Triclosan (TCS) is a widely used antimicrobial agent found in personal care products and household cleaners. While valued since the 1960s for its ability to inhibit bacterial fatty acid synthesis, its environmental persistence, ecotoxicity, and bioaccumulative potential have raised significant global concern. The increased use of disinfectants during the COVID-19 pandemic has further exacerbated its prevalence as an aquatic pollutant. In the environment, TCS is distributed through water bodies and sediments, undergoing processes such as biodegradation and photochemical degradation. Its bioaccumulation poses a substantial threat to aquatic organisms, particularly fish. A growing body of research indicates that TCS acts as an endocrine disruptor and developmental toxicant, with documented adverse effects encompassing impaired embryonic and larval development, skeletal malformations, and induction of oxidative stress, mitochondrial dysfunction, DNA damage, and inflammatory responses. Furthermore, TCS exposure is linked to reproductive toxicity, including altered sex hormone levels and diminished reproductive capacity. This review consolidates current knowledge on the chemical properties, environmental fate, biodegradation pathways, and ecotoxicological impacts of TCS, with a specific emphasis on its multifaceted health risks to fish. The synthesis aims to provide a foundation for future research, inform environmental risk assessments, and support the development of evidence-based regulatory measures.

Screening developmental (neuro)toxicity of biocides in zebrafish embryos identifies synergistic and antagonistic neurotoxic effects of biocide mixtures.

Developmental toxicity of microplastics in human stem cells using adverse outcome pathway based integrated approaches to testing and assessment approach.

Integrated transcriptomic and biochemical analysis of β-ionone induced developmental toxicity in zebrafish embryos.

6PPD exposure reduced the melanin deposition by inhibiting tyrosinase activity in larval zebrafish.

Insights into cytotoxicity and redox modulation by the herbicide linuron and its metabolite, 3,4-dichloroaniline.

Refining the AOP for retinoid-induced teratogenicity: Insights into RAR/RXR overactivation and RXR cross-talk with retinoic acid and thyroid hormone signaling.

Dose level selection for developmental and reproductive toxicology (DART) studies: Insights from the EUROTOX 2024 satellite workshop.

Early-life PFOA exposure-induced male reproductive adverse effects are associated with the activation of the NF-κB signaling pathway: The mitigative role of inulin.

The threat is in the details - critical gap in ecotoxicological assessment of Microcystis blooms revealed by critical distinctions of genotype effects induced on Medaka fish.

Promising application of microalgal-bacterial granular sludge for 17α-ethinylestradiol removal: Effective transformation and detoxification.

Green synthesis of copper oxide nanoparticles from Calotropis gigantea of antimicrobial, antidiabetic, and toxicity evaluation in zebrafish.

Embryotoxicity analysis of anti-arrhythmia drugs amiodarone, dronedarone, and their metabolites using 3D gastruloid models.

Oral gavage is ideal for studies requiring controlled dose delivery and timing, such as repeated dosing and longitudinal analysis, as shown in this study. An anesthesia-free gavage technique was used to administer daily estradiol doses to adult zebrafish for 40 days to evaluate reproductive toxicity (developmental and reproductive toxicity one stage). Results showed that neither estradiol administration nor the gavage method caused stress or injury, but both impacted reproductive capacity in a dose-dependent manner. Females exposed to the drug exhibited a reduction in gonadosomatic index (GSI) and changes in follicle maturation, while in males, only the number of cells in the testis was reduced. The authors have no interests to disclose.

Demonstration of safety for rice bran wax and sunflower wax based on bridging to other naturally derived waxes used in foods.

Toxicity and transcriptome sequencing analyses of nanoplastics combined with acetaminophen on zebrafish bone development.

Textile dyeing wastewater, rich in recalcitrant organic compounds such as azo and anthraquinone dyes, poses significant environmental concerns. This study investigates the degradation of methyl orange (MO) using two ozone (O3) oxidation systems—O3/H2O2 and O3/K2S2O8—and analyzes the degradation products and toxicity via ESR characterization. The O3/K2S2O8 system shows a higher removal rate in the initial stage (<4 min) due to rapid ·SO4- radical generation. However, O3/H2O2 produces more ·OH radicals, leading to better overall degradation performance. The O3/K2S2O8 system is more effective for pollutants with electron-rich groups, such as Congo red and sulfamethoxazole, while O3/H2O2 performs better in natural lake water. Mechanistic studies reveal that ·O2- is the dominant oxidizing species in O3/H2O2, while ·SO4- and ·O2- dominate in O3/K2S2O8. The toxicity of degradation products is assessed, showing lower bioaccumulation and developmental toxicity in most intermediate products compared to MO. This research provides valuable insights into the use of combined ozonation-peroxidation coupling technology for effective wastewater treatment.

Pentatropis capensis is traditionally used to treat several ailments, yet its potential as a bioresource for green nanotechnology remains unexplored. Selenium nanoparticles (Se NPs) synthesized via plant-based methods are gaining attention for their biomedical and environmental applications. In this study the synthesized Se NPs were characterized using DLS,TEM, SEM with EDAX, XRD, FTIR and UV-visible spectroscopy. UV analysis revealed a characteristic absorbance at 266nm, SEM and TEM imaging demonstrated both spherical and rod-shaped nanoparticles, averaging 72nm and 12nm in size, respectively. EDAX confirmed elemental composition of Selenium (96%) and oxygen (4%). The PDI was recorded as 0.237 in DLS analysis.Antibacterial assays revealed a 16mm inhibition zone against S. aureus at 100µg/mL. Antioxidant potential was demonstrated with IC₅₀ values of 75.71µg/mL (ABTS) and 72.85µg/mL (DPPH), while TAC results highest OD value at 100µg/mL is 0.51. Anti-inflammatory activities showed IC₅₀ values of 25.19µg/mL (HRBC) and 55.55µg/mL (albumin denaturation). Cytotoxicity testing on A431 epidermoid carcinoma cells revealed an IC50 of 56.69µg/mL through MTT assay. Zebrafish embryo assays revealed developmental toxicity at concentrations ≥ 1µg/mL. Photocatalytic degradation achieved 91% methylene blue removal within 70min. These findings highlight their potential applications in nanomedicine and environmental remediation, with careful consideration of dose-dependent toxicity.

1,2-Dichloroethane (1,2-DCE), a common industrial organic solvent, enters humans primarily via inhalation, damaging the central nervous system and organs like the liver and kidneys. However, its cardiotoxicity and the multi-organ developmental toxicity in zebrafish remain unclear. This study investigated its cardiotoxicity, hepatotoxicity, and nephrotoxicity using a zebrafish model. Zebrafish embryos at 4 h after fertilization (hpf) were exposed to 0, 200, 400, or 800 μg/mL 1,2-DCE until 120 hpf, and morphological and genetic changes were assessed. As the dosage of 1,2-DCE increases, the mortality rates of zebrafish also increase (p < 0.05), and the LC50 was determined as 867.5 μg/mL. Exposure to 1,2-DCE significantly increased pericardial area, heart rate, and sinus venosus-bulbus arteriosus (SV-BA) distance, upregulated nkx2.5 and gata4, and downregulated bmp4, cmlc1, vmhc, and spaw (p < 0.05). In the exposure groups, hepatic vacuolation and atrophy were observed, accompanied by downregulated cyp1a (p < 0.05). Renal tubule length decreased dose-dependently, with downregulation of pax2a, pax8, wt1a, wt1b, and nphsl (p < 0.05) in the exposure group. These data demonstrate that 1,2-DCE induces multi-organ toxicity in zebrafish, causing structural and functional impairments in the heart, liver, and kidney. This suggests that the harmful effects of 1,2-DCE on zebrafish should be taken into account when evaluating environmental risks in the future.

Prenatal exposure to per- and polyfluoroalkyl substances (PFAS) is associated with adverse birth outcomes, yet mechanistic pathways remain unclear. We measured 32 maternal serum PFAS (including their alternatives and isomers) and quantified placental mRNA levels of insulin-like growth factor 1 (IGF1), the IGF1 receptor (IGF1R), and the insulin receptor (INSR), alongside serum IGF1 and insulin levels, in 285 mother-infant pairs from the Maoming birth cohort. We applied simple, serial, and moderated mediation models to investigate placental IGF1 signaling as a mediator of PFAS-related preterm birth (PTB), low birth weight (LBW), and small-for-gestational-age (SGA). Simple mediation showed placental IGF1R mediated 15.08%-41.18% of associations between perfluorooctanesulfonate (PFOS) isomers and PTB (odds ratios [ORs-totaleffect]: 1.06-1.10), LBW (ORs: 1.05-1.10), or SGA (ORs: 1.05-1.10). Serial mediation identified a sequential pathway: PFOS exposure correlated with altered IGF1 expression, followed by IGF1R changes, and subsequent associations with PTB (ORs: 1.01-1.02), LBW (ORs: 1.01-1.02), and SGA (ORs: 1.01-1.02). Moderated mediation highlighted serum IGF1 and insulin as modifiers of these relationships. Molecular docking demonstrated preferential binding of branched PFOS to IGF1R's ligand-binding domains. This study integrates advanced mediation frameworks and molecular evidence to demonstrate that placental IGF1 signaling mediates PFAS-related adverse birth outcomes, elucidating mechanisms of developmental toxicity.