Search Results (75)

Accelerating eutrophication of aquatic ecosystems worldwide has increased concern regarding cyanotoxin exposure as an emerging environmental and public health issue, with Microcystin-LR (MC-LR) among the most extensively studied congeners due to its widespread occurrence and high toxicity. Evidence from experimental animal and cellular studies indicates that MC-LR elicits pronounced toxic impacts on both the male and female reproductive systems. In males, MC-LR induces overt testicular injury, compromises the structural and functional integrity of the blood–testis barrier, and triggers severe disorders in reproductive hormone synthesis and secretion. In females, it precipitates ovarian dysfunction, impedes normal follicular maturation and development, and induces distinct embryotoxic effects. The underlying pathogenic mechanisms involve the synergistic interplay of multiple signaling pathways, primarily including oxidative stress induction, aberrant apoptosis activation, endocrine disruption, and epigenetic modifications. Of particular significance, emerging evidence suggests that parental exposure to MC-LR may induce intergenerational or potentially transgenerational reproductive effects through epigenetic modifications in germ cells, impairing fertility and developmental outcomes in subsequent offspring and thus posing a sustained, long-term threat to population-level health. This review systematically delineates the reproductive toxicity profiles and underlying molecular mechanisms of MC-LR, evaluates its transgenerational health hazards, and aims to furnish robust scientific evidence for the formulation of targeted environmental health policies and risk management strategies. Full article

Microplastic (MP) contamination has become a defining feature of twenty-first century environmental change, yet the toxicological and ecological consequences for amphibians and reptiles—two vertebrate classes already facing severe extinction pressures—remain fragmented across taxa, regions, and methodological traditions. Here, we synthesize field and experimental evidence from five continents to provide a taxonomically balanced, mechanistically grounded, and geographically explicit assessment of MP exposure, bioaccumulation, and toxicity in herpetofauna, drawing on a structured literature search in Web of Science, Scopus, and PubMed (January 2015—March 2026). Field detection rates of MPs in amphibian larvae range from 26% in conservatively screened Central European populations to 73–80% in anuran tadpoles from high-anthropogenic-pressure Anatolian catchments, with fibrous polyethylene terephthalate (PET), polyethylene (PE), and polypropylene (PP) particles dominating the detected burden. Mechanistic evidence converges on oxidative stress cascades, hypothalamic–pituitary–thyroid axis disruption, gut and cutaneous microbiome dysbiosis, and compromised antiviral and antifungal immunity, with the latter potentially amplifying vulnerability to Batrachochytrium dendrobatidis and to ranavirus. Among reptiles, sea turtles display near-universal MP ingestion with documented maternal transfer to eggs; freshwater turtles, terrestrial squamates, and crocodilians remain critically understudied. Three structural asymmetries constrain current ecotoxicological risk characterization: taxonomic bias toward anurans and sea turtles, geographic bias toward the Global North, and experimental bias toward acute, supra-environmental laboratory exposures using pristine, single-polymer particles that fail to capture the chemical complexity of weathered field mixtures. We argue that MP burden may warrant consideration as a candidate stressor criterion within IUCN Red List assessments and within environmental risk assessment frameworks for freshwater and terrestrial biodiversity once a robust quantitative relationship between MP burden and demographic decline or population-level fitness has been established, and propose six hypothesis-driven research priorities: methodological standardization, reptile toxicokinetics, transgenerational epigenetics, MP–pathogen microbiome interactions and their translation into population viability models, temperature × MP interaction under climate warming, and population-genetic consequences of contemporary MP-driven selection, as the most tractable avenues for ecotoxicological progress and for the development of herpetofauna-specific risk characterization frameworks. Full article

Phthalic acid esters (PAEs), ubiquitous plasticizers and recognized endocrine-disrupting chemicals, pose a protracted threat to aquatic ecosystems and biodiversity. However, current ecotoxicological assessments often focus on isolated chemicals at exceedingly high laboratory doses, failing to reflect true environmental risks. This review systematically evaluates and compares the multisystemic toxicological effects of six priority PAEs (DEHP, DBP, BBP, DNOP, DEP, and DMP) using the zebrafish biological model. The synthesized evidence reveals a distinct structure–activity relationship, where long-chain and highly hydrophobic congeners exhibit substantially higher toxicity than their short-chain counterparts. Exposure to these PAEs induces severe developmental, cardiovascular, neurobehavioral, and reproductive anomalies. Specifically, DBP and BBP display the most potent cardiotoxic and neurotoxic effects, while DEHP and DBP drive profound reproductive decline and endocrine disruption at concentrations as low as 0.5–20 μg/L. Crucially, comparative environmental relevance assessments indicate that real-world PAE concentrations in industrial hotspots frequently meet or exceed these laboratory-derived lowest observed effect concentrations. These findings underscore the severe ecological risks posed by PAE contamination and position the zebrafish as a vital biological sentinel. Future ecotoxicological evaluations must prioritize chronic, low-dose mixture exposures and transgenerational toxicity to fully characterize the protracted legacy of these pollutants on zebrafish populations. Full article

Ubiquitous environmental endocrine-disrupting chemicals (EDCs), including bisphenols, phthalates, and heavy metals, pose a severe and persistent threat to mammalian reproductive health worldwide. Oxidative stress acts as the pivotal mediator which drives epigenetic dysregulation in germ cells upon EDC exposure, including aberrant DNA methylation, abnormal histone post-translational modifications and dysregulated non-coding RNA networks. EDC-induced oxidative stress damages endogenous antioxidant defense systems and inactivates key epigenetic regulators, forming a self-reinforcing cycle of redox imbalance and epigenetic dysregulation, which ultimately leads to impaired gametogenesis, reduced fertility, and transgenerational reproductive abnormalities. This review summarizes current evidence indicating that multiple antioxidants, including melatonin, vitamin C, resveratrol, and epigallocatechin gallate, alleviate EDC-induced reproductive toxicity by targeting epigenetic dysregulation. Their protective effects encompass scavenging excessive reactive oxygen species, activating endogenous antioxidant signaling cascades, restoring activity of epigenetic enzymes, and rectifying aberrant histone modification profiles, contributing to the maintenance of epigenetic homeostasis in germ cells. This review clarifies the intrinsic mechanistic link among EDC exposure, oxidative stress, epigenetic dysregulation and reproductive toxicity, which provides a theoretical basis for formulating reproductive health protection strategies against EDC exposure and guides the exploration of clinical epigenetic biomarkers. Full article

Micro(nano)plastics (MNPs) represent a pervasive and escalating threat to global ecosystems and human health. This review provides a critical synthesis of MNPs’ exposure risks across marine, atmospheric, and terrestrial compartments, with a distinct emphasis on identifying cross-media linkages and methodological inconsistencies that limit current risk assessments. Within marine environments, pollution hazard indices reveal significant spatial heterogeneity, yet their utility is constrained by the absence of toxicity weighting and particle characteristic integration. Atmospheric exposure profiles show variable risks, and the MNPs’ concentration in indoor air (up to 15.8 particles/m³) is significantly higher than in outdoor environments, posing a greater inhalation risk to infants and children who spend more time indoors. A marked increase in MNPs’ concentrations within agricultural soils is identified, where the MNP content in mulched soils (average: 570.2 particles/kg) is more than twice that of non-mulched soils (259.6 particles/kg). Critically, studies have now detected MNPs within human tissues, including the blood, intestines, liver, kidneys, tonsils, and brain, highlighting an urgent need to elucidate their multi-organ toxicity mechanisms, with a novel synthesis of gut–brain axis disruption and transgenerational effects. By integrating exposure dynamics with mechanistic toxicity data, this review advances a cross-system framework that identifies priority research directions, namely standardized detection methodologies, combined pollutant toxicity, and cross-system toxicity mechanisms, which are essential for informing mitigation strategies amid this escalating public health crisis. 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

Although chronic contamination by silver ions (Ag⁺) can persist in aquatic systems over long periods of time and can therefore have an impact on population developments, regulatory testing commonly relies on single-generation endpoints. Here, we used Daphnia magna to quantify long-term effects of pg/L to ng/L concentrations of Ag⁺ across generations and to test whether recovery depends on exposure history. Using 21 d life-cycle assays over up to seven consecutive generations, we quantified survival, key life-history traits, and population fitness (intrinsic rate of natural increase, r). In our study, low environmental concentrations of Ag⁺ caused minimal mortality, but sublethal effects persisted or multiplied over generations. Notably, continuous exposure led to significant reductions in body length and r at 50 pg/L (nominal LOEC) by the fourth generation exposed, representing population-relevant effects of Ag⁺ at very low concentrations which should be given consideration in the assessment of both water quality and the chemical itself. Recovery was concentration-dependent: low-concentration-exposed lineages recovered within a few generations, whereas 15 ng/L exposure resulted in persistent deficits even through the recovery period of three generations. Exposure-history patterns indicated that long-term outcomes were dominated by the cumulative number of exposed generations. These findings highlight the limitations of acute and single-generation assays and emphasize the importance of considering information on the effects of chemicals, including Ag⁺, across multiple generations in risk assessments. They also highlight the need to include expectations regarding recovery after the removal of pollutants in these assessments. Full article

Neonicotinoids are widely used pesticides that have caused a catastrophic decrease in bee and bumblebee populations worldwide. In addition to insects, neonicotinoids induce toxic effects in other species, including lizards, birds, and mammals. Previous studies have shown that gestational exposure to thiacloprid promotes transgenerational effects in the testes and thyroid. In this project, we described the epigenetic effects of thiacloprid on prostate tissue in directly exposed F1 and non-directly exposed F3 outbred Swiss male mice. We used paraffin sections for morphological analysis and frozen tissue for immunofluorescence analysis, RT–qPCR, and protein analysis. We purified histones and analyzed them through Western blot. We used ChIP–qPCR for histone H3K4me3 occupancy analysis. A tendency to increase in epithelial hyperplasia in F1 but not in F3 prostate was detected. Elevated levels of phosphorylated histone H3 at serine 10, a marker of mitosis, in both the F1 and F3 prostates were noted. A significant increase in the level of the Ki-67 marker of proliferation was detected in the F1 but not in the F3 anterior prostate. Hox gene expression was upregulated in the F1 and downregulated in the F3 prostate. The changes in gene expression were positively associated with histone H3K4me3 alterations at the promoters of the Hoxa and Hoxb13 genes. We determined that regions of Hox genes that play important roles in prostate development had altered DNA methylation in the sperm of F1 and F3. These alterations in DNA methylation were negatively related to gene expression. This is an observational study, as it was part of our previous research on the effects of thiacloprid on the testis and thyroid. Our analysis revealed that gestational exposure to thiacloprid induced an increase in cell proliferation in the prostates of directly exposed F1. Some persistent epigenetic alterations in the prostate of F3 males were not associated with phenotypic changes. Full article

The predatory mite Neoseiulus womersleyi is a key natural enemy in Integrated Pest Management (IPM), but its efficacy is threatened by non-target effects of acaricides like pyridaben. This study evaluated the transgenerational sublethal effects of pyridaben (LC₃₀ and LC₅₀) on N. womersleyi and explored the role of vitellogenin (Vg) genes. Using two-sex life table analysis, we found that exposure reduced longevity, fecundity, and oviposition period in F₀ females, while prolonging immature development and suppressing population growth parameters (r, λ) in F₁. Two Vg genes (NwVg1 and NwVg2) were cloned and characterized; their expression was significantly downregulated by pyridaben. RNAi-mediated silencing of NwVg1 or NwVg2 recapitulated the pyridaben-induced reproductive impairments, confirming their functional role. Our results demonstrate that pyridaben imposes multigenerational costs and that its reproductive toxicity is mediated, at least in part, through the suppression of Vg synthesis. Full article

Endocrine-disrupting chemicals (EDCs), widespread in aquatic environments, interfere with endocrine function in organisms and threaten ecosystem stability. Rotifers, critical live feed for marine fish, shrimp, and crab larvae, link EDC-induced reproductive impairment to marine ecosystem stability and aquaculture sustainability. This PRISMA-compliant review synthesizes key findings, consequences, and gaps in EDC–rotifer reproductive toxicity research. Traditional EDCs (heavy metals, per- and polyfluoroalkyl substances (PFASs), phenols, phthalate esters, polybrominated diphenyl ethers (PBDEs), and steroid hormones) and emerging EDCs (disinfection byproducts, microplastics, pharmaceutical metabolites) induce distinct reproductive harm—e.g., Hg²⁺ shows extreme toxicity (24 h LC₅₀ = 4.51 μg L⁻¹ in Brachionus plicatilis), BDE-47 damages ovaries, and microplastics cause transgenerational delays. Rotifer species and exposure duration affect sensitivity (e.g., BDE-47: 96 h LC₅₀ = 0.163 mg L⁻¹ vs. 24 h LC₅₀ > 22 mg L⁻¹ in B. plicatilis). Oxidative stress is a universal mechanism, and combined EDC exposure produces context-dependent synergistic/antagonistic effects. EDC-induced impairment reduces rotifer population density, alters structure, and propagates through food webs, threatening aquaculture and biodiversity; transgenerational toxicity (e.g., 4-nonylphenol: F₁ inhibition 28% vs. 12% in F₀) weakens resilience. This review supports EDC risk assessment, with gaps including long-term low-concentration data, transgenerational mechanisms, EDC–microbiome interactions, and emerging PFAS toxicity—priorities for future research. Full article

Pollution in aquatic ecosystems is intensifying under the combined pressures of climate change and anthropogenic contaminants, with nanoplastics (NPs) emerging as a critical threat to fish reproduction. Although extensive research has demonstrated the physiological impacts of NPs, their direct effects on sperm quality and functionality remain poorly characterized. This review synthesizes evidence from original research articles that specifically examined NPs’ impacts on fish sperm quality and related reproductive endpoints. The findings reveal that NPs consistently impair sperm motility, viability, and fertilization capacity, while inducing oxidative stress, DNA damage, mitochondrial dysfunction, and endocrine disruption. Particle size, surface chemistry, and exposure route were identified as key determinants of toxicity, with direct sperm exposure causing immediate impairments and chronic or maternal transfer exposures leading to systemic and transgenerational effects. Notably, several studies reported reduced offspring survival, altered development, and disrupted gene expression, highlighting the intergenerational risks of NPs contamination. Despite these advances, significant knowledge gaps remain, including limited research on marine wild and cultured fish species, the effects of diverse life histories on NPs toxicity, environmentally relevant exposure levels, and the combined effects of NPs with other stressors. Overall, this review underscores that fish sperm are highly sensitive to NPs pollution, with consequences that extend across generations and threaten population stability, calling for urgent mechanistic and ecologically realistic investigations. Full article

Phthalic acid esters (PAEs) are ubiquitous pollutants with reported endocrine-disruption and multiplex toxic activities in a wide range of invertebrate and vertebrate animals. In the present review, the molecular and physiological effects of phthalate exposure on invertebrates, as well as less characterized vertebrates such as amphibians, reptiles, and mammals, are thoroughly examined. PAEs induce a series of adverse effects, such as reproductive toxicity, oxidative stress, immune system impairment, and neuroendocrine disruption. The effects can extensively vary depending on the species, developmental stage, and environmental conditions, ranging from impaired hormone signaling, developmental malformations, and thyroid impairment in amphibians and reptiles to lipid metabolism disturbances and epigenetic changes in mammals. This review will place particular emphasis on transgenerational effects, mixture toxicity, and chronic low-level exposure. By integrating evidence from in vivo, in vitro, and omics studies, this review defines areas of knowledge gaps and the necessity to integrate these taxa in integrated ecological risk assessments, as well as regulatory policy. Full article

Symbiotic bacteria in insects are known to play crucial roles in detoxification metabolism and adaptation to host plant secondary metabolites. In the cotton-growing region of Xinjiang, China, the Ap. gossypii and the Ac. gossypii exhibit significant differences in sensitivity or resistance to pesticides. However, whether their detoxification-related symbiotic bacteria change under insecticide stress remains unclear. This study assessed the toxicity of nitenpyram to both aphid species and the effects of LC₂₀ treatment on their growth, development, and reproduction. Bacterial community dynamics across generations (G0–G2) were analyzed by 16S rRNA gene amplicon sequencing. The LC₂₀ of nitenpyram reduced the longevity and fecundity of the parent generation in both species. In Ap. gossypii, the intrinsic rate of increase (r_m), net reproductive rate (R₀), and finite rate of increase (λ) increased in the G1–G2 generations, whereas these parameters significantly decreased in Ac. gossypii. By the G3 generation, biological parameters in both species showed no significant differences compared to the control. Nitenpyram disrupted the stability of symbiotic bacterial communities in both aphids. In Ac. gossypii, Sphingomonas, a genus with detoxification potential, was consistently suppressed in G1–G2, while the abundance of the primary symbiont Buchnera initially decreased sharply and subsequently recovered. In contrast, the bacterial community in Ap. gossypii remained largely stable. These findings indicate that sublethal concentrations of nitenpyram exert distinct transgenerational effects on the two aphid species and disrupt the stability of their symbiotic bacterial communities. Full article

Nanoplastics have emerged as widespread environmental contaminants with toxicological properties that differ from those of microplastics. While existing reviews often examine their effects on specific organisms, they rarely provide direct comparisons with microplastics. This review aims to comprehensively assess the toxic effects of nanoplastics on animals, with a comparative perspective highlighting their distinctions from microplastics. In mammals, nanoplastics cross the blood–brain barrier and induce oxidative stress, neuroinflammation, mitochondrial dysfunction, and synaptic disruption, with consequences ranging from cognitive impairment to Parkinson’s disease-like neurodegeneration. They also impair liver, kidney, intestinal, pancreatic, and reproductive function, with evidence of transgenerational toxicity. In aquatic organisms such as fish, crustaceans, bivalves, and aquatic invertebrates, nanoplastics compromise growth, immunity, reproduction, and metabolism, while in terrestrial invertebrates they cause gut toxicity, mitochondrial damage, immune suppression, and heritable defects. Across taxa, the dominant mechanisms involve oxidative stress, apoptosis, inflammation, and interference with metabolic and signaling pathways. Comparisons with microplastics reveal that while both particle types are harmful, nanoplastics generally exert stronger and more systemic effects due to higher bioavailability, cellular uptake, and molecular reactivity. Microplastics primarily impose mechanical stress, whereas nanoplastics disrupt cellular homeostasis at lower exposure levels, often acting at the subcellular level. Evidence also indicates size-, surface chemistry-, and concentration-dependent effects, with smaller and functionalized nanoplastics exhibiting heightened toxicity. Despite growing knowledge, significant gaps remain in cross-size comparative studies, long-term and multigenerational assessments, trophic transfer analyses, and investigations involving environmentally derived nanoplastics. Addressing these gaps is critical for advancing ecological risk assessment and developing mitigation strategies against plastic pollution. Full article

Heavy metal and metalloid stress, particularly from toxic elements like cadmium (Cd), poses a growing threat to plant ecosystems, crop productivity, and global food security. Elevated concentrations of these contaminants can trigger cytotoxic and genotoxic effects in plants, severely impairing growth, development, and reproduction. In recent years, epigenetic mechanisms have emerged as crucial regulators of plant responses to heavy metal stress, offering novel insights and strategies for enhancing plant resilience in contaminated environments. This review synthesises current advances in the field of plant epigenetics, focusing on key modifications such as DNA methylation, histone acetylation and remodelling, chromatin dynamics, and small RNA-mediated regulation. These processes not only influence gene expression under metal-induced stress but also hold promise for long-term adaptation through transgenerational epigenetic memory. Recent developments in high-throughput sequencing and functional genomics have accelerated the identification of epigenetic markers associated with stress tolerance, enabling the integration of these markers into breeding programs and targeted epigenome editing strategies. Special attention is given to cadmium stress responses, where specific epigenetic traits have been linked to enhanced tolerance. As plant epigenomic research progresses, its application in sustainable agriculture becomes increasingly evident offering environmentally friendly solutions to mitigate the impact of heavy metal pollution. This review provides a foundation for future research aimed at leveraging epigenetic tools to engineer crops capable of thriving under metal stress, thereby contributing to resilient agricultural systems and sustainable food production. Full article