Search Results (1,151)

Background: The reproductive toxicity of first-line antituberculosis drugs remains poorly understood, particularly when used in combination. Rifampicin, isoniazid, pyrazinamide, and ethambutol are essential in tuberculosis therapy, but their potential influence on female fertility is uncertain. This pilot study evaluated their effects, given alone or in dual, triple, and quadruple combinations, on oxidative stress, endocrine markers, and reproductive outcomes in healthy female rats. Materials and Methods: Ninety-six albino Wistar-type female rats were divided into sixteen groups of six animals each and treated with single, dual, triple, or quadruple regimens of first-line antituberculosis drugs for 28 days. After treatment, two sexually mature males were introduced per group, and therapy continued for seven additional days. Serum malondialdehyde (MDA), total glutathione (tGSH), prolactin, and anti-Mullerian hormone (AMH) levels were measured, and fertility outcomes were evaluated. Results: In single-drug groups, MDA increased and tGSH decreased, but detectable infertility was not recorded. Prolactin remained stable except in the pyrazinamide group, where it declined. Dual-drug regimens increased oxidative imbalance; fertility failure occurred only in pyrazinamide-lacking groups and was accompanied by higher prolactin and lower AMH. Triple and quadruple combinations produced prominent oxidative imbalance. In triple-drug regimens, infertility was lower in pyrazinamide-containing groups than in the pyrazinamide-free group, but this pattern was not maintained in the quadruple regimen. Fertility impairment was not consistently aligned with the degree of oxidative stress and may involve prolactin and AMH alterations. Conclusions: These findings suggest that reproductive impairment under these experimental conditions may involve endocrine alterations and cannot be explained solely by serum oxidative imbalance. Pyrazinamide-associated fertility preservation appeared context-dependent and requires further confirmation in larger mechanistic studies with broader reproductive and endocrine assessment. Full article

Although the effectiveness of plant-derived essential oils (EOs) against several insect pests is well-documented, their high volatility presents a challenge. In this study, the potential to enhance the insecticidal activity of Satureja hortensis L. EO, an accessible natural agent, through nanoemulsification was assessed against the cosmopolitan pest Spodoptera frugiperda (J. E. Smith, 1797). The nanoemulsion of the EO (NEEO) was prepared using Tween 80 as the emulsifying agent and high-intensity ultrasonication. Oral bioassays indicated that the NEEO was more toxic (LC₅₀ = 0.922%) than the pure EO (LC₅₀ = 1.186%). Sublethal exposure to LC₃₀ of the NEEO caused evident reductions in preadult survival, developmental time, fecundity, and oviposition period, as well as the population growth parameter net reproductive rate (R₀). The exposure to the NEEO increased catalase (CAT), glutathione S-transferase (GST), and superoxide dismutase (SOD) actions and inhibited α-esterase (α-NE), β-esterase (β-NE), and cytochrome P450 (CYP450) actions. Both the NEEO and EO inhibited acetylcholinesterase (AChE) and Na⁺/K⁺-ATPase, with higher inhibition in the NEEO group. Generally, S. hortensis NEEO enhanced toxicity, intensified physiological perturbations, and caused greater negative impacts on population growth parameters. Consequently, nanoemulsification of S. hortensis EO can be considered an effective method to strengthen the insecticidal potential of this natural agent. Full article

Marine invertebrates are characterized by high species diversity, a wide distribution, ease of culture, low cost, short life cycles and high sensitivity to pollutants, which makes them excellent models for observing toxic effects and elucidating underlying mechanisms. This paper reviews representative species from three phyla—Arthropoda, Mollusca, and Echinodermata—under both single emerging contaminant exposure and combined exposure scenarios, and analyzes the reproductive and neurotoxic impacts of these contaminants on marine invertebrates. Neurotoxicity is mediated by several key mechanisms: inhibition of acetylcholinesterase activity; disruption of neurotransmitter balance, oxidative stress; and cellular damage, interference with embryonic neural development and axis specification, and impairment of neural cell differentiation and migration. Reproductive toxicity impairs reproductive development by disrupting endocrine signaling, inducing oxidative stress, downregulating reproduction-related genes and damaging gonadal structure. Studies have shown that, besides environmental factors, contaminant concentration is closely correlated with toxic potency and differing concentration ratios can lead to either antagonistic or synergistic effects in combined toxicity. Current research has largely focused on single or binary contaminant systems, whereas studies on multi-contaminant mixtures and their interactions with multiple environmental factors remain limited. Future research should prioritize combined exposure to multiple contaminants, long-term multigenerational observations and the development of comprehensive ecological risk assessment models and monitoring standards, thereby providing a scientific basis for marine ecological conservation. Full article

Emerging contaminants pose significant risks to ecosystems yet are not routinely included in standard monitoring or regulatory frameworks. Among these substances, endocrine disruptors such as β-estradiol and 17α-ethinylestradiol threaten both human and environmental health by interfering with metabolism, reproduction, and development across multiple species. These hormones are continuously released into the environment through excretion and improper disposal, and conventional water treatment processes are largely ineffective at removing them. As a result, they can accumulate in aquatic organisms and enter the human food chain. Recent studies have demonstrated that banana peel, Pleurotus ostreatus biomasses, and the nanomaterial δ-FeOOH are efficient, low-cost materials for the removal of toxic metals, suggesting their potential applicability for eliminating estrogenic compounds. Therefore, this study aimed to evaluate the removal of β-estradiol and 17α-ethinylestradiol using filters composed of banana peel and P. ostreatus biomass combined with δ-FeOOH. Hormone removal efficiency was assessed by LC-MS, and toxicity reduction was evaluated through bioassays. The results showed up to 100% removal of hormone concentrations and a significant decrease in sample toxicity, indicating that this filtration system represents a safe and effective alternative for removing organic contaminants from water. Full article

The invasive plant Datura stramonium L. possesses strong reproductive capacity and ecological adaptability, showing a tendency to spread rapidly, especially in highly human-disturbed habitats. To explore its resource utilization pathway—turning waste into wealth—and to address toxic metal pollution in strongly human-disturbed areas (such as mining regions), this study evaluates its phytoremediation potential in contaminated soils on the Qinghai–Tibet Plateau. We established a non-planted control and three planting density treatments to compare the removal rates of Pb, Cd, Cr, and As. To our knowledge, this is the first study to assess how planting density influences the multi-metal phytoremediation performance of this invasive species in a high-altitude plateau environment. The results showed that planting significantly increased toxic metal removal rates, with overall efficiency generally improving at higher densities, particularly for Cr. Analysis of bioconcentration and translocation factors revealed distinct element-specific accumulation patterns. Pb and As were primarily enriched and retained in the roots. Interestingly, while Cd exhibited a strong localized tendency to accumulate in the leaves, its overall root-to-shoot translocation remained relatively restricted at the whole-plant level, similar to Cr. Overall, D. stramonium functions primarily through root stabilization for Pb, As, and Cr, alongside partial aboveground accumulation for Cd. However, given its toxic and invasive nature, any practical phytoremediation application requires strict post-harvest biomass management and ecological monitoring to prevent secondary spread. Full article

Benthic foraminifera, single-cell marine organisms found worldwide, represent an important component of seabed ecosystems. Due to their sensitivity to environmental pollution, they are often used as bioindicators, providing an efficient tool in toxicity studies. Among the pollutants affecting marine coastal and estuarine environments, persistent flame retardants, such as polybrominated diphenyl ethers (PBDEs), are frequently found. Low-level exposure to BDE-47, a PBDE congener, is known to affect organismal development. In this framework, this study aims to assess the effects of BDE-47 exposure on benthic foraminifera from coastal marine environments. Foraminifera specimens belonging to the symbiont-bearing Peneroplidae family were sampled and exposed to two different BDE-47 concentrations for up to 48 h. Vitality indicators such as changes in pseudopodial activity, movement, reproduction, loss of symbiont algae, and occasional mortality events were monitored during the experiment. Exposure to BDE-47 induced alterations in pseudopodial activity, movement, reproduction, and symbiont retention, with the progressive loss of vitality and limited mortality at increasing exposure levels, highlighting the sensitivity of this species to BDE-47. These findings suggest the harmful repercussions of PBDE pollution on marine coastal ecosystems, affecting benthic organisms and potentially contributing to biomagnification processes within the food web, with possible implications for human health. Full article

The prevalence of plastics in the environment raises concerns about their complex and poorly understood effects on human health. Research continues to uncover more sources of exposure and wider ranges of plastics within the body. Adverse health effects have been observed in animals, but their relevance to humans remains unclear. To address the growing need for reliable toxicity assessment resources and tools to aid in the synthesis of findings and the identification of data gaps and needs, we have developed a data visualization tool to provide streamlined access to the evaluated data on the chemical impacts of plastics on human health. The Plastics-Related Toxicology Profiles Tool uses Tableau Public to organize the extracted chemical-specific information from ATSDR Toxicological Profiles, the United Nations Environmental Program’s 2023 Chemicals in Plastics Technical Report, and a literature review of relevant research in Google Scholar and PubMed. The tool organizes extracted data from 98 ATSDR Toxicological Profiles representing over 476 substances related to plastics production in 16 tabulated health outcome categories associated with plastics exposure. The chemicals are organized into four categories based on their role in plastics manufacturing. The top four health endpoints impacted by all listed substance profiles are respiratory, neurologic, hepatic, and developmental effects. More than 30% of the substance profiles affected these systems as well as other non-cancer endpoints involving the immunological, renal, and reproductive systems, as well as increased cancer risk in respiratory and hepatic systems. Most monomers negatively impact development and the respiratory system, and most metal additives affect the respiratory system. We explain how this data visualization tool combined with ATSDR’s framework for assessing health impacts from multiple chemicals could be applied to identify the target organs impacted by components of the common plastic polyvinyl chloride. Hazard quotients and index show low toxicity and health risk of components in the cured product. This data provide a valuable resource for prioritizing health risk assessments. Use of this interactive tool can enhance the ability of public health professionals to navigate the expanding literature, synthesize findings, and identify future health risk assessment and research priorities. Full article

Plastic-derived chemical additives, including bisphenols, phthalates, perfluoroalkyl substances (PFAS) and microplastic-associated contaminants, are now recognised as widespread environmental toxins that measurably affect endocrine signalling, oxidative balance, inflammation and metabolic homeostasis. Continuous exposure through food contact materials, consumer products, and environmental media raises concerns about long-term health effects. An increasing number of epidemiological and experimental studies are linking these exposures to metabolic disorders, reproductive dysfunction, neurodevelopmental alterations, and increased disease susceptibility throughout the lifespan. This narrative review summarises the latest evidence on the toxicological mechanisms of these compounds, with a focus on endocrine disruption, redox imbalance, reproductive impairment, thyroid hormone dysregulation and epigenetic modifications induced by plastic-derived chemicals. Literature was identified through searches of major scientific databases, including PubMed, Scopus, and Web of Science. Reference screening was also employed to complement these searches and ensure comprehensive coverage of vertebrate and invertebrate models. The inclusion criteria encompassed studies published within the last 10 years, focusing on experimental, experimental, and translational research. The review evaluates phytochemicals such as polyphenols, flavonoids, isoflavones, catechins, sulforaphane, and chlorogenic acid as natural agents that can mitigate the biological effects of plastic-derived toxicants. These compounds exhibit antioxidant, anti-inflammatory, and receptor-modulating properties that counteract pathways disrupted by BPA, phthalates, and PFAS. Experimental studies have demonstrated that phytochemicals can modulate oestrogen receptor activity, enhance detoxification systems, reduce oxidative biomarkers and mitigate epigenetic and metabolic alterations induced by micro- and nanoplastics. Emerging nutritional evidence suggests that diets high in polyphenols may reduce the biological impact of plastic-derived contaminants within the body, rather than reducing exposure itself. This effect appears to be especially relevant during sensitive developmental periods, such as the prenatal, early postnatal and adolescent stages. Full article

Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous combustion-derived contaminants that represent a significant cross-cutting threat to human, animal, and environmental health. Viewed through an explicit One Health lens, this review shows how the shared combustion sources, evolutionarily conserved toxicological mechanisms, and food-web linkages connecting environmental contamination to wildlife and human exposure justify an integrated, cross-domain approach to PAH risk assessment and management. PAHs are generated predominantly through incomplete combustion of organic materials and are globally distributed through atmospheric transport, aquatic runoff, and food-web transfer, persisting in soils and sediments for decades. The present review synthesizes current knowledge on PAHs through an explicit One Health lens, examining shared sources, environmental fate, and convergent health effects across species and health domains, while also highlighting the need to move beyond the classical US EPA priority PAHs to include high-molecular-weight PAHs (>302 Da), alkylated homologues, and transformation products such as oxy- and nitro-PAHs. Common pathways such as dietary intake of grilled and smoked foods, inhalation of contaminated air, and occupational exposure create parallel toxicological burdens in both human and wildlife populations, particularly through genotoxic mechanisms mediated by aryl hydrocarbon receptor (AhR) activation and CYP1A1/CYP1B1-catalyzed bioactivation to reactive diol epoxides. The resulting DNA adduct formation links environmental PAH exposure to carcinogenicity, reproductive toxicity, immunosuppression, and developmental impairment across vertebrate species with remarkable mechanistic consistency. Wildlife, especially fish, marine mammals, and seabirds, serve as critical sentinels for environmental PAH contamination, while simultaneously facing direct health impacts on immune function, reproduction, and population viability. Vulnerable human populations, including children, subsistence communities, occupational workers, and residents near combustion-intensive industries, bear disproportionate burdens reflecting underlying environmental justice concerns. Integrated intervention strategies encompassing source control, dietary exposure reduction, site remediation, and coordinated biomonitoring are urgently needed. By incorporating emerging PAH classes with distinct persistence, trophic behavior, and toxicological potency, the One Health paradigm provides a more comprehensive conceptual framework for modern environmental surveillance, food safety, and integrated risk assessment, recognizing that the health of terrestrial and aquatic ecosystems is inseparable from that of the animals and humans within them. Full article

Exposure to heavy metals remains a significant public health concern due to their environmental persistence, bioaccumulation, and ability to interfere with essential cellular processes. A large part of metal-induced toxicity converges on the establishment of a chronic oxinflammatory state, driven by the reciprocal interaction between oxidative stress and inflammation. In this review, we synthesize current mechanistic evidence describing how toxic metals, including aluminum, arsenic, cadmium, lead, mercury, and nickel, disrupt redox homeostasis, impair cellular integrity, and activate inflammatory signaling pathways. These metals promote the excessive generation of reactive oxygen and nitrogen species through multiple mechanisms, including mitochondrial dysfunction, displacement of essential metal cofactors, and inhibition of antioxidant systems. The resulting molecular damage leads to the formation of damage-associated molecular patterns (DAMPs), which activate redox-sensitive transcription factors and inflammatory cascades. Importantly, emerging metabolomic evidence indicates that these processes are accompanied by coordinated metabolic reprogramming involving amino acid, lipid, and energy metabolism, as well as microbiota-derived metabolites. These metabolic alterations not only reflect cellular adaptation to stress but also actively contribute to the propagation of a systemic inflammatory state. An integrated oxinflammatory and metabolic response underlies structural and functional alterations across multiple organ systems, including the liver, kidneys, cardiovascular system, nervous system, and reproductive organs. Persistent exposure, even at low doses, sustains this often subclinical and chronic process, reinforcing the need to understand metabolic changes as central components of metal-induced toxicity. Full article

Pomacea canaliculata, listed among the world’s 100 worst invasive alien species, poses serious threats to rice production and freshwater ecosystems. This review synthesizes current research in physiological ecology, molecular genetics, and invasion ecology to examine its invasion success from a multiscale mechanistic perspective. P. canaliculata exhibits broad environmental adaptability at physiological, molecular, and behavioral levels. These adaptations include seasonal cold tolerance, drought-induced dormancy and post-dormancy recovery, acclimation to both freshwater and brackish environments, and tolerance to a range of pollutants and pesticides, including evidence of toxicant-induced hormesis. The species also shows pronounced phenotypic plasticity in growth, reproduction, and resource utilization. Genomic plasticity, multiple introduction events, and introgressive hybridization with closely related species further enhance its evolutionary potential and dispersal capacity. In addition, P. canaliculata displays behavioral adaptations such as learning and alarm responses. The synergistic interaction of these multilayered adaptive mechanisms underpins the global invasion success of this species. This review also identifies key uncertainties in current research and emphasizes the need for greater integration of multi-omics approaches, long-term monitoring of population dynamics in hybrid zones, and experimental studies addressing the interactive effects of multiple stressors, with the ultimate aim of improving invasion risk prediction and management. Full article

Objective: This study aimed to investigate whether pomolic acid (PA), a predicted bioactive metabolite of the Dong botanical drug Madeng’ai (MDA), suppresses inflammatory cytokine expression by inhibiting nuclear factor-κB (NF-κB) pathway activation in a tumor necrosis factor-α (TNF-α)-induced human rheumatoid arthritis fibroblast-like synoviocyte (RA-HFLS) model. Methods: PA content in MDA from different regions and harvest years was quantified via High-Performance Liquid Chromatography (HPLC). Network analysis was employed as a hypothesis-generating tool to predict potential targets and pathways, followed by molecular docking to validate the binding affinity of PA to core targets of the NF-κB pathway, and ADMET prediction to evaluate its pharmacokinetic properties and safety profile. The RA-HFLS inflammatory model was induced by TNF-α. Cell viability and inflammatory cytokine secretion were assessed using Cell Counting Kit-8 (CCK-8) and enzyme-linked immunosorbent assay (ELISA). NF-κB signaling pathway activation and downstream gene expression were examined by Western blot and reverse transcription quantitative polymerase chain reaction (RT-qPCR), respectively. Results: HPLC analysis revealed that MDA samples from Guizhou harvested in 2019 contained the highest PA content (0.1117 mg/g). Network analysis predicted the NF-κB signaling pathway as a candidate mechanism underlying PA’s potential anti-inflammatory effects. Molecular docking showed that PA stably bound to IKKβ, p65, and IκBα, while ADMET prediction indicated favorable intestinal absorption, low drug–drug interaction risk, and good genetic safety, albeit with potential hepatotoxicity and reproductive toxicity risks. In the TNF-α-induced RA-HFLS model, PA dose-dependently inhibited abnormal cell proliferation and significantly reduced the secretion of pro-inflammatory cytokines TNF-α and interleukin-6 (IL-6). Mechanistic studies indicated that PA suppressed the activation of the NF-κB signaling pathway, thereby downregulating the mRNA expression of inflammatory genes such as IL-6, TNF-α, and interleukin-1β (IL-1β). Conclusions: PA, a bioactive metabolite of the Dong botanical drug MDA, may inhibit NF-κB signaling pathway activation, thereby downregulating TNF-α-induced inflammatory cytokine expression in RA-HFLS, demonstrating its in vitro anti-inflammatory potential. Full article

Paroxetine, a selective serotonin reuptake inhibitor commonly used to treat various psychiatric disorders, may adversely affect female reproductive function. Although apigenin has been shown to ameliorate reproductive abnormalities and ovarian dysfunction, its effect on paroxetine-induced reproductive toxicity in females remains unclear. Therefore, this study investigated the potential protective effects of apigenin against paroxetine-induced reproductive alterations in female rats. Female rats with regular estrous cycles were randomly assigned to four groups (n = 9 per group): control, apigenin, paroxetine, and paroxetine + apigenin. The rats received saline, apigenin (20 mg/kg), paroxetine (10 mg/kg), or their combination by oral gavage once daily for about 29 consecutive days. Compared with paroxetine treatment alone, apigenin co-administration restored decreased serum anti-Müllerian hormone (AMH) levels, enhanced PAS reactivity in the zona pellucida, reduced ovarian iNOS immunoreactivity, increased follicle and corpus luteum numbers, and increased ovarian VEGF immunoreactivity. However, apigenin administration alone was associated with reduced testosterone levels and alterations in certain ovarian and uterine histological features in female rats. In conclusion, the findings suggest that apigenin may ameliorate paroxetine-induced reproductive alterations in female rats by modulating AMH levels, follicle and corpus luteum numbers, and ovarian histochemical and molecular parameters. Full article

Male infertility is an increasing global health concern associated with declining population growth. Mancozeb (MZ) exposure may induce reproductive toxicity through endocrine disruption and oxidative stress, impairing spermatogenesis. This study evaluated the effects of White Bualuang extract (WBE) on sexual behavior, testicular histomorphometry, and spermatogenic parameters in rats exposed to MZ. Thirty mature male rats were randomly assigned to the following five groups (n = 6): Control, MZ 500 mg/kg, MZ + 0.55 mg/kg WBE, MZ + 1.10 mg/kg WBE, and MZ + 2.20 mg/kg WBE, for 30 days. Sexual behaviors, relative testis weight, antioxidant properties, and histomorphometry parameters were determined. MZ-exposed rats had significantly decreased courtship behavior, seminiferous tubule diameter, and a tendency toward decreased spermatogenic cell numbers, along with enlarged interstitial spaces. However, pretreatment with WBE, especially at a dose of 0.55 mg/kg, showed improvements in courtship behavior and several histomorphometry parameters and was associated with increased Sertoli cell efficiency and spermatogenic organization compared with the MZ group. WBE showed potential to reduce lipid peroxidation (LPO) and advanced oxidation protein products (AOPP) in MZ-exposed rats, particularly, the 0.55 mg/kg dose improved courtship behavior and reproductive parameters, supporting further investigation of WBE as an antioxidant and potential functional supplement. Full article

The molecular mechanism underlying male reproductive toxicity associated with Perfluorooctanoic acid (PFOA), a persistent environmental endocrine disruptor (EDC), has not yet been fully elucidated. Six-week-old male C57BL/6 mice were treated with PFOA by oral gavage at 0, 1.25, 5, 10, and 20 mg/kg/day for 35 days to explore its toxic effects on the male reproductive system and the underlying mechanisms. Analyses of semen quality, testicular histopathology, and blood–testis barrier (BTB) integrity revealed that PFOA caused dose-dependent structural and functional damage to the BTB, leading to markedly reduced semen quality. Based on transcriptomic sequencing and differential gene enrichment analysis, the glycolytic pathway was identified as a key regulatory target for PFOA-induced damage to the reproductive system. Further validation revealed that PFOA exposure inhibited glycolysis-related enzymes (Hexokinase 1 (HK1), Glucose Transporter 1 (GLUT1), and Lactate Dehydrogenase A (LDHA)), reduced lactate production and ATP synthesis, lowered Pan-Kla and H3K18la levels, and diminished H3K18la enrichment at the Hk1, Glut1, and Ldha promoters, whereas exogenous sodium lactate reversed these changes. This study is the first to identify the “glycolysis–lactate–H3K18la” chain as a key regulator in PFOA-induced BTB damage and spermatogenesis impairment, offering a new theoretical foundation for understanding EDC-induced male reproductive toxicity. Full article