Search Results (2,466)

Chloroidium saccharophilum is a resilient green microalga with a broad ecological distribution and an increasing biotechnological interest due to its tolerance of extreme environmental conditions. In this study, a sample of C. saccharophilum from the Laguna Blanca aquifer (Magallanes, southern Chile) was physiologically and phylogenetically characterized. This is the first confirmed evidence of this strain in the Southern Cone. Molecular identification based on ITS rDNA sequencing and ITS2 secondary structure analysis confirmed its taxonomic location, showing high similarity with reference strains and no compensatory base changes. Growth performance was analyzed under controlled laboratory conditions and under outdoor desert cultivation in the Atacama Desert, focusing on temperature, salinity, nutrients limitation, and high solar irradiance operational conditions. The strain exhibited optimal growth at 22 °C under laboratory conditions and demonstrated a strong tolerance to high salinity (150 g L⁻¹ NaCl). Outdoor raceways cultivation revealed a negative relationship between temperatures above 25 °C and biomass accumulation, while nutrients depletion and strong irradiance caused moderate carotenoid accumulation. However, the low amount of carotenoid yields remained constant, even under combined stress conditions. In general, the results highlight the ecological adaptability and the stress tolerance of C. saccharophilum, supporting its potential application in saline bioprocesses and bioremediation. Nevertheless, the limited production of carotenoid synthesis suggests that additional or combined stress strategies will be required to enhance the production of high-value metabolites. This study expands the biogeographical knowledge of C. saccharophilum and provides a physiological baseline for future optimization studies in extreme and Mars-analog environments. Full article

This scientometric review examines the evolution and scope of invasive (blood and tissue) and non-invasive (faeces, hair, and saliva) sampling in terrestrial mammal population genetics, with particular emphasis on the comparability of observed heterozygosity (Ho), expected heterozygosity (He), and the inbreeding coefficient (Fis) between studies published from 1985 to 2026. Searches in Web of Science and Scopus, filtered under PRISMA/PRISMA-S criteria, yielded a compendium of articles analysed with Bibliometrix and VOSviewer 1.6.20 to quantify temporal production, keyword evolution, collaborative networks, and publication outlets. Searches in Web of Science and Scopus, filtered under PRISMA/PRISMA-S criteria, yielded a broad corpus of 145 articles for general scientometric analyses, of which 85 met the eligibility criteria for the focused analysis of Ho, He, and Fis. The field shows steady growth (annual rate ≈ 6.1%), substantial authorship and international collaboration, and increasing thematic diversity. Adoption of non-invasive sampling has accelerated, broadening spatial and taxonomic coverage, but also increasing exposure to DNA degradation and genotyping error when laboratory quality control is insufficient. Across the literature, reporting of quality control practices (e.g., extraction blanks, negative PCR controls, multi-tube replication, and error-rate estimation) has improved over time but remains inconsistent. Comparisons indicate that differences in Ho, He, and Fis between invasive and non-invasive sampling are generally modest once marker system and species are taken into account. These findings indicate that quality control and transparency in reporting, rather than invasiveness per se, are the main factors determining comparability among studies. The scientometric patterns also reveal a methodological transition from microsatellites to SNP-based and reduced representation approaches, with implications for synthesis across marker types. Overall, this review identifies geographic and taxonomic biases in research effort and highlights the need for standardised reporting of DNA quality indicators, inclusion thresholds, and validation protocols to strengthen genetic monitoring in mammalian conservation. Full article

DNA methylation constitutes a primary layer of epigenetic regulation in plants, operating across three sequence contexts (CG, CHG, and CHH) through distinct enzymatic pathways. Over the past fifteen years, accumulating evidence has shown that DNA methylation varies substantially among individuals and populations of wild plants, sometimes independently of underlying genetic polymorphism. This variation can influence gene expression, transposable element activity, and phenotypic traits relevant to ecological adaptation. Population epigenetics, the study of methylation variation at the population scale, has matured from initial surveys using methylation-sensitive amplified fragment length polymorphism (MS-AFLP) into a discipline increasingly reliant on reduced-representation bisulfite sequencing (epiGBS, bsRADseq), whole-genome bisulfite sequencing (WGBS), enzymatic methyl-seq (EM-seq), and direct long-read detection by nanopore sequencing. These methodological advances are opening population epigenetics to non-model organisms across the full breadth of the plant phylogeny, from angiosperms and gymnosperms to ferns and bryophytes. We cover (i) the molecular machinery underlying plant DNA methylation, including the debated status of N6-methyladenine (6mA); (ii) empirical evidence for natural epigenetic variation in plant populations, spanning clonal, invasive, and outcrossing species; (iii) the methodological toolkit available for population-scale methylation profiling, with emphasis on approaches suitable for non-model taxa; and (iv) the ecological and evolutionary significance of population epigenetic variation, including transgenerational inheritance, stress memory, epigenetic clocks, conservation applications, and the emerging integration of epigenetics into the extended evolutionary synthesis. We identify critical knowledge gaps, particularly the near-complete absence of population-level epigenetic data for bryophytes, ferns, and lycophytes, and outline priorities for future research. Full article

Chemotherapy-induced mucositis (CIM) is a dose-limiting toxicity of cancer therapy that is mainly associated with mitochondrial dysfunction in epithelial cells. We investigated whether GV1001, a mitochondrial protective peptide from human telomerase reverse transcriptase (hTERT), attenuates 5-fluorouracil (5-FU)-induced mucositis in a murine model. 5-FU induced notable mortality, leukopenia, and mucositis in the gastrointestinal (GI) tract, including tongue, esophagus and small intestine. It promoted epithelial–mesenchymal transition (EMT), nuclear factor kappa-B (NF-κB) activation, systemic and mucosal inflammation, DNA damage, impaired cell proliferation, and apoptosis throughout the GI tract. GV1001 blocked 5-FU–associated mortality, significantly attenuated leukopenia, and notably prevented mucositis. GV1001 also suppressed 5-FU-induced DNA damage, EMT, loss of proliferative capacity, apoptosis, and NF-κB activation in mucosal epithelium. In normal human keratinocytes, 5-FU inhibited the cell proliferation, disrupted mitochondrial function, as evidenced by reduced mitochondrial membrane potential, increased reactive oxygen species (ROS) production, impaired electron transport chain (ETC) complex integrity, decreased ATP synthesis, and cytochrome c release into the cytosol. GV1001 markedly mitigated these 5-FU-induced mitochondrial defects. Taken together, GV1001 mitigates CIM by most likely preserving mitochondrial integrity and function, supporting its potential as a strategy to prevent cancer chemotherapy-associated mucosal injury in patients. Full article

Antarctic terrestrial photosynthetic biota is dominated by cryptogamic communities, which are largely restricted to scarce ice-free areas. Among these, nunataks constitute habitats of remarkable biogeographical interest, as they may harbor distinctive biotic assemblages worthy of investigation. This work presents a comprehensive assessment of lichen diversity on Antarctic nunataks. The lichen flora of four nunataks on the Hurd Peninsula (Livingston Island, maritime Antarctica) was investigated. Specimens were identified using an integrative approach combining morphological assessment and DNA barcoding. This survey revealed a high and potentially underestimated species richness, with 39 confidently identified and several additional taxa requiring further taxonomic resolution. A review of published records of lichen occurrence in nunatak and non-nunatak environments throughout Antarctica was used to evaluate patterns in taxonomic, biogeographical, and morphotype composition. This synthesis showed that nunataks support lower species richness than other ice-free environments. Most of their taxa occur in non-nunatak areas, consistent with patterns observed locally on the Hurd Peninsula. Floristic overlap seems greater in continental Antarctica, suggesting a stronger influence of nunatak-associated environmental constraints in the maritime region. These results underscore the ecological significance of nunataks as environmentally filtered habitats and highlight their relevance for understanding biodiversity patterns and community assembly in Antarctica’s terrestrial ecosystems. Full article

Background/Objectives: Triple-negative breast cancer (TNBC) is frequently characterized by notably elevated Ki-67 expression, a hallmark of uncontrolled rapid cell-cycle progression. However, the underlying mechanisms remain unclear, leading to limited therapeutic options. Methods: In this study, hub gene was identified through integrated bioinformatic analysis of public datasets (TCGA-BRCA and METABRIC). Subsequent functional validation was performed both in vitro and in vivo using siRNA-mediated knockdown and small-molecule inhibitors. Phenotypic effects—including cell viability, cell cycle distribution, DNA synthesis, and clonogenic survival—were comprehensively assessed using MTT assays, flow cytometry, EdU, and colony formation assays. Protein-level changes were confirmed by Western blotting and immunohistochemistry (IHC). To dissect the transcriptional regulation of the key hub gene TTK, we first predicted potential upstream transcription factors using the JASPAR database; binding specificity was then validated through in silico motif analysis, luciferase reporter assays, and chromatin immunoprecipitation followed by quantitative PCR (ChIP-qPCR). Results: The mitotic kinase TTK is significantly overexpressed in TNBC compared with non-TNBC breast cancers. Notably, TTK overexpression exhibited a strong positive correlation with elevated Ki-67 indices and reduced overall survival in TNBC patients. Functional validation demonstrated that pharmacological or genetic inhibition of TTK effectively induced G2/M cell-cycle arrest and potently suppressed TNBC proliferation in both in vitro cell cultures and in vivo xenograft models. Mechanistically, TTK overexpression stems from enhanced transcriptional initiation driven by the transcription factor NFYA binding to the CCAAT box in the TTK promoter—an interaction newly identified here. Concurrently, TTK blockade disrupted spindle assembly checkpoint (SAC) signaling via BUB1B/MAD1L1 downregulation, triggering mitotic arrest and catastrophe. Conclusions: Collectively, these findings establish TTK as a key cell-cycle regulator driving TNBC proliferation. More importantly, targeting mitotic control through TTK inhibition represents an efficient strategy to impede the aberrantly fast cell cycle progression in TNBC. Full article

Background/Objectives: Endometrial cancer frequently develops resistance to apoptosis-based therapies, highlighting the need for alternative strategies that control tumor growth independently of cell death induction. Three-dimensional (3D) tumor models more accurately recapitulate tumor architecture, cellular interactions, and treatment resistance compared to conventional two-dimensional (2D) cultures. This study aimed to investigate whether imatinib-based combination treatments can enforce sustained cytostatic responses in a 3D endometrial cancer model. Methods: Ishikawa spheroids were treated with imatinib alone or in combination with lithium chloride or medroxyprogesterone acetate. Proliferation was assessed by bromodeoxyuridine incorporation, cell cycle distribution by flow cytometry, and apoptosis by Annexin V/propidium iodide staining over 96 h. Results: Imatinib monotherapy produced modest antiproliferative effects, whereas combination treatments resulted in sustained suppression of DNA synthesis, increased G₀/G₁ accumulation, and reduced S-phase entry. Despite strong growth inhibition, apoptotic fractions remained low across all groups. Conclusions: Imatinib-based combinations suppress 3D endometrial cancer growth predominantly through sustained cell cycle arrest rather than apoptosis induction. Targeting apoptosis-resistant proliferation through cytostatic mechanisms may represent a complementary therapeutic strategy for hormone-responsive endometrial cancer and warrants further translational evaluation. Full article

Breast cancer remains the most frequently diagnosed malignancy in women worldwide, accounting for approximately 2.3 million new cases and 670,000 deaths annually. The diagnostic landscape has undergone a paradigm shift over the past two decades, evolving from morphology-based classification toward molecularly informed, precision-guided strategies. Early and accurate diagnosis is fundamental to improving outcomes; advances in imaging technology, including digital breast tomosynthesis (DBT), contrast-enhanced mammography (CEM), and abbreviated magnetic resonance imaging (MRI), have improved sensitivity and specificity in diverse patient populations. Simultaneously, the integration of artificial intelligence (AI) and radiomics into screening workflows offers unprecedented potential for risk stratification and a reduction in false-positives. At the pathological level, multi-gene expression profiling assays such as Oncotype DX, MammaPrint, Prosigna, and EndoPredict have refined prognostic classification and guide adjuvant chemotherapy decisions in early-stage hormone receptor-positive disease. The emergence of liquid biopsy, circulating tumor DNA (ctDNA), circulating tumor cells (CTCs), and exosomal biomarkers provides minimally invasive tools for real-time monitoring of response, residual disease, and the evolution of resistance mechanisms. Precision diagnostics now encompass next-generation sequencing (NGS)-based comprehensive genomic profiling, enabling identification of actionable alterations such as PIK3CA mutations, HER2 amplification, BRCA1/2 pathogenic variants, and NTRK fusions, each linked to approved therapeutic agents. The purpose of this review is to provide a comprehensive synthesis of current and emerging diagnostic modalities in breast cancer—from population-level screening to individualized molecular profiling—and to examine how integrative, multimodal diagnostic platforms are reshaping clinical decision-making in the era of precision medicine. Full article

Purpose: Cannabidiol (CBD) is a primary bioactive, non-intoxicating cannabinoid found in the cannabis plant. Studies have shown that CBD causes anticancer activity by inhibiting the expression of growth factors and inducing apoptosis, leading to cell cycle arrest. In this study, we aimed to determine how CBD influences the expression of genes that affect cancer pathways in doxorubicin-sensitive (MCF-7) and doxorubicin-resistant (MCF-7/Adr) breast cancer cells. Materials and Methods: IC₅₀ concentrations of CBD in MCF-7 and MCF-7/Adr cell lines were determined by the MTT cell cytotoxicity assay. RNA isolation and subsequent cDNA synthesis were performed for qPCR experiments with the determined IC₅₀ values. The effects of CBD on the cell cycle and apoptosis were studied using flow cytometry. IC₅₀ values of CBD were determined in MCF-7 and MCF-7/Adr breast cancer cell lines at eight different concentrations and at three different incubation periods (24 h, 48 h, and 72 h) with different doses. RT-qPCR was used to investigate the molecular mechanisms underlying the expression of genes involved in cancer pathway analysis. Results: Treatment with CBD at concentrations of 17.57 μM (MCF-7) and 11.41 μM (MCF-7/Adr) for 48 h decreased colony formation, induced apoptosis, and inhibited cell invasion in both cell lines. In addition, we observed significant alterations of angiogenesis, apoptosis, cell cycle, cellular senescence, DNA damage and repair, epithelial-to-mesenchymal transition, hypoxia, metabolism, telomeres, and telomerase in both cell lines. Conclusions: Our research indicates that CBD could be an effective natural bioactive compound for breast cancer treatment, inhibiting tumor cell proliferation and inducing apoptosis. Full article

Plant-derived antimicrobial compounds are emerging as promising alternatives to synthetic preservatives in the food industry due to their efficacy against a broad spectrum of pathogenic and spoilage microorganisms, as well as their consumer acceptance. This review critically examines the main classes of bioactive phytochemicals, including essential oils, polyphenols, alkaloids, terpenoids, and saponins, comparing their relative antimicrobial effectiveness and highlighting representative examples. Notably, essential oils rich in thymol or carvacrol have shown strong inhibitory activity against Listeria monocytogenes and Salmonella spp., while polyphenols and alkaloids exhibit moderate to strong activity depending on concentration and food matrix. Their mechanisms of action include cell membrane disruption, inhibition of key enzymes, and interference with DNA or protein synthesis. Applications in food systems (i.e., incorporation into coatings, emulsions, or controlled-release formulations) demonstrate potential for extending shelf life and enhancing safety. However, practical implementation is challenged by matrix-dependent efficacy, compound stability, sensory impact, and regulatory and toxicological considerations. By synthesizing current knowledge, identifying the most promising compound classes, and highlighting key limitations, this review provides a critical framework to guide future research and the development of effective, sustainable natural preservatives in the food industry. Full article

Alpha-Ketoglutarate (AKG), a central intermediate of the tricarboxylic acid cycle, is a crucial metabolic and signaling molecule that connects mitochondrial function with cellular homeostasis, immunological modulation, epigenetic remodeling, and lifespan. While mitochondrial AKG maintains energy metabolism, the nuclear AKG pool influences chromatin remodeling through DNA and histone modifications, which together control hypoxia responses and shape gene expression patterns. This dual role demonstrates AKG’s significance in mediating metabolic state, gene expression, and long-term cellular adaptability. AKG modulates immunological responses, reduces reactive oxygen species (ROS), promotes the polarization of anti-inflammatory macrophages, and suppresses nuclear factor kappa B (NF-κB) activation, thereby reducing chronic inflammatory processes. AKG restricts pro-inflammatory cytokine production, increases extracellular matrix synthesis, and reduces cartilage degradation in arthritic models, suggesting potential therapeutic benefits in autoimmune diseases and joint degeneration. Additionally, AKG affects lifespan in several model organisms, where supplementation enhances metabolic resilience, lowers age-related inflammation, modifies mTOR signaling, and preserves youthful epigenetic profiles. Additionally, because endogenous AKG levels decrease with age, oral supplementation of AKG, especially with calcium and arginine, has drawn attention to its potential benefits in longevity and metabolic health. Thus, AKG is versatile and has encouraging therapeutic promise for cancer, aging, and inflammatory illnesses. However, a lack of human clinical evidence prompts further research to determine ideal dosage, tissue selectivity, and long-term safety. The goal of this review is to critically examine the current mechanistic knowledge related to AKG biosynthesis and breakdown and its future implications in maintaining cellular homeostasis and controlling chronic inflammation. Full article

Background/Objectives: Malignant salivary gland tumors (MSGTs) are rare, biologically heterogeneous neoplasms in which histopathologic diagnosis and classification are challenging and subject to interobserver variability. Artificial intelligence (AI) approaches using radiologic, histopathologic, and molecular data, including radiomics, deep learning, and biomarker-based models, have been proposed as adjunctive diagnostic tools. This systematic review aimed to identify and critically appraise AI/ML models across radiologic, histopathologic, and molecular domains for distinct diagnostic tasks in MSGTs, and to integrate their diagnostic roles through a functional meta-synthesis. Methods: We conducted a PRISMA 2020-compliant systematic review. Embase, PubMed/MEDLINE, and Scopus were searched from inception to February 2026. Eligible studies developed or validated AI/ML diagnostic or classification models in human salivary gland tumor cohorts and reported extractable performance metrics. Results: From 1265 records, eight studies (1922 participants) met the inclusion criteria, spanning CT/MRI radiomics or deep learning (n = 4), whole-slide histopathology deep learning (n = 3), and DNA methylation-based classification (n = 1). External validation was reported in two CT-based benign–malignant discrimination studies, with AUCs of 0.890 (95% CI 0.844–0.937) and 0.745 (95% CI 0.699–0.791). Heterogeneity in model construction, outcome definitions, and validation strategies precluded meta-analysis. Risk of bias was frequently high in QUADAS-2/PROBAST assessments, driven by retrospective sampling, limited blinding, and analysis-related concerns, while calibration and utility were rarely assessed. Conclusions: AI/ML models for MSGTs demonstrate promising diagnostic performance, particularly for preoperative benign–malignant discrimination, but the current evidence base is limited by heterogeneity, predominantly internal validation, and high risk of bias. The functional meta-synthesis identified three convergent diagnostic domains: malignancy discrimination, histopathologic subtype classification, and molecular/epigenetic taxonomy refinement. Full article

Antimicrobial resistance (AMR) poses a significant global health threat, with multidrug-resistant pathogens undermining the effectiveness of conventional antibiotics. Natural alkaloids, a diverse group of nitrogen-containing compounds mainly derived from plants, are gaining attention as potential antimicrobial agents due to their broad-spectrum activity, structural variety, and unique mechanisms of action. This review examines the antimicrobial properties of natural alkaloids, classifying them by chemical structure (e.g., quinoline, isoquinoline, pyridine, indole, and imidazole alkaloids). Their antibacterial, antifungal, and antiviral activities are discussed, along with the mechanisms by which they target pathogenic microorganisms, including disruption of cell walls and membranes, inhibition of protein synthesis, interference with DNA replication, and viral assembly. The review also explores the synergistic effects of alkaloids when combined with conventional antimicrobial agents. Alkaloids demonstrate potent antimicrobial activity against various pathogens. Quinoline alkaloids, such as quinine, inhibit DNA replication and damage cell membranes. Isoquinoline alkaloids like berberine and sanguinarine exhibit broad-spectrum antibacterial effects. Pyridine alkaloids, including nicotine, disrupt bacterial membranes. In fungi, alkaloids such as sanguinarine and indole derivatives prevent cell wall synthesis and spore germination. Antiviral alkaloids like lycorine target viral RNA polymerases. Additionally, alkaloids enhance the activity of traditional antibiotics by overcoming resistance. Natural alkaloids represent a promising source of antimicrobial agents with diverse mechanisms to combat AMR. Future research should focus on optimizing alkaloid structures, ensuring safety and efficacy, and exploring combination therapies to address the escalating AMR challenge. Full article

Chlorinated paraffins (CPs) are widely used, structurally complex mixtures of chlorinated alkanes whose ecological risks in aquatic ecosystems have raised increasing concern. However, the toxic effects and molecular mechanisms of CPs on primary aquatic producers remain poorly understood. In this study, we used the eukaryotic green algae Chlorella sp. and the prokaryotic cyanobacterium Microcystis aeruginosa (M. aeruginosa) as test organisms to systematically investigate the effects of CPs with different carbon chain lengths, namely short-chain CPs (SCCPs), medium-chain CPs (MCCPs), and long-chain CPs (LCCPs), on algal growth, photosynthetic pigment content, antioxidant systems, cellular ultrastructure, and the underlying molecular responses. Our results showed that CPs toxicity to algae is significantly dependent on both CPs carbon-chain length and algal species. Exposure to 1.0 mg/L SCCPs for 96 h produced a growth inhibition of Chlorella sp. of 14.45%. CPs’ exposure significantly altered algal Chl-a content and elicited antioxidant defense responses, and affected the synthesis and extracellular release of MC-RR and MC-LR in M. aeruginosa. Ultrastructural observations revealed cell surface wrinkling and deformation in both Chlorella sp. and M. aeruginosa. Chlorella sp. additionally exhibited thylakoid disintegration and plasmolysis. Transcriptomic analysis indicated that CPs with different chain lengths significantly downregulated genes in Chlorella sp. associated with DNA replication and mismatch repair, suggesting impairment of replication initiation and elongation and compromised genome stability. Concurrently, genes encoding photosynthetic antenna proteins and carbon fixation were upregulated. In M. aeruginosa, CPs exposure markedly disturbed energy metabolism pathways, including glycolysis/gluconeogenesis and oxidative phosphorylation, which were generally downregulated. This study provides a comparative assessment of CPs’ toxicity between the eukaryotic algae Chlorella sp. and the prokaryotic algae M. aeruginosa, revealing that toxicity is co-determined by carbon chain length and algal species. Additionally, it provides critical toxicological data and establishes a theoretical foundation for the scientific assessment of the aquatic ecological risks posed by CPs with different carbon chain lengths. Full article

Microplastics (MPs) are synthetic polymer particles that are generally less than 5 mm in size and have attracted heightened scrutiny due to their pervasive presence in the environment, along with their toxicological significance. Several research investigations documented its presence in humans as a profound finding in biological tissues and fluids crossing barriers, leading to oxidative and inflammatory pathways alterations associated with blood, placenta, cardiovascular, pulmonary, nephrotic, other systems, and their disorders. Given the ubiquitous utilization of microplastics across diverse sectors, it is imperative to systematically investigate and elucidate their potential toxicological effects on biological systems through rigorous and mechanistically informed research. This review will also provide the synthesis of recent mechanistic data on the toxicity that can be caused by MPs and will determine key gaps that impede efficient human health risk evaluation. A structured literature search was conducted via PubMed, Web of Science, and Scopus databases, mostly from the studies published between 2010 and 2026. The studies of exposure characteristics and biological effects were analyzed in vitro, in vivo, and in human biomonitoring, and the primary focus of the interventions includes oxidative stress, inflammation, apoptosis, hepatotoxicity, and metabolic malfunction. MPs possess various physicochemical properties, such as a low particle size, various shapes, surface area, polymer composition, and the presence of sorbed or intrinsic additives. When MPs are taken up by cells, they can induce oxidative stress via increasing ROS, eventually leading to high lipid peroxidation, mitochondrial malfunction, DNA fragmentation, and eventually cell death. MPs also cause pro-inflammatory cytokine responses, including TNF-α, IL-1β, and IL-6, altering the immune system and cell profile, leading to systemic inflammation. In aquatic and terrestrial organisms, these microplastics have a harmful impact on growth, reproduction, and behavior in a time- and dose-dependent manner. Under conditions of controlled exposure, the organ-specific toxicities that have been reported include hepatic, renal, neurological, reproductive, and cardiovascular systems. Although the fields of mechanistic knowledge are growing, there is still a substantial amount of uncertainty; there is a lack of characterization of the long-term effects of low-dose chronic exposure, the kinetics of bioaccumulation, biodegradation potential, and transgenerational effects. In addition, there are no standardized procedures for the characterization of MPs, nor the reporting of the distribution of size or exposure measurements, which limits the comparability of cross-studies and makes it difficult to assess risks quantitatively. The dynamics of interactions of MPs between co-adsorbed contaminants like heavy metals, polycyclic aromatic hydrocarbons, and endocrine-disrupting chemicals are also yet to be explored. Although all evidence available to date does indicate biologically plausible mechanisms of MP-induced toxicity, integrated research employing standardized analytical protocols, an environmentally relevant exposure model, and human epidemiological data is required to ensure that laboratory results are translated into evidence-based public health and regulatory actions. This review offers an in-depth analysis of the existing molecular understanding of MP-induced toxicity, demonstrates organism-level impacts throughout species, and establishes vital fields for future studies. In order to develop competent guidelines to minimize MP exposure and its adverse health effects, it is crucial to cover these gaps via research that incorporates toxicology and environmental science. Full article