Nanoplastics (NPs; ≤1 µm) have been detected in human placenta, blood, lung, atherosclerotic plaque, testis, semen, olfactory bulb, and brain, shifting the field from environmental description toward mechanistic interrogation of barrier crossing. This review synthesises current evidence on NP translocation across the intestinal epithelium, the blood–brain barrier (BBB) and the placental syncytiotrophoblast. We distinguish four evidence categories throughout the review: detection, association, mechanism, and causality. We also apply model-system labels (in silico, in vitro, ex vivo, animal, and human) to every mechanistic claim, so that the strength of each statement can be read off directly. Most current studies use pristine polystyrene nanoplastics at concentrations 3–6 orders of magnitude above plausible human exposure, so the mechanistic conclusions below are hypothesis-generating for human disease rather than definitive. We propose a working conceptual framework—corona-driven barrier selectivity (CDBS)—in which the particle–corona–surface complex, rather than the bare polymer, is hypothesised to dictate which receptor and transport machinery (TfR1, LRP1, FcRn, P-gp/BCRP, caveolae) each barrier engages. CDBS is offered as a hypothesis-stage organising tool requiring experimental validation, not as an established mechanism. We outline reported transport modes, including clathrin- and caveolin-mediated endocytosis, paracellular leakage via ROS-induced tight-junction disassembly, receptor-mediated transcytosis, and the candidate olfactory route. We emphasise that pristine polystyrene-bead doses commonly exceed plausible human exposure by 3–6 orders of magnitude, that detection methods underestimate sub-micrometre particles, and that causal links between NPs and human disease remain hypothesis-generating. A research agenda built on weathered reference materials, microphysiological systems, and integrative human biomarker science is proposed.

Purpose: The objective of our study was to ascertain whether the SARS-CoV-2 virus exerts direct cytotoxic and genotoxic effects on human blood defence cells. Materials and Methods: An in vitro analysis was conducted to assess the cytotoxic and genotoxic effects of the virus using three established tests: the mitotic index (MI), micronucleus (MN), and comet assay (CA). These tests were applied to blood samples from 101 patients. The blood samples were simultaneously analyzed using the polymerase chain reaction (PCR) test. The study population included patients of all ages and genders who presented to the outpatient clinic with symptoms suggestive of a respiratory tract infection and fever. Results: The frequency of MN in the human lymphocytes of COVID-19-infected patients (1.06) was higher compared to COVID-19-negative patients (0.68). Similarly, in COVID-19-positive individuals, parameters such as tail length (3.67), tail moment (1.786), and tail intensity in the comet assay showed a significant increase compared to the negative control, indicating DNA damage. In the cytotoxicity assessment, the MI frequency of COVID-19-positive individuals (0.041) was significantly lower than that of negative controls (0.051). Gender did not influence the cyto/genotoxicity (except for tail length) in SARS-CoV-2-infected patients. Among age groups, the SARS-CoV-2 virus increased MI frequency and tail intensity only in middle-aged individuals (26–36 years). Conclusion: The SARS-CoV-2 virus has the potential to induce cytotoxic and genotoxic effects in the human lymphocytes of infected individuals.

The extensive use of herbicidal products in agriculture and forestry has raised concerns over potential adverse effects on human health and the environment. Chloroacetanilide herbicides are a group of synthetic chemicals used to control weeds in agriculture and forestry. However, so[me of their members have been characterized as possible carcinogens. The genotoxicity and carcinogenicity of two chloroacetanilide herbicides, delachlor and xylachlor, are discussed. This article proposes to use tools to predict their potential toxicities based on their chemical structure. Four software tools, Vega Hub, Toxtree, Lazar, and TEST, are used to predict the potential genotoxic and carcinogenic effects of the herbicides. Vega Hub uses QSAR models, Toxtree uses a decision tree approach, Lazar uses data mining algorithms, and TEST uses QSAR methods to estimate toxicity. The canonical Simplified Molecular Input Line Entry Specification (SMILES) systems of delachlor and xylachlor are entered into each software tool to create a prediction. The study found that delachlor and xylachlor is a class 3 highly toxic compounds with potential mutagenic and carcinogenic effects based on Toxtree and Vega Hub. Meanwhile, Lazar and TEST predicted that delachlor and xylachlor are unlikely to be mutagenic. This study to determine the toxicity of the herbicides delachlor and xylachlor has shown that the possible effects of these herbicides on health and the environment need to be further investigated. The results provide valuable insights into chloroacetanilide herbicide toxicity and help develop safer, more environmentally friendly alternatives.

Valproic acid (VPA) is among the most commonly used antiepileptic drugs in childhood and adult epilepsy. Although VPA is well tolerated, it can cause life-threatening side effects. VPA has toxic and genotoxic effects. Antioxidants can reverse drugs' toxic and genotoxic effects. Therefore, our study aimed to evaluate the antigenotoxic protective effect of quercetin (QUE) against VPA genotoxicity by in vitro comet assay analysis method. Comet assay analysis was performed in five different groups. Group I; negative control (Sterile H2O), Group II; positive control (H2O2), Group III; VPA was applied in four different dose ranges, Group IV; QUE was applied in four different dose ranges, Group V; For the simultaneous combined administration of VPA and QUE, three different doses of VPA + four different doses of QUE were administered. Low-dose administration of QUE was more effective in ameliorating the damage caused by low-dose VPA (62.5 μg/ml) administration. It is seen that the genotoxic damage caused by the application of 125 μg/ml VPA can be eliminated by QUE at all doses. It was determined that different doses of QUE exhibited a significant antigenotoxic effect against damage caused by 125 µg/mL VPA (P<0.05). In our study, the curative effect of QUE on DNA damage was determined by in vitro comet analysis. Our analysis results showed that QUE ameliorates VPA-induced genetic damage.

Global antibiotic consumption continues to rise across pediatric and adult populations, while the genotoxic consequences of host eukaryotic exposure remain less systematically characterized than the parallel problem of antimicrobial resistance. Several lines of evidence, from molecular cytogenetics, redox biology, and systems toxicology, now permit a more mechanistically resolved synthesis of antibiotic-induced genome stress than was previously possible, although a substantial fraction of this evidence is preclinical and warrants cautious clinical extrapolation. This narrative review evaluates the molecular mechanisms, cytogenetic biomarkers, and translational implications of antibiotic-induced genotoxicity, with a primary focus on six clinically prominent classes (fluoroquinolones, nitroimidazoles, aminoglycosides, macrolides, β-lactams, and tetracyclines) and a brief extension to glycopeptides and glycylcyclines. We organize the evidence around three convergent mechanistic axes rather than around individual drugs. Accumulating evidence supports three intersecting off-target axes: (i) eukaryotic topoisomerase II interference, principally documented for fluoroquinolones; (ii) mitochondrial dysfunction, reflecting the evolutionary kinship between the mitoribosome and bacterial ribosomes; and (iii) inflammation-coupled redox stress, often amplified by microbiome perturbation. These pathways converge on a common spectrum of DNA lesions—including double-strand breaks, oxidatively modified bases, replication-fork stalling, and chromosomal mis-segregation) detected by complementary assays (CBMN-Cyt, comet, γH2AX, and oxidative and mitochondrial biomarkers). Pediatric, pregnant, geriatric, and oncology populations may represent biologically distinct susceptibility strata, although direct human evidence for several of these inferences remains limited. Causal inference is constrained by infection as a confounder, frequent use of supratherapeutic in vitro concentrations, reliance on immortalized cell lines that may not recapitulate primary-cell repair capacity, inter-laboratory variability across cytogenetic assays, and a marked scarcity of pediatric and pregnancy biomonitoring data. Most existing positive signals derive from preclinical models; clinically validated long-term outcomes, particularly carcinogenic endpoints, remain inconsistently demonstrated for most antibiotic classes outside metronidazole. Antibiotic-induced genotoxicity appears to be a measurable and mechanistically tractable dimension of drug safety, though its clinical magnitude in real-world exposure scenarios requires further investigation. Integrating multi-omics, microphysiological systems, single-cell genotoxicology, and AI-assisted prediction may improve risk resolution, particularly in vulnerable populations. We argue that antimicrobial stewardship discussions should consider host genome integrity alongside resistance, while remaining mindful that the mechanistic case currently outpaces clinical-endpoint validation.