Nanoparticles (NPs), due to their small size and unique physico-chemical properties are now being increasingly utilized in agriculture, commerce, industry and medicine, raising concerns about their systemic health effects on human health. Amongst vulnerable systems, the endocrine glands have been identified as critical target(s) of NP toxicity. Present review highlights current understanding of mechanisms viz. oxidative stress, inflammation, apoptosis disruption of hormone synthesis and metabolism, involved in endocrine toxicity of metallic nanoparticles. Experimental evidence suggests that NPs can enter endocrine glands, mimic hormones, interact with hormone receptors and disrupt downstream signaling pathways. Specific effects of NPs thus induced in endocrine glands viz. thyroid, parathyroid, thymus, pineal, pancreas, adrenals, placenta and hypothalamo-pituitary axis have been documented. Since, a few nanoparticles do exhibit antioxidant properties or therapeutic potential, their dual role as endocrine disruptors and therapeutic agents contributes to diverse and complex biological manifestations. The review emphasizes the need for advanced experimental models, including organ chip systems and multi-omic approaches to better evaluate NP-induced endocrine disruption. The review concludes that endocrine toxicity remains crucial for risk assessment and safe integration of nanotechnology into health care, theranostics, industrial, commercial and environmental applications.
With the increasing use of pesticides, particularly glufosinate ammonium (Finale®), and the herbicide-resistant weeds, specifically those resistant to glyphosate, alongside the development of transgenic crops tolerant to glufosinate ammonium, it has become crucial to better understand the effects of herbicides on terrestrial ecosystems. This study aimed to assess the ecotoxicological effects of glufosinate ammonium on earthworms (Eisenia andrei), with a focus on acute and chronic toxicity, as well as avoidance behavior. The tests were conducted under controlled laboratory conditions. The trials included five concentrations of glufosinate ammonium and an untreated control (acute: 0, 175, 340, 505, 670, and 835 mg ai kg−1; chronic and avoidance: 0.0, 3.3, 5.0, 6.7, 8.3, and 10.0 mg ai kg−1), with four replicates for the acute and chronic tests, and five replicates for the avoidance test. The results revealed significant impacts on the survival, biomass, reproduction, and avoidance behaviors of earthworms at certain concentrations. The LC50-14d was determined to be 611.68 mg ai kg−1, indicating moderate herbicide toxicity. The EC50 for reproductive effects at 56 days and avoidance behavior within 48 h were 4.49 mg ai kg−1 and 3.30 mg ai kg−1, respectively. Concentrations of 8.3 and 10 mg ai kg−1 triggered the highest escape responses. This study demonstrates that even sublethal levels of glufosinate ammonium can significantly impair the reproductive capacity and avoidance behavior of E. andrei.
Organophosphate (OP) poisoning is a major public health concern in Nigeria, driven by the widespread availability of pesticides such as Sniper (dichlorvos) and Otapiapia. Despite its high morbidity and mortality, local evidence remains fragmented across isolated case reports and single-centre reviews. This systematic review aggregated the clinical patterns, exposure characteristics, management approaches, and outcomes of OP poisoning in Nigeria. A comprehensive search was conducted (January 2000–August 2025) across PubMed, AJOL, Scopus, and Google Scholar, using PRISMA guidelines. Eligible studies were case reports, case series, retrospective or prospective clinical reviews, cross-sectional and cohort studies that reported OP-specific data in Nigerian patients. Data on demographics, exposure, clinical features, management, and outcomes were extracted using a standardised form and pooled together descriptively. Twenty-three studies (176 OP cases) were reported. Males constituted 54.5
Chronic arsenic exposure represents a major public health concern in regions with contaminated groundwater, where long-term bioaccumulation may lead to adverse health outcomes. This study explores the potential genotoxic effects of arsenic exposure in women residing in an arsenic-endemic region by integrating multi-matrix arsenic quantification with whole exome sequencing (WES). Arsenic concentrations were measured in blood, urine, and breast milk samples from nine participants. Elevated arsenic levels were detected across all biological matrices, with each participant exceeding WHO or CDC recommended limits in at least one sample type. Notably, eight of the nine women exhibited breast milk arsenic concentrations above the 1 µg/L reference level, indicating a potential exposure pathway for infants during lactation. Whole exome sequencing identified rare or novel variants in key DNA repair genes in two participants, including a likely pathogenic ATM missense variant (c.590G > A; p.Gly197Glu) and a novel MSH6 variant (c.3716 T > C; p.Ile1239Thr) predicted to be damaging by computational analyses. These genes play essential roles in DNA damage response and mismatch repair pathways that are important for maintaining genomic stability. Although the small sample size (n = 9) limits causal interpretation, these findings provide preliminary evidence suggesting a possible association between chronic arsenic exposure and alterations in DNA repair genes. The study highlights the value of integrating environmental exposure assessment with genomic analysis and provides a hypothesis-generating foundation for future large-scale investigations into gene–environment interactions in arsenic-exposed populations.
The rapid progress of nanotechnology has inevitably led to the increasing presence of nanopollutants in aquatic environments. Silver nanoparticles (AgNP), or nanosilver, are among the most widely used nanomaterials owing to their unique biocidal properties; however, nanotoxicological concerns have risen in parallel with their expanding applications. Freshwater systems represent one of the most important final sinks for these contaminants, and fish are widely used test organisms for toxicological assessment due to their sensitivity, physiological complexity, and multiple exposure routes. This mini-review aimed to synthesize current knowledge on surface-driven AgNP toxicity in freshwater fish, focusing on the role of capping agents, eco-corona formation, and environmentally relevant transformations. A structured literature search across five databases was conducted following the reporting guidelines of the PRISMA extension for scoping reviews (PRISMA-ScR), retrieving 21 studies that met the inclusion criteria of waterborne exposure and at least one comparative ecotoxicological assessment of surface modulators. Evidence indicates that surface coating clearly influences toxicological outcomes; however, contradictions remain regarding whether toxicity is driven by the coating itself, the nanoparticle, or Ag⁺ release, with particle size and surface charge emerging as the most consistent physicochemical drivers. Humic and fulvic substances represent the most studied environmental modifiers and generally exert mitigating effects on AgNP toxicity, while also markedly influencing particle fate and bioavailability. Knowledge gaps persist regarding exposures at environmentally relevant concentrations, the ecotoxicity of green-synthesized AgNP in fish, and the underrepresentation of eco-corona studies relative to coating-focused research, reflecting the current state of the literature in this field.
Bihar, a densely populated region in eastern India, faces significant public health challenges due to environmental contamination by heavy metals. Arsenic (As) and lead (Pb) are persistent toxicants known to adversely affect multiple physiological systems. This study assessed blood As and Pb concentrations and their associations with haematological parameters among adults residing in thirteen districts of Bihar. A cross-sectional biomonitoring study was conducted on 1279 adults, around rural and semi-urban populations. Mean blood As and Pb concentrations were 41.86 and 369.19 µg/L, respectively, indicating widespread exposure. Haematological assessment revealed a high prevalence of abnormalities, including low red blood cell counts (42.7
Reno-cardiac syndrome or toxicity, a significant global health concern, involves underlying factors like inflammation, programmed cell death, and oxidative stress. Arsenic, a pervasive environmental contaminant, poses significant health risks to vertebrates due to its widespread distribution. Acute exposure has been associated with cardiovascular disorders and, more recently, renal dysfunction, contributing to increased morbidity and mortality. This study is designed to evaluate whether low-dose vitamin E (α-tocopherol) supplementation mitigates arsenic-induced reno-cardiac toxicity and elucidate the molecular mechanisms underlying its protective effects. Thirty-five adult male Wistar rats were randomly assigned into five groups of seven animals each and orally administered vitamin E (25 and 50 mg/kg) for 7 days prior to concurrent co-administration of sodium arsenite (10 mg/kg) and vitamin E for a further 7 consecutive days. Animals challenged with sodium arsenite exhibited marked increases in serum creatinine, lactate dehydrogenase, and urea, as well as elevated cardiac biomarkers, including creatine kinase-MB, alkaline phosphatase, antioxidant enzyme activities, and glutathione levels, reducing oxidative stress and inhibiting apoptosis. Notably, vitamin E shifted the Bax/Bcl-2 ratio towards Bcl-2, thereby favouring cell survival. Overall, these findings indicate that vitamin E not only counteracts arsenic-induced oxidative and redox disturbances in renal and cardiac tissues but also modulates the intrinsic apoptotic pathway to confer protective effects.
Aluminum cookware remains widely used in household and commercial food preparation, particularly in small-scale food vending systems, raising concerns regarding environmental quality and human exposure through food-contact materials. This pilot study evaluated aluminum migration into foods under typical cooking conditions and examined behavioral and socio-educational determinants influencing cookware usage. A structured questionnaire survey of food vendors (n = 35) was statistically analyzed using chi-square tests and correlation analyses to assess associations between education level, awareness of aluminum-related health risks, and cookware-use behavior. Aluminum concentrations in food samples were quantified following standardized laboratory analytical procedures. Survey results indicated that 82.9
Developmental exposure to environmental neurotoxicants can program persistent vulnerability to oxidative and genomic injury. We compared the long-term effects of developmental manganese (Mn) and the dietary flavonoid quercetin in Drosophila melanogaster. Larvae were exposed to ordered doses of Mn or quercetin; adult outcomes (n = 4 vials/group unless stated) included survival, negative geotaxis (RING), hydrogen peroxide (H2O2), glutathione redox state (GSH/GSSG), malondialdehyde (MDA), antioxidant enzymes (SOD, CAT), acetylcholinesterase, dopamine, DNA fragmentation index (DFI) and advanced glycation end-products (AGEs). Conventional omnibus and pairwise post-hoc tests (ANOVA/Tukey or Kruskal–Wallis/Dunn) identified significant, dose-dependent increases in H2O2 and DFI with Mn exposure. Quercetin developmental exposure produced protective trends in redox markers and reduced genomic fragmentation signals. These findings implicate oxidative burden and DNA damage as measurable biomarkers of developmental Mn programming and identify candidate endpoints for targeted mechanistic and translational studies.
Plant protection products (PPP) contain active substance(s) and co-formulants. As complex mixtures, PPPs are susceptible to toxicokinetic or toxicodynamic interactions, enhancing toxicity. Considering these interactions is crucial to avoid underestimating risk. In vitro testing identifies toxicokinetic interactions among PPP components and establishes toxicological threshold values for these products. In vitro-in vivo extrapolation (IVIVE) using physiologically based kinetic (PBK) modeling helps derive organism-based threshold values for PPPs. Currently, PBK modeling is primarily applied to single substances. We present a proof-of-concept for generating data for whole-mixture PBK modeling for PPP operator risk assessment. A PPP containing difenoconazole and mandipropamid was selected based on our previous study, which identified their metabolic interactions. Since PPP operators are predominantly dermally exposed, traditional rapid equilibrium dialysis (RED) for determining fraction unbound and pooled human liver microsomes (HLM) for hepatic clearance are insufficient. We integrated RED and HLM with EpiDerm Full Thickness 400 (EFT-400), a skin-penetration model. EFT-400 was spiked with concentrated and dilutions of formulated product and pure difenoconazole for 24 h before transferring receptor contents to RED or HLM. Difenoconazole concentration was measured using LC-MS/MS, and fraction unbound and hepatic clearance were determined. Hepatic clearance of difenoconazole decreased significantly in concentrated formulated product and dilutions compared to pure difenoconazole, indicating CYP enzyme inhibition by mandipropamid. Difenoconazole fraction unbound remained unchanged in concentrated formulated product but increased with product dilution. This strategy provides a framework for PBK modeling of mixtures, acknowledging potential combination effects and toxicokinetic interactions within complex mixtures with clear risk drivers such as PPPs.
Exposure to fluoride above the recommended dose has been shown to have toxicological consequences on several body systems. There is a paucity of information on neurotoxic effect of exposure of varying doses of sodium fluoride (NaF) on specific brain regions. Hence, we investigated the toxicological consequences of 30- and 60-day exposure to varying doses of NaF on neurobehavioral outcomes and region-specific brain alterations in adult Wistar rats, with biochemical analyses conducted in the hippocampus and striatum, and immunohistochemical assessment of astrocytic activation in the striatum and myelin integrity in the corpus callosum. Eighty-four Wistar rats of 100–120 g were randomly divided into six groups. Rats in experimental groups (groups B–F) were administered NaF in deionized water at concentrations of 25, 50, 100, 150, and 300 ppm, respectively, via oral administration for 30 and 60 days. The control group (group A) received only deionized water for the same duration. Neurobehavioral assessments were carried out, and brain samples (striatum and hippocampus) were collected for biochemical assays and immunohistochemistry. Sodium fluoride caused a significant influence on locomotor activities and anxiety. Moreover, NaF caused a significant increase in malondialdehyde and decreased GSH level, superoxide dismutase and glutathione peroxidase activities. The activity of acetylcholinesrase (AchE) was also significantly reduced by all the administered doses of NaF. There was increased GFAP immunoreactivity in the NaF treated rats, and reduced myelin basic protein immunoreactivity in the corpus callosum. NaF exposure compromises brain health by disrupting antioxidant defenses, altering neurochemical balance, promoting astrocytic activation, and inducing demyelination, ultimately resulting in neurobehavioral impairments.
Paracetamol has a wide safety margin at therapeutic doses but overdose may cause life-threatening hepatotoxicity particularly in children. We report a case of a 3-year-old African female who presented to Malindi Sub County Hospital (MSCH) with severe dehydration, pneumonia, and convulsions. A detailed clinical history from her grandmother and medication reconciliation at the hospital revealed that she had inadvertently received a 5000 mg supratherapeutic dose of paracetamol over 48 h. Liver function tests (LFTs) showed marked amino transferases (peak ALT: 1566.2 IU/L, AST: 302.3 IU/L), rising gamma-glutamyl transferase (GGT) and hypoalbuminemia. Clinical coagulopathy was suspected based on blood oozing at the cannula site and epistaxis triggered by nasogastric tube insertion. Given the resource-limited nature of MSCH, measurements on serum paracetamol, international normalized ratio (INR), and prothrombin time (PT) were not done prompting empirical administration of fresh frozen plasma (FFP). N-acetylcysteine (NAC) was initiated more than 84 h after paracetamol exposure due to regional stockouts and barriers in procurement. Despite this delay, patient liver enzymes improved rapidly (ALT: 431.1 IU/L, AST: 105.6 IU/L) and she regained consciousness several hours post-NAC administration. This case report highlights how system failures in a resource-limited setting may compromise the management of paracetamol poisoning. This case highlights how system failures such as medication errors, misdiagnosis, poor caregiver education, and limited antidote access in resource-limited healthcare settings may result in sub-optimal care in pediatric paracetamol poisoning. Proper history taking, patient examination, and medication reconciliation are key in managing suspected paracetamol poisoning. Fortunately, even the late administration of N-acetylcysteine (> 24 h) abrogates severe hepatotoxicity in children with paracetamol poisoning. The close monitoring of liver function and clinical status is essential in managing pediatric paracetamol poisoning.
The emergence of New Psychoactive Substances (NPSs) has become a growing concern for global public health and security. The nitazene analogues, a group of synthetic opioids that could present a higher potency than morphine and fentanyl, have been associated with fatal overdoses. Nitazene analogues have been frequently found on the drug market, often combined with other substances, which significantly increases the risk of poisoning. This work aims to review the toxic effects and abuse potential of nitazene analogues, through the review of scientific articles and technical notes, from 2020 to 2024, in the databases PubMed/Medline, Scielo, and Google Scholar. The desired effects associated with the use of nitazene include euphoria and relaxation, but they can also lead to undesirable effects, such as edema, dizziness, drowsiness and respiratory depression, in addition to the risk of cardiac arrest. Prolonged exposure is associated with the development of dependence and withdrawal symptoms after abrupt cessation. One of the main clinical concerns is the difficulty in the use of traditional overdose reversal methods, such as naloxone, due to the higher potency of some analogues compared to morphine or heroine. Laboratory analysis is one of the main challenges due to the low concentration of nitazene analogues in samples. The complexity of toxicity, abuse potential, and difficulties in reversing intoxication reinforce the need for specific intervention protocols and training for health professionals on the risks of synthetic opioids. Better understanding the toxicokinetics and effects of nitazenes group are essential steps to develop effective drug policies and minimize the harm to human health caused by these compounds.
New psychoactive substances (NPS) represent an emerging public health concern, with synthetic cannabinoid receptor agonists (SCRAs) among the most prevalent classes worldwide. Although widely reported in seizures and toxicological casework, their pharmacology and toxicity remain poorly characterized. In this study, we investigated the acute toxicity and behavioral effects of two emerging SCRAs—ADB-INACA and CHO-4′Me-5′Br-FUBOXPYRA—using zebrafish (Danio rerio) as an in vivo model. Fish embryo acute toxicity (FET) and maximum tolerated concentration (MTC) assays were performed to assess lethality and sublethal effects in early developmental stages. Social behavior was evaluated at 21 days post-fertilization (dpf) using the Fishbook assay, and drug-seeking behavior was investigated in adult zebrafish through a self-administration paradigm. Both SCRAs produced low embryonic mortality across the tested range (0.001–10 µM). CHO-4′Me-5′Br-FUBOXPYRA induced sublethal effects including pericardial edema, loss of posture, and reduced heart rate at higher concentrations, whereas ADB-INACA produced mainly impaired escape responses without significant lethality. Neither compound significantly altered social interaction in juvenile zebrafish, and CHO-4′Me-5′Br-FUBOXPYRA failed to elicit reinforcing effects in adult zebrafish, in contrast to the hydrocodone positive control. Taken together, these results indicate that both SCRAs exhibit limited cannabinoid-like effects at the tested concentrations, with only modest cardiotoxic findings for CHO-4′Me-5′Br-FUBOXPYRA. This study highlights the applicability of zebrafish assays, including Fishbook and self-administration paradigms, for investigating the toxicological and behavioral properties of novel NPS.
Heavy metal contamination, resulting from pollution, presents serious threats to aquatic species and has far-reaching consequences for ecosystem health. This study investigates the acute toxicity of copper (Cu) on grass shrimp (Palaemon spp.), a key species in North American estuaries. We exposed shrimp to a range of copper concentrations (0, 0.25, 0.50, 1.0, and 2.0 ppm) and salinities (1, 5, 10, and 20 ppt) over periods of 3, 6, 9, 12, 24, 48, 72, and 96 h. We hypothesized that exposure to 1.0 ppm Cu and 10 ppt salinity would reduce copper toxicity; but contrary to our expectations, optimal shrimp survival occurred at 20 ppt salinity and 0.25 ppm Cu. Copper solutions were prepared using CuSO₄·5H₂O, and toxicity was monitored using indicators such as mortality, abdominal curvature, discoloration, and mobility. Water quality remained stable throughout the study, with dissolved oxygen consistently at 8.675 ± 0.187 ppm, pH at 6.88 ± 0.088, and temperature at 28.75 ± 0.244 ℃. Copper toxicity increased at lower salinities, with the highest mortality and quickest onset observed at 1 ppt. Mortality was lowest at 0.25 ppm Cu, while 2.0 ppm Cu induced the highest mortality across all salinities, supporting a dose–response relationship. LC50 values increased with salinity, with the highest survival rates occurring at 20 ppt. These findings highlight the protective role of higher salinity in mitigating copper toxicity, emphasizing the need for further research on the long-term ecological consequences of copper contamination in estuarine ecosystems.
Neurotoxic pollutants are increasingly recognized as significant environmental threats, significantly impacting vertebrates’ neurological health. This is particularly due to their detrimental effects on the neurological health of vertebrates. Key contributors include heavy metals such as cadmium, arsenic, mercury, and lead, pesticides such as organophosphates, carbamates, and organochlorines, and various industrial chemicals including polychlorinated biphenyls, polybrominated diphenyl ethers, and dioxins. These substances disrupt normal neurophysiological functions by impairing neurotransmission, generating oxidative stress, provoking neuroinflammation, and initiating neuronal cell death. Such disturbances are linked to cognitive deficits, motor impairments, and abnormal neural development. Chronic exposure even at low concentrations poses serious ecological and health concerns due to the tendency of these toxins to bioaccumulate in organisms and biomagnify through food chains, ultimately threatening biodiversity and ecosystem balance. Recent studies highlight the growing use of molecular biomarkers, neuroimaging techniques, and behavioural assays to detect and assess neurotoxic impacts. Particularly alarming is the evidence that exposure during prenatal and early developmental stages may lead to persistent neurobehavioral disorders. To counteract these risks, current mitigation efforts focus on neuroprotective interventions such as antioxidant therapy and nutritional strategies, as well as on strengthening environmental regulations to reduce pollutant emissions. This review highlights the current knowledge on the mechanisms of neurotoxicity, advances in monitoring approaches, and emerging strategies for risk reduction. A comprehensive understanding of how these pollutants affect vertebrate neurophysiology is essential for shaping effective policies aimed at protecting both wildlife and human populations. Future research must adopt integrative, cross-disciplinary approaches that link toxicology, ecology, and public health to better address the complex challenges posed by environmental neurotoxicants.
The rapid industrialisation and agricultural expansion in Nigeria have intensified environmental contamination challenges and created an urgent need for advanced biotechnological interventions in toxicological research. This comprehensive review examines the integration of cutting-edge molecular biotechnology tools, AFLP-PCR, RAPD-PCR, qPCR, and Next-Generation Sequencing (NGS), into the toxicological research landscape of Nigeria. Despite the rich biodiversity and agricultural heritage in Nigeria, positioning it as a potential leader in biotechnology innovation, significant systemic barriers persist. These barriers include inadequate regulatory frameworks, limited research infrastructure, insufficient funding mechanisms, and fragmented policy implementation. The manuscript analyses global advances in molecular biotechnology applications, particularly omics technologies and CRISPR/Cas9 gene editing, and examines the transformative potential for toxicological assessments and environmental monitoring. Key findings reveal that while Nigeria has established foundational institutions such as the Nigerian Toxicology Information Centre and implemented the National Biosafety Management Agency Act, critical gaps remain in advanced molecular technology integration and capacity building. The review proposes a novel trans-disciplinary framework encompassing three strategic pillars: scientific capacity building through international collaborations and specialised training programs, comprehensive policy and regulatory reform incorporating advanced molecular technologies, and sustainable funding mechanisms aligned with the United Nations Sustainable Development Goals. The manuscript concludes that strategic implementation of this integrated framework could position Nigeria as a regional leader in biotechnology-driven environmental solutions while addressing critical public health challenges. The proposed recommendations emphasise balancing innovation with safety, establishing robust regulatory oversight, and fostering public-private partnerships to accelerate biotechnology adoption. This work contributes to the growing body of literature on biotechnology applications in developing countries and provides a roadmap for sustainable biotechnology integration in toxicological research within the Nigerian context. This review not only summarises the state of molecular biotechnology in Nigeria but also proposes a practical roadmap tailored to the country’s institutional, regulatory, and socioeconomic realities.
Soil contamination is becoming a major source of concern because of its consequences on the overall well-being of the soil ecosystem. The presence of microplastics in the environment which may co-exist with other contaminants could serve as double jeopardy to the life forms in the soils. This study investigates the effects of polypropylene (PP) microplastics and lead (Pb) contamination on soil physicochemical properties and the growth performance of Ficus benjamina, a widely cultivated ornamental plant. The soil samples used in this study were obtained from a Research Farm, Obafemi Awolowo University (OAU), Ile-Ife, Nigeria. The soil was air-dried at room temperature, crushed, and sieved using a 2 mm steel sieve to ensure homogeneity before being packed into 5 kg pots. Three sizes of polypropylene (PP) microplastics (1 mm, 2 mm, and 4 mm) and Pb applied as nitrate salts (250, 500, and 750 mg/kg) were used for artificial contamination of the soil. Thereafter, two weeks old seedlings of. Ficus benjamina were planted into experimental pots. The experiment was in a factorial combination (2 × 2 × 2) arranged in a completely randomized design with three replications. Standard methods were adopted in determining all the soil physiochemical parameters (pH, organic carbon, total nitrogen, available phosphorus, particle size distribution), Pb, Cd, exchangeable acidity and cation exchange capacity (CEC: Na⁺, K⁺, Ca²⁺, Mg²⁺). Fourier-transform Infrared Spectroscopy (FT-IR) was used to identify the presence of Microplastics (MPs) in the soil. Plant responses were evaluated based on leaf area, root length, number of roots, and biomass accumulation. Descriptive statistics and analysis of variance (ANOVA) using SPSS software with Duncan’s Multiple Range Test (DMRT) were employed in this study. The findings showed that MPs reduced the soil pH from 6.57 to 5.57. Exchangeable cations (Ca²⁺, Mg²⁺, K⁺, and Na⁺) decreased progressively with decrease in PP MP sizes while the exchangeable acidity (H⁺ and Al³⁺) increased with higher Pb concentrations regardless of the sizes of PP MP. Increased Pb concentrations significantly (p < 0.05) impaired plant growth (leaf area, root length, and total biomass). However, the combination Pb and PP MPs had more pronounced negative effects on the growth of Ficus compared to individual contaminants. Significant (p < 0.05) interactions existed between Pb contaminations and PP MPs irrespective of the Pb concentrations and microplastics sizes. Further studies on the effects of interactions between various sizes of microplastics and heavy metals on terrestrial environment should be explored.
Elevated environmental temperatures associated with climate change may potentiate heavy metal toxicity in aquatic ecosystems, yet the mechanisms underlying this interaction remain poorly characterized. Most prior studies have examined either Cadmium (Cd) toxicity or thermal stress in isolation, whereas integrated assessments of how chronic temperature elevation modulates Cd toxicokinetics and toxicodynamics are limited. In this study, adult zebrafish (Danio rerio) were chronically exposed to Cd (21 days) at control (26 °C) and elevated (34 °C) temperatures. Tissue-specific analyses revealed pronounced hepatic Cd accumulation that was significantly amplified (2.4-fold increase) at 34 °C compared to 26 °C, accompanied by enhanced metallothionein induction. Histopathological assessment documented progressive hepatocellular deterioration characterized by cytoplasmic vacuolation, sinusoidal dilation, and leukocyte infiltration—effects exacerbated at elevated temperature. Comprehensive biochemical profiling demonstrated marked dysregulation of glucose homeostasis, protein metabolism, lipid parameters, and calcium regulation, with temperature-dependent perturbation patterns. Mechanistic investigations revealed that high temperature synergistically enhanced Cd-induced oxidative stress, evidenced by elevated reactive oxygen species generation, lipid peroxidation, and compensatory antioxidant enzyme modulation. Flow cytometric analysis using Annexin V-FITC/PI and JC-1 staining confirmed that temperature amplified Cd-induced hepatocyte apoptosis through mitochondria-dependent pathways. These findings establish temperature as a critical determinant of Cd toxicokinetics and toxicodynamics in fish, providing mechanistic insights into metal–temperature interactions. While extrapolation from laboratory zebrafish to natural ecosystems must be made cautiously, this work establishes a framework for understanding how climate warming could alter metal toxicity in aquatic organisms and inform ecological risk assessment in thermally fluctuating aquatic environments under climate change scenarios.
