating antioxidant defense, ion homeostasis, and auxin, jasmonic acid/ethylene signaling pathways.

The mechanism of oxidative stress induced by nanoplastics in Caenorhabditis elegans: Integrated analysis of transcriptomics and metabolomics.

Integrated phenotypic, physiological, transcriptomic and metabolomic analyses uncover the mechanisms underlying root and leaf responses of Osmanthus fragrans to Pb toxicity.

Zearalenone induces hepatic metabolic disruption in common carp: Multi-omics evidence linking to the gut microbiota-PPARδ axis.

Against a backdrop of increasingly severe marine heavy-metal pollution, bioaccumulation now poses a grave threat to aquaculture species and sector sustainability. To investigate the response mechanisms of bivalve mollusks under heavy metal stress, Crassostrea hongkongensis were exposed to 0.506 mg/L Hg (96-h LC 50 ) in filtered seawater. The activities of antioxidant enzymes were subsequently measured at 0 h, 24 h, 48 h, 72 h, and 96 h post-exposure, while transcriptomic and metabolomic analyses were performed on hepatopancreas samples collected at designated time points. The results showed that the antioxidant enzyme responses, including SOD, CAT, and GSH-Px, were both time- and tissue-dependent. While activities in the adductor muscle, gills, and mantle peaked at 24 h before declining, the hepatopancreas showed significant suppression until 72 h, followed by partial recovery at 96 h, indicating the activation of tissue-specific repair mechanisms against prolonged oxidative stress. Transcriptome sequencing revealed 5383 DEGs enriched in the NF-κB and Lysosome pathways. Metabolomics analysis identified 297 and 181 unique DEMs in positive and negative ion modes, respectively, with significant enrichment in key metabolic pathways such as amino acid and pyruvate metabolism. Integrated analysis revealed co-enrichment of DEGs and DEMs across 119 pathways including Lysosome and Glutathione metabolism, which demonstrate C. hongkongensis counteracts Hg toxicity through coordinated activation of antioxidant, detoxification, and immune responses. This study reveals the comprehensive mechanisms by which C. hongkongensis adapts to Hg-induced stress, providing candidate biomarkers for early warning of coastal Hg pollution and laying a theoretical foundation for stress-resilient breeding in shellfish. • Hepatopancreas exhibits unique suppression-recovery antioxidant pattern under Hg stress in C. hongkongensis . • Integrated transcriptomic and metabolomic analysis reveals 5383 DEGs and 478 DEMs under Hg exposure. • Glutathione and cytochrome P450 pathways co-enriched, indicating coordinated detoxification response. • Hg exposure activates NF-κB and NOD-like receptor innate immune pathways in the oyster hepatopancreas.

A systems-level understanding of Radix Bupleuri-Radix Paeoniae Alba in depression: multi-omics reveals synergistic regulation of Neuroinflammation and synaptic plasticity.

Glutathione depletion activates cGAS-STING signaling via oxidative stress in preeclampsia.

A multimodal ROS logic-gated therapeutic platform disrupts the vicious cycle of senescence to promote aged bone defect repair.

Thielaviopsis paradoxa is a widespread soil-borne fungus and a major pathogen of oil palm, responsible for substantial yield losses worldwide. Understanding host–pathogen interactions is critical for developing resistant cultivars. In this study, we examined the pathogenicity and transcriptomic responses of two oil palm cultivars, Tenera and Malaysian Dwarf, following inoculation with 11 T. paradoxa isolates, including the highly virulent DA002 and the low-virulence AA034. Pathogenicity assays revealed strong isolate- and cultivar-dependent disease outcomes: Tenera was highly susceptible to DA002, displaying chlorosis, spear collapse, and tissue necrosis, whereas Malaysian Dwarf remained asymptomatic with both isolates, reflecting enhanced tolerance. Transcriptome profiling identified 2,093 and 1,577 differentially expressed genes (DEGs) in Tenera and Malaysian Dwarf, respectively, following DA002 infection, compared with 1,130 and 244 DEGs after AA034 infection. Tenera mounted a broad but energetically costly defense, characterized by mixed regulation of PR proteins, R-gene homologs, receptor-like kinases, oxidative enzymes, and phenylpropanoid, flavonoid, and lignin biosynthesis genes. In contrast, Malaysian Dwarf exhibited a targeted and coordinated transcriptional response, including selective activation of glutathione metabolism and antioxidant enzymes to maintain redox balance, alongside efficient upregulation of secondary metabolite pathways, such as alkaloids, terpenoids, and phenylpropanoids. This integrated strategy likely underlies its asymptomatic phenotype and effective containment of pathogen colonization within the duration of the experiment. Functional enrichment analyses revealed cultivar- and isolate-specific activation of immune components, ROS detoxification, and specialized metabolism, highlighting how host genetic and physiological traits shape responses to pathogen virulence. Collectively, these findings elucidate the relationship between pathogen virulence, host transcriptional reprogramming, and cultivar-specific defense strategies, providing a molecular basis for breeding of oil palm varieties with improved disease resistance and sustainable yield performance. • Pathogenicity of Thielaviopsis paradoxa varies strongly with isolate virulence and oil palm cultivar. • The virulent isolate DA002 causes severe disease in Tenera but not in Malaysian Dwarf. • Tenera activates a broad, energetically costly defense involving PR genes, RLKs, and phenylpropanoid pathways. • Malaysian Dwarf mounts a targeted defense emphasizing redox balance and secondary metabolism. • Cultivar-specific transcriptional strategies explain tolerance and disease containment in oil palm.

Metabolomic cues from Salmonella Typhi drive neuroimmune modulations and behavioural adaptation in Caenorhabditis elegans.