Sci Rep. 2025 Apr 30;15(1):15201. doi: 10.1038/s41598-025-97684-y.

ABSTRACT

Boolean networks (BNs) are vital modeling tools in systems biology for biomolecular regulatory networks. After a transient phase, BNs converge to attractors that represent distinct cell types or conditions. Therefore, methods to control the long-term behavior of BNs have important implications for biological and genetic applications. In this paper, we propose a method to enforce convergence of a BN to a desired attractor from any initial state through a simple intervention: fixing a specific subset of network variables at definite values. We refer to this method as the global stabilization of a BN to a target attractor. Utilizing the algebraic state space representation of BNs, we introduce novel matrix tools to formulate this intervention method, as well as develop a foundation for analyzing the stabilizability of BNs. We derive necessary and sufficient conditions for the global stabilizability of BNs and utilize these criteria to identify a minimal subset of network variables-termed the global stabilizing kernel-whose regulation ensures that the BN converges to the desired attractor. Finally, we apply our proposed method to determine the stabilizing kernels of several biomolecular regulatory network models and demonstrate how they can be steered to their target attractors, showcasing the applicability of our approach. We also apply our method to identify the stabilizing kernels of 480 randomly generated BNs. Our experiments suggest that, on average, only a relatively small portion (approximately 25%) of the network nodes need to be manipulated for the networks to converge to their primary attractors.

PMID:40307350 | DOI:10.1038/s41598-025-97684-y

J Theor Biol. 2025 Apr 28:112135. doi: 10.1016/j.jtbi.2025.112135. Online ahead of print.

ABSTRACT

During the COVID-19 pandemic, the emergence of novel variants of concern (VoCs) prompted different responses from governments across the world aimed at mitigating the impacts of more transmissible or more harmful strains. We model the invasion of a novel VoC into a population with heterogeneous vaccine- and infection-acquired immunity using a multi-type branching process framework with immigration. We define the number of cases needed to be reached to ensure stochastic extinction of this strain is unlikely and, therefore, the strain has become established in the population. To estimate the first-passage time distribution to reach this number of cases we use a mixture of stochastic simulations and analytic results. The first-passage time distribution gives a time window that is useful for policymakers planning interventions aimed at suppressing or delaying the introduction of novel VoC. We apply our method to a model of COVID-19 in the United Kingdom, though our results are applicable to other pathogens and settings.

PMID:40306569 | DOI:10.1016/j.jtbi.2025.112135

Clin Immunol. 2025 Apr 28:110507. doi: 10.1016/j.clim.2025.110507. Online ahead of print.

ABSTRACT

This study explores immune responses in mild Omicron-era COVID-19 breakthrough cases, focusing on cytokine dysregulation, antibody dynamics, and Long COVID. Samples from 114 mild COVID-19 patients across multiple waves were analyzed at three timepoints (T1: 2-4 weeks, T2: 3-4 months, T3: 6-8 months post-infection). Persistent IP-10 elevation up to 8 months suggests prolonged low-grade immune activation. Hybrid immunity from Omicron breakthrough infections provided broad cross-variant antibody recognition but showed declining neutralization over time. Among vaccination regimens, mRNA-inclusive combinations were associated with lower Long COVID scores. CoV-229E antibody levels correlated with Long COVID scores. These findings underscore the need for extended monitoring of mild COVID-19 cases and highlight the potential of mRNA vaccines in reducing post-COVID-19 complications. Insights into immune alterations and vaccine effects can inform the development of future vaccination strategies and approaches for managing post-COVID-19 conditions.

PMID:40306350 | DOI:10.1016/j.clim.2025.110507

Semin Cell Dev Biol. 2025 Apr 29;171:103612. doi: 10.1016/j.semcdb.2025.103612. Online ahead of print.

ABSTRACT

Cardiovascular diseases remain the leading cause of death worldwide-claiming one-third of all deaths every year. Current two-dimensional in vitro cell culture systems and animal models cannot completely recapitulate the clinical complexity of these diseases in humans. Therefore, there is a dire need for higher fidelity biological systems capable of replicating these phenotypes to inform clinical outcomes and therapeutic development. Cardiac tissue engineering (CTE) strategies have emerged to fulfill this need by the design of in vitro three-dimensional myocardial tissue systems from human pluripotent stem cells. In this way, CTE systems serve as highly controllable human models for a variety of applications-including for physiological and pathological modeling, drug discovery and preclinical testing platforms, and even direct therapeutic interventions in the clinic. Although significant progress has been made in the development of these CTE technologies, critical challenges remain and necessary refinements are required to derive more advanced human heart tissue technologies. In this review, we distill three focus areas for the field to address: I) Generating cardiac muscle cell types and scalable manufacturing methods, II) Engineering tissue structure, function, and analyses, and III) Curating system design for specific application. In each of our focus areas, we emphasize the importance of designing CTE systems capable of mimicking the intricate intercellular connectivity of the human heart and discuss fundamental design considerations that subsequently arise. We conclude by highlighting cutting-edge applications that use CTE technologies for clinical modeling and the direct repair of damaged and diseased hearts.

PMID:40306230 | DOI:10.1016/j.semcdb.2025.103612

Biomed Pharmacother. 2025 Apr 29;187:118088. doi: 10.1016/j.biopha.2025.118088. Online ahead of print.

ABSTRACT

Mitochondrial dysfunction and mitophagy are closely linked with human diseases such as neurodegenerative diseases, metabolic diseases, and cancer. High-mobility group box 1 (HMGB1) has been shown to mediate a wide range of pathological responses by binding with the receptor for advanced glycation end-products (RAGE) and toll-like receptors (TLRs). Extracellular HMGB1 and its ligand RAGE stimulate the growth, metastasis, invasiveness, and treatment resistance of different cancer cells. Through extracellular signal-regulated kinase 1/2 (ERK1/2) signaling, HMGB1 and RAGE lead to the phosphorylation of Drp1-S616 and Drp1-mediated mitochondrial fission, which consequently causes autophagy. Although the structure of the RAGE and HMGB1 complex is not clearly known, the complex has emerged as a potential therapeutic target. In the present study, the structure of the RAGE and HMGB1 complex was determined at a resolution of 5.19 Å using cryogenic electron microscopy. The structure revealed that the residues P66, G70, P71, S74, and R77 in RAGE and E145, K146, E153, and E156 in HMGB1 were the sites of interaction between the two proteins. Additionally, an HMGB1 peptide (151 LKEKYEK 157) was synthesized based on the RAGE-HMGB1 complex. We investigated the inhibitory function of the HMGB1 peptide and demonstrated that it inhibits tumor growth, metastasis, and invasion by binding to the RAGE protein in lung cancers. The HMGB1 peptide significantly suppressed mitochondrial dysfunction and the initiation of autophagy. Furthermore, the HMGB1 peptide dramatically reduced cell viability, migration, and mitophagy in the colorectal and pancreatic cancer cell lines HCT-116 and AsPC-1, respectively.

PMID:40306174 | DOI:10.1016/j.biopha.2025.118088

Biomolecules. 2025 Mar 26;15(4):485. doi: 10.3390/biom15040485.

ABSTRACT

Calcium is a ubiquitous second messenger and plays a major role in a variety of cellular functions, both within the same cell and between different cells [...].

PMID:40305225 | DOI:10.3390/biom15040485

Chem Commun (Camb). 2025 Apr 30. doi: 10.1039/d5cc00961h. Online ahead of print.

ABSTRACT

Mitochondrial autophagy is closely related to abnormal NAD(P)H and pH. Here, we synthesized a dual-response fluorescent probe with high selectivity for NAD(P)H and sensitivity in the physiological pH range, for simultaneous imaging analysis of mitochondrial NAD(P)H and pH, holding potential as a novel tool for understanding mitochondria-associated diseases.

PMID:40305089 | DOI:10.1039/d5cc00961h

Elife. 2025 Apr 30;12:RP90668. doi: 10.7554/eLife.90668.

ABSTRACT

The Staphylococcus aureus clonal complex 8 (CC8) is made up of several subtypes with varying levels of clinical burden; from community-associated methicillin-resistant S. aureus USA300 strains to hospital-associated (HA-MRSA) USA500 strains and ancestral methicillin-susceptible (MSSA) strains. This phenotypic distribution within a single clonal complex makes CC8 an ideal clade to study the emergence of mutations important for antibiotic resistance and community spread. Gene-level analysis comparing USA300 against MSSA and HA-MRSA strains have revealed key horizontally acquired genes important for its rapid spread in the community. However, efforts to define the contributions of point mutations and indels have been confounded by strong linkage disequilibrium resulting from clonal propagation. To break down this confounding effect, we combined genetic association testing with a model of the transcriptional regulatory network (TRN) to find candidate mutations that may have led to changes in gene regulation. First, we used a De Bruijn graph genome-wide association study to enrich mutations unique to the USA300 lineages within CC8. Next, we reconstructed the TRN by using independent component analysis on 670 RNA-sequencing samples from USA300 and non-USA300 CC8 strains which predicted several genes with strain-specific altered expression patterns. Examination of the regulatory region of one of the genes enriched by both approaches, isdH, revealed a 38-bp deletion containing a Fur-binding site and a conserved single-nucleotide polymorphism which likely led to the altered expression levels in USA300 strains. Taken together, our results demonstrate the utility of reconstructed TRNs to address the limits of genetic approaches when studying emerging pathogenic strains.

PMID:40305082 | DOI:10.7554/eLife.90668

Proc Natl Acad Sci U S A. 2025 May 6;122(18):e2427151122. doi: 10.1073/pnas.2427151122. Epub 2025 Apr 30.

ABSTRACT

In the common cellular space, hundreds of binding reactions occur reliably and simultaneously without disruptive mutual interference. The design principles that enable this remarkable compatibility have not yet been adequately elucidated. In order to delineate these principles, we consider the intracellular sensing of transition metals in bacteria-an integral part of cellular metal homeostasis. Protein cytosolic sensors typically interact with metals through three types of lateral chain residues, containing oxygen, nitrogen, or sulfur. The very existence of complete sets of mutually compatible sensors is a nontrivial problem solved by evolution, since each metal sensor has to bind to its cognate metal without being "mismetallated" by noncognate competitors. Here, based solely on theoretical considerations and limited information about binding constants for metal-amino acid interactions, we are able to predict possible "sensor compositions," i.e., the residues forming the binding sites. We find that complete transition-metal sensor sets are severely limited in their number by compatibility requirements, leaving only a handful of possible sensor compositions for each transition metal. Our theoretical results turn out to be broadly consistent with experimental data on known bacterial sensors. If applicable to other cytosolic binding interactions, the results generated by our approach imply that compatibility requirements may play a crucial role in the organization and functioning of intracellular processes.

PMID:40305046 | DOI:10.1073/pnas.2427151122

Microbiol Spectr. 2025 Apr 30:e0284824. doi: 10.1128/spectrum.02848-24. Online ahead of print.

ABSTRACT

As primary colonizers of the tooth surface, oral streptococci play a crucial role in dental caries development. Numerous natural compounds, including flavonoids, are emerging as promising agents for inhibiting dental biofilm formation without compromising bacterial viability, underscoring their potential in non-bactericidal antibiofilm strategies. This study investigated the effects and mechanism of action of the unmodified plant flavonoid cyanidin on the growth and sucrose-dependent biofilm formation of oral streptococci, with a particular focus on the cariogenic pathogen Streptococcus mutans. At concentrations above 100 µg/mL, cyanidin significantly inhibited biofilm formation by S. mutans without impacting bacterial viability. The flavonoid reduced the biomass of surface-associated bacteria and exopolysaccharides (EPS), particularly by inhibiting water-insoluble glucan (WIG) production mediated by the glucosyltransferases GtfB and GtfC. While cyanidin did not exhibit a bactericidal effect on early colonizer streptococci, such as Streptococcus sanguinis, Streptococcus gordonii, Streptococcus oralis, and Streptococcus mitis, it showed a significant inhibitory effect on bacterial acidogenicity and mixed-species streptococcal biofilms in the presence of S. mutans. Remarkably, cyanidin gradually reduced the proportion of S. mutans in the mixed biofilm, suggesting a selective impact that may promote a more commensal-dominant community by disrupting S. mutans glucan production and biofilm competitiveness.

IMPORTANCE: The identification of compounds with potent antibiofilm effects that do not compromise bacterial viability presents a promising strategy for oral health management. By preventing biofilm formation and keeping bacteria in a planktonic state, such agents could enhance bacterial susceptibility to targeted therapies, including probiotics or phage-based treatments. Cyanidin, which exhibits strong antibiofilm activity against oral streptococcal biofilms, reduces bacterial acidogenicity and may promote a more commensal-dominant biofilm in vitro, potentially hindering the maturation of cariogenic biofilms.

PMID:40304465 | DOI:10.1128/spectrum.02848-24

Phys Chem Chem Phys. 2025 Apr 30. doi: 10.1039/d5cp00604j. Online ahead of print.

ABSTRACT

Gas-phase activation and dissociation studies of biomolecules, proteins and their non-covalent complexes using X-rays hold great promise for revealing new insights into the structure and function of biological samples. This is due to the unique properties of X-ray molecular interactions, such as site-specific and rapid ionization. In this perspective, we report and discuss the promise of first proof-of-principle studies of X-ray-induced dissociation of native (structurally preserved) biological samples ranging from small 17 kDa monomeric proteins up to large 808 kDa non-covalent protein assemblies conducted at a synchrotron (PETRA III) and a free-electron laser (FLASH2). A commercially available quadrupole time-of-flight mass spectrometer (Q-Tof Ultima US, Micromass/Waters), modified for high-mass analysis by MS Vision, was further adapted for integration with the open ports at the corresponding beamlines. The protein complexes were transferred natively into the gas phase via nano-electrospray ionization and subsequently probed by extreme ultraviolet (FLASH2) or soft X-ray (PETRA III) radiation, in either their folded state or following collision-induced activation in the gas phase. Depending on the size of the biomolecule and the activation method, protein fragmentation, dissociation, or enhanced ionization were observed. Additionally, an extension of the setup by ion mobility is described, which can serve as a powerful tool for structural separation of biomolecules prior to X-ray probing. The first experimental results are discussed in the broader context of current and upcoming X-ray sources, highlighting their potential for advancing structural biology in the future.

PMID:40304431 | DOI:10.1039/d5cp00604j

Nucleic Acids Res. 2025 Apr 22;53(8):gkaf355. doi: 10.1093/nar/gkaf355.

ABSTRACT

The structure-specific endonuclease, XPF-ERCC1, plays a central role in DNA damage repair. This nuclease is known to be important for nucleotide excision repair, interstrand crosslink repair, and DNA double-strand repair. We found that the arginine methyltransferase, CARM1/PRMT4, is essential for XPF stabilization and maintenance of intracellular protein levels. Loss of CARM1 results in a decrease in XPF protein levels and a concomitant decrease in ERCC1 protein. A similar destabilization of XPF protein was observed in cells expressing a mutant in which XPF arginine 568 was replaced by lysine. Loss of CARM1 impaired XPF-ERCC1 accumulation at the site of damage and delayed removal of cyclobutane pyrimidine dimers by UV. As a result, CARM1-deficient cells showed increased UV sensitivity. Our results provide insight into the importance of CARM1 not only in the mechanism of XPF-ERCC1 complex stabilization but also in the maintenance of genome stability.

PMID:40304182 | DOI:10.1093/nar/gkaf355

Front Plant Sci. 2025 Apr 15;16:1539641. doi: 10.3389/fpls.2025.1539641. eCollection 2025.

ABSTRACT

Peanut (Arachis hypogaea L.), a key oilseed crop in the U.S., plays a significant role in agriculture and the economy but faces challenges from biotic and abiotic stresses, including aflatoxin contamination caused by Aspergillus flavus and A. parasiticus. Despite many large-effect QTLs identified for yield and key traits, their use in breeding is limited by unfavorable genetic interactions. To overcome this, we aimed to identify consensus genomic regions and candidate genes linked to key traits by analyzing QTL data from 30 independent studies conducted over the past 12 years, focusing on biotic, abiotic, aflatoxin, morphological, nutritional, phenological, and yield-associated traits. Using genetic map information, we constructed consensus maps and performed a meta-analysis on 891 QTLs, leading to the identification of 70 Meta-QTLs (MQTLs) with confidence intervals ranging from 0.07 to 9.63 cM and an average of 2.33 cM. This reduction in confidence intervals enhances the precision of trait mapping, making the identified MQTLs more applicable for breeding purposes. Furthermore, we identified key genes associated with aflatoxin resistance in MQTL5.2 (serine/threonine-protein kinase, BOI-related E3 ubiquitin-protein ligase), MQTL5.3, MQTL7.3, and MQTL13.1. Similarly, for yield-related traits in MQTL3.1-MQTL3.4 (mitogen-activated protein kinase, auxin response factor), MQTL11.2 (MADS-box protein, squamosa promoter-binding protein), and MQTL14.1. Genes related to oil composition within MQTL5.2 (fatty-acid desaturase FAD2, linoleate 9S-lipoxygenase), MQTL9.3, MQTL19.1 (acyl-CoA-binding protein, fatty acyl-CoA reductase FAR1), MQTL19.4, and MQTL19.5. Nutritional traits like iron and zinc content are linked to MQTL1.1 (probable methyltransferase, ferredoxin C), MQTL10.1, and MQTL12.1. These regions and genes serve as precise targets for marker-assisted breeding to enhance peanut yield, resilience, and quality.

PMID:40303861 | PMC:PMC12038908 | DOI:10.3389/fpls.2025.1539641

Hortic Res. 2025 Mar 11;12(6):uhaf076. doi: 10.1093/hr/uhaf076. eCollection 2025 Jun.

NO ABSTRACT

PMID:40303429 | PMC:PMC12038890 | DOI:10.1093/hr/uhaf076

medRxiv [Preprint]. 2025 Apr 11:2025.04.11.25325572. doi: 10.1101/2025.04.11.25325572.

ABSTRACT

BACKGROUND: The catechol-O-methyltransferase (COMT) gene is involved in brain catecholamine metabolism, but its association with Parkinson's disease (PD) risk remains unclear.

OBJECTIVE: To investigate the relationship between COMT genetic variants and PD risk across diverse ancestries.

METHODS: We analyzed COMT variants in 2,251 PD patients and 2,835 controls of European descent using whole-genome sequencing from the Accelerating Medicines Partnership-Parkinson Disease (AMP-PD), along with 20,427 PD patients and 11,837 controls from 10 ancestries using genotyping data from the Global Parkinson's Genetics Program (GP2).

RESULTS: Utilizing the largest case-control datasets to date, no significant enrichment of COMT risk alleles in PD patients was observed across any ancestry group after correcting for multiple testing. Among Europeans, no correlations with cognitive decline, motor function, motor complications, or time to LID onset were observed.

CONCLUSIONS: These findings emphasize the need for larger, diverse cohorts to confirm the role of COMT in PD development and progression.

PMID:40297458 | PMC:PMC12036390 | DOI:10.1101/2025.04.11.25325572

Genome Biol. 2025 Apr 29;26(1):109. doi: 10.1186/s13059-025-03565-y.

ABSTRACT

Normalization of spatial transcriptomics data is challenging due to spatial association between region-specific library size and biology. We develop SpaNorm, the first spatially-aware normalization method that concurrently models library size effects and the underlying biology, segregates these effects, and thereby removes library size effects without removing biological information. Using 27 tissue samples from 6 datasets spanning 4 technological platforms, SpaNorm outperforms commonly used single-cell normalization approaches while retaining spatial domain information and detecting spatially variable genes. SpaNorm is versatile and works equally well for multicellular and subcellular spatial transcriptomics data with relatively robust performance under different segmentation methods.

PMID:40301877 | DOI:10.1186/s13059-025-03565-y

BMC Infect Dis. 2025 Apr 29;25(1):623. doi: 10.1186/s12879-025-10992-6.

ABSTRACT

BACKGROUND: The management of many chronic diseases requires a multidisciplinary and holistic approach. Long Covid is a recent, poorly understood disease with several symptoms. Most recommendations suggest a multidisciplinary approach. While there are a few programs aimed to the management of Long Covid, to our knowledge very few were assessed. The SPACO + study therefore aims to evaluate an innovative program which combines the methods used in therapeutic education and in personalized multifactorial intervention for management of Long Covid. Here, we present the protocol of our study, which aims to evaluate the effectiveness of an educational intervention in terms of changes in quality of life at 6 months in comparison with standard clinical practice in patients suffering from Long Covid.

METHODS: To achieve our objectives, we have planned to carry out a prospective, multicentre, two-arm randomized controlled trial with a convergent parallel mixed methods design. Two countries are involved in this study: France and Cameroon. The study concerns patients aged 18 and over, who have been infected with Covid-19. They must also be diagnosed as having Long Covid in accordance with the WHO definition. The number of subjects required for the study is 400 individuals. Participants will be randomly assigned to either the intervention or control group using a dynamic randomization process to ensure balanced group characteristics. The SPACO + program is an educative intervention with individual follow-up by a nurse dedicated to the program. The SPACO + program offers five workshops, two of which are compulsories. Patients take part in the other workshops according to their needs. The program includes an 8 - 10 weeks intervention period. Each session lasts two hours and includes breaks (pacing). The main outcome measure will be quality of life, evaluated through the SF-36. Primary and secondary outcomes, with few exceptions, are assessed before the intervention ("T0"), at 8 weeks ("T1" corresponding to the end of SPACO + program's session period) and then 3 months later ("T2").

DISCUSSION: If the SPACO + program is effective and accepted by professionals and patients, it could be disseminated in other regions to assess its transferability. The medico-economic evaluation will also make it possible to assess the benefits provided.

TRIAL REGISTRATION: This trial is registered under the number NCT05787366 (March 24, 2023). Protocol Version N°3.0 (May 31, 2024).

PMID:40301772 | DOI:10.1186/s12879-025-10992-6

Nat Biotechnol. 2025 Apr 29. doi: 10.1038/s41587-025-02660-6. Online ahead of print.

ABSTRACT

Microbiomes are complex communities of microorganisms that are essential for biochemical processes on Earth and for the health of humans, animals and plants. Many environmental and host-associated microbiomes are dominated by anaerobic microbes, some of which cannot tolerate oxygen. Anaerobic microbial communities have been extensively studied over the last 20 years using molecular techniques, especially next-generation sequencing. However, there is a renewed interest in microbial cultivation because isolates provide the basis for understanding the taxonomic and functional units of biodiversity, elucidating novel biochemical pathways and the mechanisms underlying microbe-microbe and microbe-host interactions and opening new avenues for biotechnological and clinical applications. In this Perspective, we present areas of research and applications that will benefit from advancement in anaerobic microbial cultivation. We highlight key technical and infrastructural hurdles associated with the development and deployment of sophisticated cultivation workflows. Improving the performance of cultivation techniques will set new trends in functional microbiome research in the coming years.

PMID:40301656 | DOI:10.1038/s41587-025-02660-6

Cell Death Differ. 2025 Apr 29. doi: 10.1038/s41418-025-01514-7. Online ahead of print.

ABSTRACT

Ferroptosis and apoptosis are widely considered to be independent cell death modalities. Ferroptotic cell death is a consequence of insufficient radical detoxification and progressive lipid peroxidation, which is counteracted by glutathione peroxidase-4 (GPX4). Apoptotic cell death can be triggered by a wide variety of stresses, including oxygen radicals, and can be suppressed by anti-apoptotic members of the BCL-2 protein family. Mitochondria are the main interaction site of BCL-2 family members and likewise a major source of oxygen radical stress. We therefore studied if ferroptosis and apoptosis might intersect and possibly interfere with one another. Indeed, cells dying from impaired GPX4 activity displayed hallmarks of both ferroptotic and apoptotic cell death, with the latter including (transient) membrane blebbing, submaximal cytochrome-c release and caspase activation. Targeting BCL-2, MCL-1 or BCL-XL with BH3-mimetics under conditions of moderate ferroptotic stress in many cases synergistically enhanced overall cell death and frequently skewed primarily ferroptotic into apoptotic outcomes. Surprisingly though, in other cases BH3-mimetics, most notably the BCL-XL inhibitor WEHI-539, counter-intuitively suppressed cell death and promoted cell survival following GPX4 inhibition. Further studies revealed that most BH3-mimetics possess previously undescribed antioxidant activities that counteract ferroptotic cell death at commonly employed concentration ranges. Our results therefore show that ferroptosis and apoptosis can intersect. We also show that combining ferroptotic stress with BH3-mimetics, context-dependently can either enhance and convert cell death outcomes between ferroptosis and apoptosis or can also suppress cell death by intrinsic antioxidant activities.

PMID:40301648 | DOI:10.1038/s41418-025-01514-7

Sci Rep. 2025 Apr 29;15(1):15049. doi: 10.1038/s41598-025-99425-7.

ABSTRACT

This study investigates the impact of irrigation water sources on the quality of olive oil from the Chemlal olive variety in the Hadjadj region, northeast of Mostaganem, Algeria, a coastal area known for its semi-arid climate and intensive olive cultivation. Olive trees (n = 50 per irrigation group) were irrigated with treated wastewater, spring water, and normal water, and the resulting oils were assessed for physicochemical properties, fatty acid composition, and bioactive compound profiles. Treated wastewater demonstrated distinct water quality characteristics, including elevated temperature (15.00 °C), chemical oxygen demand (COD: 58.38 mg/L), biochemical oxygen demand (BOD5: 29.00 mg/L), ammonium (15.60 mg/L), nitrite (2.55 mg/L), suspended solids (14.00 mg/L), pH (7.40), and conductivity (2.80 µS/cm), reflecting residual organic material and ionic content post-treatment. Heavy metal concentrations in all water sources were within permissible limits for irrigation and drinking purposes, affirming their safety for agricultural use. Olive oil from treated wastewater-irrigated trees exhibited superior quality parameters, including low acidity (1.99%), low peroxide value (6.8 meq O2/kg), enhanced oxidative stability, higher fat content (96.5%), and favorable saponification values. Fatty acid analysis revealed a higher oleic acid content (62.6 mg/kg), known for cardiovascular health benefits. Bioactive compound analysis indicated significantly elevated levels of α-tocopherol (180.25 mg/kg), squalene (7500.8 mg/kg), carotenoids (25.1 mg/kg), and polyphenols (604.76 mg GAE/kg), contributing to increased antioxidant capacity (63.50% DPPH inhibition, a measure of free radical scavenging) and lower lipid peroxidation (0.25 TBARS, an index of oxidative degradation), indicative of superior oxidative stability. Spring water-irrigated oils showed higher acidity, peroxide values, and linoleic acid concentrations, alongside notable antibacterial efficacy against Escherichia. coli, Pseudomonas. aeruginosa, and Staphylococcus. aureus. Oils from normal water irrigation were characterized by higher linolenic acid levels, providing a more balanced fatty acid profile. These findings underscore treated wastewater's potential to enhance olive oil's nutritional and functional qualities, particularly its antioxidant activity and stability, while highlighting the role of spring water in enhancing antibacterial properties despite slightly reduced antioxidant stability. These findings are relevant to water-scarce Mediterranean and arid regions, informing sustainable irrigation strategies in line with global climate-resilient agriculture policies.

PMID:40301569 | DOI:10.1038/s41598-025-99425-7