Huntington’s disease (HD) is an inherited progressive neurodegenerative disorder marked by motor impairments, oxidative stress, neuroinflammation, and selective neuronal loss. The 3-nitropropionic acid (3-NP)-induced rat model recapitulates key pathological features of HD. Baicalein, a naturally occurring flavonoid, recognized for its anti-inflammatory and antioxidant properties. This study investigates the neuroprotective efficacy of Baicalein against 3-NP-induced HD-like neurotoxicity, with a specific emphasis on the initiation of Nrf2 signalling pathway. For this study male Wistar rats were allocated into five groups: Saline control, 3-NP alone (10 mg/kg) and 3-NP co-treated with Baicalein at doses of 50, 100, and 150 mg/kg. Behavioural performance was assessed using the rotarod, open field, and grip strength tests. Biochemical parameters such as reduced glutathione (GSH), superoxide dismutase (SOD), succinate dehydrogenase (SDH), lipid peroxidation (LPO), and nitrite level were quantified. Pro-inflammatory cytokines (IL-6, TNF-α, and IL-1β), Neurotransmitters (GABA and Glutamate), and Nrf2 level were also measured. Histopathological analysis of brain tissues (cortex) was conducted to evaluate neuropathological changes. Baicalein administration significantly ameliorated motor deficits and improved muscle strength in a dose dependent manner. It restored antioxidant enzyme levels (GSH, SOD, SDH), enhanced Nrf2 expression, and attenuated oxidative and nitrosative stress (LPO and nitrite levels). Additionally, Baicalein markedly suppressed the upregulation of pro-inflammatory cytokines and normalized neurotransmitter imbalances induced by 3-NP. Histological examination revealed a reduction in neuronal degeneration, particularly at the highest dose (150 mg/kg). Thus, Baicalein exhibited significant neuroprotective effects in the 3-NP-induced experimental model of HD. Its modulation of the Nrf2 pathway, along with the attenuation of oxidative damage, and neuroinflammation, highlights its potential as a therapeutic candidate for HD management.
To investigate the potential association between di(2-ethylhexyl) phthalate (DEHP) and psoriasis using an integrated approach that combines network toxicology, bioinformatics, and computational simulations. We identified shared targets between DEHP and psoriasis from public databases. Differential expression genes in the GSE13355 dataset were analyzed to obtain potential targets of DEHP-induced psoriasis. Core genes were screened using machine learning algorithms (LASSO and Random Forest) and validated in the GSE226244 dataset. Enrichment analysis, immune infiltration assessment, molecular docking, and molecular dynamics (MD) simulations were performed to explore underlying mechanisms and binding stability. A total of 453 shared targets were identified, and 34 potential targets were derived from differential expression analysis. Six core genes—AKR1B10, S100A9, TGM1, CLEC7A, CXCR2, and CCR7—were selected and showed significant upregulation in psoriatic lesions, with high diagnostic value (cross-validated AUC > 0.951). Enrichment analysis linked these genes to pathways such as viral protein–cytokine receptor interaction, chemokine signaling, cornified envelope formation, and cytokine–cytokine receptor interaction. Immune infiltration analysis revealed moderate correlations with neutrophils and activated CD4+ T cells. Molecular docking showed a moderate binding affinity for DEHP-AKR1B10 (− 8.7 kcal/mol), and MD simulations indicated relatively stable binding of the complex under simulated conditions (supported by consistent RMSD, Rg, RMSF, and SASA values). These computational findings suggest that DEHP may influence psoriasis through multi-target and multi-pathway mechanisms. However, experimental and epidemiological validation is required to confirm these predictions.
This study aimed to elucidate the molecular mechanisms underlying bisphenol A (BPA)-induced cytotoxicity in human retinal pigment epithelial (RPE) cells, focusing on oxidative stress-associated signaling pathways involved in retinal injury. Human RPE cells were exposed to BPA with or without the antioxidant N-acetylcysteine (NAC). We evaluated cell viability, membrane damage, intracellular reactive oxygen species (ROS), redox status, endoplasmic reticulum (ER) stress markers, oxidative DNA damage, autophagy, and apoptosis-related signaling pathways using biochemical, fluorescence-based, and immunoblotting analyses. BPA exposure significantly inhibited RPE cell viability and disrupted membrane integrity in a concentration-dependent manner. Intracellular ROS generation was markedly elevated, accompanied by a depletion of the GSH/GSSG ratio, indicating severe redox imbalance. NAC treatment effectively suppressed ROS accumulation and restored cell survival, suggesting that oxidative stress is a key mediator of BPA-induced cytotoxicity. BPA also triggered ER stress responses, evidenced by increased intracellular Ca2+ accumulation, PERK phosphorylation, and CHOP expression. Additionally, oxidative DNA damage was enhanced, as demonstrated by elevated levels of γH2AX and 8-hydroxy-2′-deoxyguanosine. BPA further stimulated autophagic activity, indicated by increased Cyto-ID fluorescence, LC3-II accumulation, and p62 degradation; these changes were attenuated by NAC co-treatment. Apoptotic cell death was subsequently induced, characterized by an increased Bax/Bcl-2 ratio, caspase-3 activation, and PARP cleavage, all of which were substantially reversed by antioxidant treatment. These findings demonstrate that BPA induces injury in RPE cells through ROS-mediated mechanisms involving Ca2+ imbalance, ER stress, oxidative DNA damage, autophagy activation, and apoptosis. These findings provide mechanistic evidence linking BPA exposure to RPE cell injury and suggest that antioxidant-based strategies warrant further investigation in physiologically relevant in vivo models as potential approaches for mitigating BPA-induced retinal damage.
Lead (Pb) is a persistent environmental toxicant that induces oxidative stress, disrupts antioxidant defenses, and causes cellular damage with effects that can persist across generations. This study uses Drosophila melanogaster to examine transgenerational oxidative and antioxidant dysregulation following maternal lead exposure. Wild-type Drosophila melanogaster (W1118) were maintained under controlled laboratory conditions on a standard cornmeal diet. In a randomized experimental design, parental flies (F0) were assigned to a control or a lead-exposed group. They received either a normal diet or one with 500 ppm lead acetate for 20 days. Transgenerational lineages (F1–F3) were produced through controlled crosses, with only maternal lead exposure transmitted. All offspring were reared on a lead-free diet. Oxidative stress was evaluated by measuring SOD, CAT, GSH, vitamins A, C, and E, and MDA using standard protocols. Expression of CAT and SOD1 was also assessed. Data were analyzed by one-way ANOVA followed by Tukey’s post hoc test and presented as mean ± SD. Maternal lead (Pb) exposure in D. melanogaster caused pronounced transgenerational oxidative stress, significantly affecting both enzymatic and non-enzymatic antioxidant defenses across four generations (F0–F3). In the F0 generation, direct exposure to Pb led to sharp reductions in GSH, vitamins A, C, and E, and suppressed CAT and SOD activities, while MDA levels were elevated, indicating enhanced lipid peroxidation (p < 0.05). These disruptions persisted in F1 and F2 progeny reared on a lead-free diet, with antioxidant molecules and enzyme activities remaining depleted and CAT and SOD1 mRNA downregulated. Recovery trends varied: in F1 and F2, females began to recover GSH and vitamin A earlier than males, while by F3, GSH and vitamin A levels returned to control values in most groups. However, SOD, CAT, vitamin C, vitamin E, and MDA levels remained significantly altered in both sexes in F3, indicating partial recovery and continued impairment of certain antioxidant pathways. Maternal lead exposure produced persistent transgenerational redox imbalance, marked by sex-specific recovery trajectories and enduring disruption of crucial antioxidant defenses.
To evaluate the knowledge, perceptions, and practices of Portuguese perinatal healthcare professionals regarding environmental and lifestyle exposures during the periconceptional period. Cross-sectional survey. An anonymous online questionnaire was distributed between September and December 2024 through professional associations, targeting gynecologist–obstetricians (senior and resident), nurses, and nutritionists. The survey assessed demographic and professional characteristics, routine screening of nine key exposures (smoking, alcohol use, occupational hazards, physical activity, environmental chemicals, diet, fish intake, drinking water source, and plastic use), perceived barriers, familiarity with ACOG/FIGO recommendations, and preferred educational formats. Logistic regression analyses explored associations between demographics and responses. A total of 126 professionals participated (87.3
This study evaluated the acute toxicity and interaction patterns of chromium (Cr), zinc (Zn), and copper (Cu) in single and combined exposures in Diaphanosoma celebensis, and examined associated transcriptional responses of antioxidant defense-related genes. Acute toxicity tests (48h) were conducted to determine LC50 values for single metals and binary/ternary mixtures. Mixture toxicity was assessed using toxicity units (TU) and compared with concentration addition (CA) and independent action (IA) models. Gene expression was analyzed by qRT-PCR after exposure to sublethal concentrations (1/10 and 1/2 LC50 or ΣTULC50). LC50 values were 2.342 mg/L for Cr, 2.256 mg/L for Zn, and 0.286 mg/L for Cu, indicating highest toxicity of Cu. Mixtures showed LC50 values of 2.533 mg/L (Cr–Zn), 5.414 mg/L (Cr–Cu), 2.546 mg/L (Zn–Cu), and 1.714 mg/L (Cr–Zn–Cu). Based on the ΣTULC50, Cr–Zn and Cr–Zn–Cu exhibited additive effects, whereas Zn–Cu and Cr–Cu showed antagonistic interactions. Gene expression analysis showed that single-metal exposure upregulated CuZn-SOD, catalase, Nrf, and GST-S. Under mixture exposure, Nrf was consistently upregulated in all groups, whereas GST-S and GST-mu were most strongly induced in the antagonistic Cr–Cu and Zn–Cu mixtures, suggesting distinct detoxification responses depending on metal combination. This study highlights that the toxicity of Cr, Zn, and Cu mixtures varies depending on metal combination, showing both additive and antagonistic interaction. The marked upregulation of GST-S and GST-mu in the antagonistic Cr–Cu and Zn–Cu mixtures suggests enhanced activation of glutathione-mediated detoxification pathways, although the underlying mechanisms require further investigation. Overall, these findings emphasize the importance of considering metal interactions and integrating molecular and organism-level endpoints in ecotoxicological assessment.
Calcium sulfide (CaS) nanoparticles are emerging luminescent materials with potential applications in optoelectronics and cancer therapeutics. Surface modification with polyethylene glycol (PEG) enhances their stability, dispersibility, and biocompatibility, making them suitable for biomedical use. PEG-capped CaS nanoparticles were synthesized via a solvothermal method at three different temperatures. Structural and morphological characteristics were evaluated using X-ray diffraction (XRD) and scanning electron microscopy (SEM). Optical properties were investigated using UV–visible spectroscopy and photoluminescence (PL) analysis. Crystallite size was estimated using the Debye–Scherrer equation. The optical bandgap was determined from Tauc plots. Cytotoxicity against MCF-7 human breast cancer cells was assessed using the MTT assay after 24 and 48 h incubation time. The XRD results revealed well-crystallized cubic CaS nanoparticles with average crystallite sizes ranging from 32 to 38 nm. The SEM images showed a transition from flake-shaped to nearly spherical morphology with increasing synthesis temperature. The PL emission spectra exhibited broad peaks from 350 to 580 nm, which were attributed to intrinsic point defects in the CaS host lattice. The samples prepared at 150 °C demonstrated superior structural and optical properties, with the highest bandgap of 4.94 eV. In vitro cytotoxicity studies on MCF-7 human breast cancer cells using the MTT assay revealed a significant reduction in cell viability with increasing nanoparticle concentrations, with an IC50 value of 114 µg/mL after 48 h of incubation time. PEG-capped CaS nanoparticles synthesized via solvothermal processing exhibit desirable structural, morphological, and luminescent properties, along with notable cytotoxic activity against breast cancer cells. These findings support their potential utility in optoelectronic devices and nanomedicine, particularly as promising candidates for anticancer applications.
Microplastics (MPs), which refer to plastic components less than 5 mm in diameter, have become a common pollutant in the environment as a result of the degradation of larger plastic materials and through spillage from packaging. Their existence in the drinking water sources has led to growing concerns on human exposure and possible health hazards. This paper is a narrative review of literature on microplastic contamination in drinking water, particularly in bottled water, sachet water, and tap water. Considerable scientific databases were sought out to find relevant studies which were then analyzed according to contamination levels, sources, methods of detection, and the effects reported on the health. Results have shown that microplastics are ubiquitous in all drinking water sources, and bottled water commonly has higher contamination rates than tap water, in large part because of packaging degradation during production, storage, and handling. Polymer degradation also correlates with contamination under environmental stressors, including heat and ultraviolet radiation, of sachet water which is a common consumption practice in West Africa. The satchet water is a source of invisible threat of microplastics pollution in Nigeria. Health effects that have been reported with exposure to microplastics include inflammation, activation of the immune system, endocrine disruption, and possible bioaccumulation of toxic substances. Contamination of drinking water with microplastic is a new public health issue, especially in areas that use packaged water extensively. Standardized detection methodologies, better water treatment technologies, and effective regulatory arrangements are in dire need. The future studies need to focus on long-term health effects studies, the construction of effective microplastic elimination measures, and adopting more environmentally friendly options such as plastic-free packaging.
Mosquito-borne diseases such as malaria, dengue, and chikungunya continue to pose major global public health challenges, aggravated by increased insecticide resistance and ecological concerns related to synthetic products. Seaweeds (marine macroalgae) are promising sources of secondary metabolites with diverse mosquitocidal properties. This review examines the diversity, chemical composition, and biological effects of seaweed-derived compounds, including phlorotannins, terpenoids, flavonoids, alkaloids, and halogenated derivatives, on mosquito vectors like Aedes aegypti, Anopheles stephensi, and Culex quinquefasciatus. These compounds exhibit ovicidal, larvicidal, pupicidal, adulticidal, and repellent activities by inhibiting acetylcholinesterase, inducing oxidative stress, disrupting hormonal balance, and causing tissue deterioration. Nanoparticle-based formulations further enhance the delivery and efficacy of seaweed-derived mosquitocidal compounds. The review discusses the potential integration of these compounds into integrated mosquito management (IMM) programs, including their ecological safety, non-target impacts, and biodegradability. Despite promising laboratory results, obstacles remain in standardizing extraction techniques, isolating compounds, obtaining regulatory permission, and implementing large-scale programs in the field. Future directions prioritize mechanistic validation, synergistic formulations, and uniform risk assessment frameworks to facilitate commercialization. This research highlights the potential of seaweed metabolites as eco-sustainable biopesticides, advocating for their integration into future mosquito control efforts.
Microcystin-LR (MC-LR) targets Sertoli cells (SCs), induces reproductive toxicity, disrupts the immune-privileged microenvironment of the blood–testis barrier (BTB), and consequently impairs spermatogenesis. However, whether the bitter taste receptor mT2R143 is involved in the mechanisms by which SCs resist toxicant uptake and preserve immune homeostasis following MC-LR exposure remains unclear. In this study, TM4 cells were exposed to different concentrations of MC-LR (1 μM, 0.5 μM, and 0.05 μM) for 24 h and 48 h, and the expression of related molecular markers was examined using qPCR, Western blot, and immunofluorescence. MC-LR exposure significantly upregulated mT2R143 mRNA expression (P < 0.05). Co-treatment with MC-LR and siRNA-mT2R143 markedly downregulated the expression of the BTB tight junction proteins ZO-1 and Occludin compared with the control group (P < 0.01). Immunofluorescence analysis further confirmed the reduction of ZO-1 and Occludin. Similarly, combined exposure to MC-LR and an NF-κB inhibitor led to a significant decrease in ZO-1 and Occludin (P < 0.01). These findings suggest that MC-LR exposure activates mT2R143 expression in TM4 cells and that mT2R143 mediates NF-κB signaling to regulate the expression of BTB tight junction proteins. This work provides a theoretical basis for exploring the regulatory roles of bitter taste receptors in the reproductive system, highlights their potential involvement in the chemosensory regulation of spermatogenesis, and offers new perspectives for testicular reproductive toxicology research.
This study aimed to determine the minimum toenail mass needed for reliable fluoride analysis, and to compare fluoride extraction efficiency (
Stress has become an integral part of life, often triggering various biological systems involved in maintaining homeostasis and causing a range of physiological and pathological changes depending on the type and duration of the stress. Further, environmental chemical significantly contributes to intensify the stress. This study investigated how prior exposure to chronic psychological stress (immobilization stress, IMS) or physical stress (forced swim stress, FSS) modifies lambda-cyhalothrin (LCT)-induced dopaminergic and neurobehavioral impairments.Neither IMS (one session, 15 min/day in restrainer for 28 days), FSS (one session,3 min/day for 28 days), nor LCT alone (3.0 mg/kg body weight, p.o. for 3 days on days 26–28) produced significant changes in motor activity, rotarod performance, or DA-D2 receptor in the corpus striatum brain region as compared with controls. These treatments alone caused only marginal alterations in tyrosine hydroxylase (TH) mRNA expression, TH immunoreactivity, and Nissl staining in the striatum region. However, pre-exposure to IMS or FSS for 28 days followed by LCT treatment distinctly impaired motor activity and rotarod performance. Exhibit changes in striatal dopamine receptor binding, TH mRNA expression and immunoreactivity and altered Nissl staining compared with IMS, FSS, or LCT alone. These findings suggest that chronic psychological or physical stressors enhance the brain's susceptibility to LCT-induced dopaminergic impairments, leading to measurable neurobehavioral deficits. Enhanced vulnerability to lambda-cyhalothrin induced neurotoxicity in rats pre-exposed to stress.
Pyrethroids have been documented to accumulate in animal bodies. Multiple experimental studies suggest potential disruption of male reproductive function, yet findings remain inconsistent. Therefore, a comprehensive synthesis is required to clarify overall reproductive risks. Herein, we aim to quantitatively synthesize evidence from mammalian studies investigating the impact of pyrethroid exposure on male reproductive outcomes. A systematic search of Google Scholar, EMBASE, PubMed, and Scopus was conducted. Data extraction included species, exposure characteristics, outcomes, and methodological quality. Meta-analyses were conducted using standardized mean differences. Heterogeneity was evaluated using I2 and Q statistics. Subgroup and sensitivity analyses were performed to explore sources of variation. Sixty-two studies were selected, which primarily involved rats, with oral exposure as the dominant route. Geographically, studies originated mainly from India, Egypt, and Tunisia. Across pooled analyses, pyrethroid exposure showed no statistically significant overall effect on sperm count, motility, viability, testes weight, or testosterone levels. Leave-one-out analyses demonstrated robust but consistent pooled effects. Rats showed stronger negative trends than mice. Overall, the pooled SMD for all reproductive outcomes combined was –2.30 (95
The aim of the current study is assessing the in vitro anti-inflammatory and antioxidant properties of Laurus nobilis methanolic extract (LNME) and to investigate their impacts on experimental oxidative stress in ulcerative colitis caused by acetic acid (AA). The in vitro antioxidant ability of LNME was evaluated using four tests (DPPH, ABTS, FRAP, and CUPRAC). The anti-inflammatory capacity was assessed using the protein denaturation technique, on the basis of total polyphenol measurement. In an in vivo study, 28 rats were equitably divided into four groups: (1) control group, (2) Laurel group: Rats receiving 250 mg/kg B.W of LNME, (3) AA group: Rats receiving 2 mL/kg B.W of AA (3 The current study suggests that LNME displays anti-inflammatory, and antioxidant potential and a cytoprotective impact supporting its uses to alleviate ulcerative and colonic oxidative stress.
Antibiotic resistance is a significant health issue that continues to rise, leading to the emergence of multidrug-resistant (MDR) bacteria. There is an urgent need to propose alternative strategies to combat the spread of antibiotic resistance. Nanoparticles are one such method that showed promising effects on MDR bacteria. In this study, MDR bacteria inhabiting wastewater were isolated and treated with different nanoparticles. Bacterial susceptibility was tested against a panel of antibiotics, followed by identification of those showed resistance to at least three different classes of antibiotics were further analysed and identified. The selected MDR bacterial isolates were treated with three nanoparticles (Ag NPs, TiO2 NPs, and ZnO NPs) by broth microdilution method. The study findings indicated that 73
In recent years, sea hares (family Aplysiidae) have attracted growing interest as potential bioindicators for environmental research in coastal regions, although they are not yet as widely utilized as other marine organisms commonly found in these habitats. Sea hares exhibit several characteristics that make them promising candidates for local environmental monitoring: They are easy to sample, relatively small in size, and reside in sedentary coastal environments that are especially susceptible to pollution. Their grazing behavior also increases their potential for bioaccumulating environmental contaminants. While methodological standardization and regulatory frameworks for using sea hares in both field and laboratory studies are less developed compared to more established molluscan bioindicators, numerous studies have documented their ability to accumulate organic and inorganic pollutants. In addition, their physiological and behavioral responses, such as alterations in feeding, locomotion, and neural activity, offer valuable insights into the neurotoxic effects of environmental stressors. This review outlines the current ecotoxicological and environmental applications of sea hares and underscores the importance of integrating molecular and biochemical approaches to further establish their utility as a promising molluscan model. In particular, we emphasize their potential for site-specific assessments of contaminant exposure and ecological impact in coastal ecosystems. Despite certain limitations in their use as laboratory toxicity models, we hope this review encourages broader adoption of sea hares as effective bioindicators in coastal environmental monitoring and research.
This review discusses the potential hazards of exposure to micro- and nano-plastics in the workplace and its mitigation. The literature reviewed was obtained by searching the papers used in most research for the necessary data, including PubMed, specifically for the last five years. The search was performed using the key terms “microplastics”, “nano-plastics”, “toxicity”, “health”, and “workers”. Unless the plastic value chain is changed, the threats to the environment, marine ecosystems, species, human health, the economy, and communities will become intolerable. But these hazards also present special opportunities to contribute to the shift to a more sustainable world. The review underlines the need for more investigation into the intricate biological relationships and hazards associated with the buildup of MPs/NPs in the workplace, and suggests possible avenues for future research on the health of employees.
4-Methylbenzylidene camphor (4-MBC) is a widely used ultraviolet (UV) filter found in sunscreens, cosmetics, and plastic materials, resulting in increased human exposure. Due to its environmental persistence and bioaccumulation, 4-MBC poses significant health concerns, including skin sensitivity, hepatotoxicity, endocrine disruption, and potential carcinogenicity. This in silico study explores the toxicological mechanisms of 4-MBC using network toxicology and a molecular docking approach. Disease-related targets of 4-MBC were identified using network toxicology analysis. A total of 22 targets were screened and subsequently evaluated through molecular docking to assess the binding interactions and affinities between 4-MBC and the identified proteins. Additionally, pathway enrichment analysis was conducted to understand the biological pathways involved. Out of 22 identified targets, 13 targets showed interaction through hydrogen bonding and pi–pi stacking. Importantly, several targets were shared across multiple health conditions, with STAT3 and MPO consistently implicated in cancer, endocrine disruption, liver toxicity, and skin sensitivity. Pathway enrichment analysis indicated a predominant involvement of these targets in cell surface-mediated signaling, particularly the AGE-RAGE pathway associated with diabetic complications. High binding affinities were observed for ABCB1 (− 7.003 kcal/mol), STAT3 (− 6.014 kcal/mol), and CYP19A1 (− 5.807 kcal/mol), suggesting their relevance in mediating toxic effects. These findings offer mechanistic insights into 4-MBC-induced toxicity and highlight STAT3 and MPO as central molecular mediators. The study underscores the need for stricter regulatory oversight and environmental monitoring to mitigate 4-MBC exposure linked to health issues and safeguard both public health and ecological systems.
Marine invertebrates represent the majority of ocean biodiversity and are continuously exposed to rapidly changing environmental conditions, including temperature fluctuations, ocean acidification, pollution, and hypoxia. To cope with these challenges, marine invertebrates rely not only on genetic variation but also on epigenetic regulatory mechanisms that enable flexible and rapid modulation of gene expression. Epigenetic processes such as DNA methylation, histone modifications, chromatin remodeling, and the action of non-coding RNAs operate without altering DNA sequences and play fundamental roles in controlling development, physiology, and stress responses. Importantly, these mechanisms link environmental signals to functional biological outcomes by regulating transcriptional programs that influence growth, reproduction, larval survival, and stress tolerance, thereby affecting population dynamics and ecosystem resilience. This review provides a comprehensive synthesis of current knowledge on epigenetic regulation in marine invertebrates, with a focus on major taxonomic groups including mollusks, crustaceans, echinoderms, annelids, and cnidarians. We examine how epigenetic mechanisms contribute to key biological processes such as embryonic development, larval plasticity, immune defense, host-microbiome interactions, and symbiotic associations. Particular attention is given to the role of epigenetic modifications in mediating responses to environmental stressors, including climate change-related pressures and anthropogenic contaminants. Emerging evidence suggests that environmentally induced epigenetic changes may persist across generations, influencing offspring performance, recruitment success, and population resilience. This study also highlights recent methodological advances in epigenomic and multi-omics approaches that have expanded epigenetic research beyond traditional model organisms. Despite significant progress, important knowledge gaps remain regarding the stability, reversibility, and ecological relevance of epigenetic marks in natural marine populations. Overall, this review underscores the importance of epigenetic mechanisms in shaping phenotypic plasticity and adaptive potential in marine invertebrates, with implications for conservation, ecosystem management, and sustainable aquaculture.
